Proclination of lower incisors: a design to maximize food penetration and minimize torque.

Human upper and lower incisors are both tilted forward in the sagittal plane. Previous theoretical and in vitro studies have investigated how proclination may help the teeth either to penetrate or to fracture food more effectively or both. We study the proclination of lower incisors in relation to efficiency and to the protection it may offer from potentially damaging torque forces. Lateral cephalographs from 57 normal human subjects were traced. In one study, a line was drawn joining the centre of the condyle to the tip of the lower incisor. The results showed the lower incisor is oriented so that it is closely parallel to the arc of a circle centred at the condyle. In another study, lines were drawn joining the tips of upper and lower incisors at different openings. Each line showed the direction of the force that must be used to bite an object held between the tips of the incisor teeth. Its direction was compared with the direction of the long axis of the lower incisor when the mandible was graphically rotated open. The results showed the long axis of the lower incisor is closest to the direction of the bite force at 12 degrees and 15 degrees of jaw openings (roughly 20-25 mm incisal separation). This is the opening where the maximum incisal force is normally produced. The findings suggest that to reduce the torque, lower incisors implanted or relocated during orthodontic treatment should be oriented parallel to the closing arc.

The effect of normal occlusal forces on fluid movement through human dentine in vitro.

Receptors inside human incisors appear to respond to stress (comparable to pressure as opposed to force) on the crown. This ability may be used to limit the stress applied to teeth or to discriminate between the hardness of objects clenched between upper and lower teeth. Here the hypothesis that these receptors are activated by fluid squeezed out of dentinal tubules when the loaded tooth is stressed was tested. Vertically compressing the crowns of extracted human teeth with loads of from 20 to 120 N, similar to those used in other studies and during natural chewing, did indeed displace fluid into the pulp. The fluid was displaced away from the crown immediately after the tooth had been loaded and moved back into the crown when the load was removed. The volume ranged from 3.5 to 22.2x10(3) pl, similar to that known to stimulate single pulpal nerve fibres. Thus, normal chewing forces could displace sufficient fluid out of dentine to excite putative mechanoreceptors somewhere inside the dentine/pulp complex.

Angiotensin and osmoreceptor inputs to the area postrema: role in long-term control of fluid homeostasis and arterial pressure.

1. The role of the area postrema (AP) in the long-term control of body fluid homeostasis and arterial pressure under conditions of increased dietary salt intake is reviewed. A model is proposed in which sympathetic nerve activity is suppressed when dietary salt is increased. It is hypothesized that the AP acts as an essential integrative site in the hind-brain for this response. 2. An essential component of the hypothesis is that basal levels of circulating angiotensin II support arterial pressure in animals consuming a normal salt diet by acting on the AP to drive sympathetic nerve activity. This hypothesis is supported by the observation that the long-term hypotensive response to losartan, the AT1 receptor antagonist, is attenuated in AP-lesioned (APx) rats. 3. The role of hepatoportal sodium receptors in signalling the AP about changes in dietary salt intake is discussed. Intragastric hypertonic saline infusion increases portal venous, but not systemic plasma, osmolality and increases Fos-like immunoreactivity in the AP, nucleus tractus solitarius and the supraoptic, paraventricular and lateral parabrachial nuclei. Other studies have shown that stimulation of these receptors decreases renal sympathetic nerve activity. 4. The hypothesis that the AP is critical in long-term control of arterial pressure and body fluid homeostasis under conditions of altered dietary salt intake was studied. The responses of arterial pressure and sodium and water balance to changes in dietary salt intake were measured in intact and APx rats. Contrary to the hypothesis, APx rats did not exhibit impaired regulation of arterial pressure or water balance. However, APx rats did demonstrate an impaired ability to excrete sodium when salt intake was elevated. 5. Based on these observations, it is concluded that the AP is important in the control of sodium balance, but not arterial pressure, when dietary salt intake is altered.

Beat-to-beat modulation of heart rate is coupled to coronary perfusion pressure in the isolated heart.

A goal of clinicians caring for heart transplant recipients has been to use heart rate variability as a noninvasive means of diagnosing graft rejection. The determinants of beat-to-beat variability in the surgically denervated heart have yet to be elucidated. We used an isolated, blood buffer-perfused porcine heart preparation to quantitatively assess the relationship between coronary perfusion and sinus node automaticity. Hearts (n = 9) were suspended in a Langendorff preparation, and heart rate (HR) fluctuations were quantified while perfusion pressure was modulated between 70/50, 80/60, 90/70, and 100/80 mmHg at 0.067 Hz. In 32 of 32 recordings, the cross spectrum of perfusion pressure vs. HR showed the largest peak centered at 0.067 Hz. In eight of nine experiments during nonpulsatile perfusion, HR accelerated as perfusion pressure was increased from 40 to 110 mmHg (mean increase 24.2 +/- 3.0 beats/min). HR increased 0.34 beats/min per mmHg increase in perfusion pressure (least squares linear regression y = -25.8 mmHg + 0.34x; r = 0.88, P < 0.0001). Administration of low- and high-dose nitroglycerin (Ntg) resulted in a modest increase in flow but produced a significant decrease in HR and blunted the response of HR to changes in perfusion pressure (HR increase 0.26 beats. min-1. mmHg-1, r = 0.87, P < 0.0001 after low-dose Ntg; 0.25 beats. min-1. mmHg-1, r = 0.78, P < 0.0001 after high-dose Ntg). These experiments suggest that sinus node discharge in the isolated perfused heart is mechanically coupled to perfusion pressure on a beat-to-beat basis.

The chronic infusion of hexamethonium and phenylephrine to effectively clamp sympathetic vasomotor tone. A novel approach.

There are several ways to assess the sympathetic nervous system (i.e. , nerve recording, sympathectomy, etc.), each of which has its own limitations. The present study was conducted to establish a standard, testable chronic ganglionic blockade protocol with a fixed level of adrenergic vasomotor tone. Rats were instrumented with radio telemetry pressure transducers and venous catheters for continuous measurement of arterial pressure and infusion of pharmacologic agents, respectively. After 3 days of control measurements, rats were infused for 9 days with a continuous dose of the ganglionic blocking agent, hexamethonium and the alpha-adrenergic agonist, phenylephrine. In this way, sympathetic tone was effectively "clamped," which maintained a normal level of arterial pressure. Control pressure between hexamethonium + phenylephrine (HEX + PE) treated rats (101+/-2 mm Hg) and saline (VEHICLE) treated rats (101+/-2 mmHg) was not different. By day 9 of the infusion, there was no difference in arterial pressure between groups (VEHICLE: 101+/-3 mm Hg, HEX + PE: 103+/-3 mm Hg) or from the control period, although heart rate was significantly less in HEX + PE rats (VEHICLE: 406+/-9 beats/min vs. HEX + PE: 343+/-6 beats/min). The effectiveness of this technique was validated by measuring cardiac baroreceptor reflex sensitivity, as well as the pressor response to the direct ganglionic stimulating agent, 1, 1-dimethyl-4-phenylpiperazinium iodide (DMPP). Compared to VEHICLE rats, HEX + PE rats showed no tachycardic response to depressor stimuli and an absence of a pressor response to DMPP. We conclude that this protocol is a useful technique to chronically, yet reversibly, block the sympathetic nervous system in experimental settings.

The area postrema modulates hypothalamic fos responses to intragastric hypertonic saline in conscious rats.

We have recently reported that an acute intragastric hypertonic saline load increases Fos immunoreactivity in several central nuclei, including the supraoptic nucleus (SON), paraventricular nucleus (PVN), nucleus of the solitary tract (NTS), area postrema (AP), and lateral parabrachial nucleus (LPBN). We have also shown that these responses are mediated by stimulation of peripheral osmoreceptors with splanchnic and vagal afferent projections. However, it is unclear whether the primary projections of peripheral osmoreceptors terminate in the NTS or the AP, both of which project to the SON and PVN. This study tested the hypothesis that efferent projections from the AP were necessary for the Fos responses in the SON, PVN, and LPBN. We examined the effect of AP lesion on the response of central Fos immunoreactivity to intragastric hypertonic saline infusion in conscious rats. Compared with sham-lesioned rats (n = 5), Fos expression in AP-lesioned rats (n = 6) was similar in the SON following the intragastric sodium load. However, in contrast to the sham group, Fos expression was significantly reduced in the PVN of AP-lesioned rats. Fos levels observed in the NTS and LPBN were similar in both groups. These results suggest that the PVN response to intragastric hypertonic saline is dependent on efferent projections from the AP. In contrast, Fos responses to this stimulus in the NTS, SON, and LPBN are independent of the activity of the AP.

Arterial baroreceptor denervation impairs long-term regulation of arterial pressure during dietary salt loading.

Experiments were performed to examine the contribution of arterial baroreceptors to long-term regulation of mean arterial pressure (MAP) during changes in dietary salt intake. Normotensive Sprague-Dawley rats were subjected to either sinoaortic denervation (SAD; n = 8) or Sham surgery (n = 6) and instrumented 1 wk later with radiotelemetry transmitters for continuous minute-to-minute monitoring of MAP and heart rate (HR) over the 8-wk protocol. Rats consumed three levels of dietary NaCl: 0.4% NaCl (week 1), 4.0% NaCl (weeks 2-4), and 8.0% NaCl (weeks 5-7). Rats returned to a 0.4% NaCl diet during the eighth week of the experiment. During week 1 (0.4% NaCl), there were no differences between Sham and SAD groups for 24-h averages of MAP or HR. However, by the third week of 4.0% NaCl, 24-h MAP was elevated significantly from baseline in SAD (10 +/- 2 mmHg) but not Sham (1 +/- 1 mmHg) rats. By the end of the third week of 8.0% NaCl diet, 24-h MAP was elevated 15 +/- 2 mmHg above control in SAD rats compared with a 4 +/- 1 mmHg increase in Sham rats (P < 0.05). Hourly analysis of the final 72 h of each level of dietary salt revealed a marked effect of dietary NaCl on MAP in SAD rats, particularly during the dark cycle. MAP increased approximately 20 and 30 mmHg in SAD rats over the 12-h dark cycle for 4.0 and 8.0% NaCl diets, respectively. In contrast, increased dietary NaCl had no effect on MAP during any phase of the light or dark period in Sham rats. These data support the hypothesis that arterial baroreceptors play a critical role in long-term regulation of MAP under conditions of altered dietary salt intake. Finally, hourly analysis of MAP revealed that the majority of the hypertensive response to increased NaCl occurs during the dark cycle in SAD rats. Hence, previous investigations may have underestimated the magnitude of the hypertensive response to increased dietary NaCl in animals with baroreceptor dysfunction.

Effects on human maximum bite force of biting on a softer or harder object.

A recent study concluded that the pulps of human incisor teeth may contain mechanoreceptors. These provide the input for a protective mechanism that reflexly limits the maximum bite force by monitoring the stress on compressed dentine. In separate experiments it was later shown that individuals can accurately detect whether they are biting on a harder or softer surface when it seemed that the only receptors which could have detected the difference must have been in the tooth pulps. Thus, pulpal mechanoreceptors may be used subconsciously to limit the maximum bite force and consciously to detect differences in hardness. If these conclusions are correct the maximum bite force should be larger when incising on a soft (rubber) surface than on a hard (acrylic) surface because when the teeth sink into the rubber the bite force is spread over a larger area, thereby reducing the local stress. A reduction in stress allows an increase in bite force. But if the tooth were previously covered with an acrylic crown, which would already reduce the stress by distributing the bite force over a large area of the incisor crown, there would be little or no difference in the maximum bite force whether biting on rubber or acrylic. The results of experiments on 15 participants confirm these predictions and support the hypothesis that the pulps of human incisors contain high-threshold mechanoreceptors.

Relationship between growth and the pattern of tooth initiation in alligator embryos.

The temporal and spatial patterns in which teeth are initiated in the growing jaws of embryos are constant for a species but different for different species. The sources of the patterns have been explained in two ways. First, they are the outcome of reactions between molecules created at stationary targets and those which diffuse through embryonic tissues (e.g., Edmund, 1960). Second, Osborn (1978) supposed that the patterns mirror the way a (mixed) population of parent cells, the tooth clone, grows. Westergaard and Ferguson (1986, 1987, 1990) concluded, from their observations of the sequence of tooth initiation in alligators, that the complicated sequences in which 20 teeth are initiated in each tooth quadrant could not be explained by jaw growth. The present study attempts to refute this criticism by means of measurements made from the raw data published by Westergaard and Ferguson. These data reveal that new teeth, here called primary teeth, are added at a constant rate at the back of the jaw. Interstitial growth of the cells between primary teeth creates space for secondary teeth in secondary regions. The secondary regions increase in length exponentially with time. The sequence in which teeth are initiated in the growing secondary regions was found to be the same in every part of the upper and lower jaws. It was accurately reproduced by a computer program based on a linear contraction rate of inhibitory zones and exponential growth of secondary regions. The results suggest that the posterior progress zone in alligator embryos grows about 125 microm a day. Newly initiated tooth germs are surrounded by an inhibitory zone about 250 microm in diameter. These zones contract from 20 to 30 microm a day until they are about 170 microm in diameter. The sequences in which tooth positions are initiated in embryos may be more the result of the pattern in which cells escape from molecules that inhibit induction rather than the pattern in which cells create molecules that initiate induction.

The area postrema does not modulate the long-term salt sensitivity of arterial pressure.

The hindbrain circumventricular organ, the area postrema (AP), receives multiple signals linked to body fluid homeostasis. In addition to baroreceptor input, AP cells contain receptors for ANG II, vasopressin, and atrial natriuretic peptide. Hence, it has been proposed that the AP is critical in long-term adjustments in sympathetic outflow in response to changes in dietary NaCl. The present study was designed to test the hypothesis that long-term control of arterial pressure over a range of dietary NaCl requires an intact AP. Male Sprague-Dawley rats were randomly selected for lesion of the AP (APx) or sham lesion. Three months later, rats were instrumented with radiotelemetry transmitters for continuous monitoring of mean arterial pressure (MAP) and heart rate and were placed in individual metabolic cages. Rats were given 1 wk postoperative recovery. The dietary salt protocol consisted of a 7-day period of 1.0% NaCl (control), 14 days of 4.0% NaCl (high), 7 days of 1.0% NaCl, and finally 14 days of 0.1% NaCl (low). The results are reported as the average arterial pressure observed on the last day of the given dietary salt period: APx (n = 7) 114 +/- 2 (1.0%), 110 +/- 3 (4.0%), 110 +/- 3 (1.0%), and 114 +/- 4 (0.1%) mmHg; sham (n = 6) 115 +/- 2 (1.0%), 114 +/- 3 (4.0%), 111 +/- 3 (1. 0%), and 113 +/- 2 (0.1%) mmHg. Neither group of rats demonstrated significant changes in MAP throughout the entire dietary salt protocol. Furthermore, no significant differences in MAP were detected between groups throughout the protocol. All lesions were histologically verified. These results suggest that the area postrema plays no role in long-term control of arterial pressure during chronic changes in dietary salt.

Endogenous ANG II supports lumbar sympathetic activity in conscious sodium-deprived rats: role of area postrema.

This study tests the hypothesis that the area postrema (AP) is necessary for endogenous ANG II to chronically maintain lumbar sympathetic nerve activity (LSNA) and heart rate (HR) in conscious sodium-deprived rats. The effect of the ANG II type 1-receptor antagonist, losartan, on LSNA and HR was determined in rats that were either AP lesioned (APX) or sham lesioned. The sham rats were divided into groups, with (SFR) or without (SAL) food restriction, to control for the decreased food intake of APX rats. Before losartan, basal mean arterial pressure (MAP), HR, and baroreflex control of LSNA and HR were similar between groups, with the exception of lower maximal reflex LSNA and higher maximal gain of the HR-MAP curve in APX rats. In all groups, losartan similarly shifted (P < 0.01) the LSNA-MAP curve to the left without altering maximal gain. Losartan also decreased (P < 0.05) minimal LSNA in all groups, and suppressed (P < 0.01) maximal LSNA (% of control) in SFR (240 +/- 13 to 205 +/- 15) and SAL (231 +/- 21 to 197 +/- 26) but not APX (193 +/- 10 to 185 +/- 8) rats. In general, losartan similarly shifted the HR-MAP curve to a lower MAP in all groups. The results suggest that the AP is not necessary for endogenous ANG II to chronically support LSNA and HR at basal and elevated MAP levels in sodium-deprived rats. However, the AP is required for endogenous ANG II to increase maximal reflex LSNA at low MAP levels.

Hepatic denervation chronically elevates arterial pressure in Wistar-Kyoto rats.

Several lines of evidence suggest that peripheral osmoreceptors respond to alterations in dietary NaCl by adjusting renal sympathetic nerve activity, but the impact of this reflex on the long-term regulation of mean arterial pressure (MAP) remains unclear. The present study tested the hypothesis that denervation of peripheral osmoreceptors elevates arterial pressure and induces NaCl-sensitive hypertension in normotensive rats. Hepatic denervated and sham-operated Wistar-Kyoto rats were instrumented with telemetry probes for continuous monitoring of MAP and heart rate. After 1 week on a basal (0.6%) NaCl diet, the rats were fed a high (8%) NaCl diet for 2 weeks. On the basal NaCl diet, MAP in hepatic denervated rats was 15+/-1 mm Hg higher than in sham-operated rats. The high NaCl diet did not significantly increase MAP above baseline levels in either denervated or sham-operated rats, but the amplitude of the 24-hour rhythm of arterial pressure increased significantly more in the denervated than in the sham-operated rats. In a second experiment, two similar groups of rats were fed a very low (0.05%) NaCl diet. Mean arterial pressure of the denervated group was significantly higher than that of the sham-operated rats on either the basal or the very low NaCl diet, but the very low NaCl diet did not affect arterial pressure in either group. These results suggest that in the rat, although hepatic osmoreceptors contribute to long-term arterial pressure regulation, they contribute much less to dietary NaCl-induced changes in arterial pressure.

Respiratory sinus dysrhythmia persists in transplanted human hearts following autonomic blockade.

1. The present study was performed to test whether beat-to-beat cardiovascular control in cardiac allograft recipients resides in cholinergic and/or adrenergic nerves that are intrinsic to the heart. 2. Heart rate (HR) fluctuations synchronous with respiration during spontaneous, double tidal volume and metronome-synchronized breathing were quantified in 13 human heart transplant recipients. We also examined the effects of sequential cholinergic and beta-adrenoceptor (combined) autonomic blockade on respiratory sinus arrhythmia (RSA). We computed RSA amplitude and the correlation between respiration and changes in HR (cardiopulmonary synchronization; CPS). Group means were compared using repeated-measures analysis of variance. Transplant recipients served as their own controls. 3. In the basal state, moderate RSA amplitude and CPS were observed. During cholinergic and combined blockade, we observed no significant change in RSA amplitude, whereas CPS increased significantly during combined blockade (P < 0.05). The amplitude of RSA increased during respiration at double baseline tidal volume, but not at any of the other breathing manoeuvres (P < 0.01). In contrast, CPS increased significantly during both patterned breathing manoeuvres. No significant correlation was seen between mean right atrial pressure and RSA amplitude. In 23% of subjects with low CPS, HR oscillated with arterial pressure. These oscillations were independent of respiration. During all three patterns of respiration, a significant inverse correlation was observed between CPS and pulse pressure (r = -0.53 to -0.73). Thus, as the amplitude of pulse pressure increased, respiration accounted for a smaller percentage of HR variation. 4. In conclusion, RSA persists and the magnitude of CPS increases following combined autonomic blockade. These studies suggest that while RSA after cardiac transplantation is not cholinergically or adrenergically mediated, it may be related to mechanical stretch of the sinus node caused by changes in intrathoracic pressure and perfusion pressure.

Splanchnic and vagal denervation attenuate central Fos but not AVP responses to intragastric salt in rats.

We have recently reported that an acute intragastric hypertonic saline load increases plasma arginine vasopressin (PAVP) and Fos immunoreactivity in several central nuclei, including the supraoptic nucleus (SON), paraventricular nucleus (PVN), nucleus of the solitary tract (NTS), area postrema (AP), and lateral parabrachial nucleus (LPBN). We hypothesized that these responses are mediated by stimulation of peripheral osmoreceptors with splanchnic and/or vagal afferent projections. To test this hypothesis, we examined the effect of bilateral subdiaphragmatic vagotomy and bilateral splanchnic denervation on the PAVP and Fos immunoreactivity responses to intragastric hypertonic saline infusion in awake rats. Compared with responses in sham rats, Fos immunoreactivity responses were significantly reduced in vagotomized rats in the AP, SON, and PVN, whereas normal Fos levels were observed in the LPBN. However, vagotomized rats exhibited a normal increase in PAVP. Splanchnic-denervated rats also exhibited similar changes in PAVP in response to intragastric hypertonic saline compared with sham-denervated rats, and no differences were observed in Fos immunoreactivity in the LPBN, SON, and PVN compared with sham rats. However, splanchnic-denervated rats were observed to have significantly lower Fos staining in the NTS and AP compared with sham rats. The inability of splanchnic or vagal denervation alone to block the PAVP response to intragastric hypertonic saline suggests that either peripheral osmoreceptors project via both splanchnic and vagal afferents to mediate AVP release or that the observed response of PAVP is due to the activation of central osmoreceptors in the absence of measurable changes in plasma osmolality.

Discrimination of hardness by human teeth apparently not involving periodontal receptors.

Periodontal receptors are generally thought to provide the input used to detect the hardness of food. Whether hardness can be sensed by teeth without periodontal assistance was tested here. A bite-force transducer was sandwiched between a hard acrylic strip on one side and rubber on the other side, both sides being covered with masking tape to prevent participants from sensing a difference in touch. Participants were asked to increase the bite force on the sandwich until, and if, they could detect which material, hard acrylic or rubber, was on the upper side. The positions of acrylic and rubber were randomly chosen. Fifteen participants each undertook three separate experiments each involving 10 tests using (1) bare incisors, (2) incisors capped with acrylic and (3) bare molars. The accuracy of responses and the direction and magnitude of bite forces were recorded. Participants most correctly detected the surfaces with bare incisors (91% correct, SD = 11%). Performance was significantly worse with capped incisors (79%, SD = 19%) (p < 0.01) and worse still with molars (57%, SD = 24%) (p < 0.001). The detection threshold using bare incisors was increased in 14 out of the 15 participants when the incisors were capped, but the increase was statistically significant (0.002 < p < 0.01) in only six of them. The molar threshold was significantly increased (0.002 < p < 0.01) in comparison with the bare incisor threshold in 12 of 15 participants. There was no correlation between bite direction and the position of the rubber. Because in each trial the upper and lower periodontal input was the same whether the rubber was on the top or on the bottom, it was concluded that the periodontal ligament was not involved. The observed discrimination was probably based on a difference in the pressure on the upper and lower teeth. Incisal edges sank more deeply into the rubber and reduced the pressure (force/unit area) on a tooth crown.

Area postrema lesion attenuates the long-term hypotensive effects of losartan in salt-replete rats.

We reported that the AT1 receptor antagonist losartan decreases arterial pressure in sodium-replete rats and that this response is attenuated in area postrema-lesioned (APx) rats (J. P. Collister, B. J. Hornfeldt, and J. W. Osborn. Hypertension 27: 598-606, 1996). In that study, food intake for the 3-wk period after sham lesion was restricted to that observed in APx rats. Food-restricted sham rats had lower arterial pressures and attenuated responses to losartan compared with control rats fed ad libitum. The present study examined whether these differences persisted months, rather than weeks after APx or sham lesions. Losartan was administered for 10 days to APx and two groups of sham rats 3 mo after APx or sham surgery. The first sham group was food restricted (SFR) for 3 wk after surgery, whereas the second sham group was allowed ad libitum (SAL) access to food. By day 8 of losartan administration, both sham groups demonstrated a marked hypotension (SFR: -38 +/- 4; SAL: -33 +/- 4 mmHg). This response was attenuated (P < 0.05) on the same day in APx rats (-17 +/- 3 mmHg). This trend continued throughout days 9 and 10. Because both sham groups responded similarly to losartan (yet significantly different from APx rats), these results demonstrate that transient decreases in food intake do not affect the response to losartan if rats are allowed an adequate recovery period. We conclude that the area postrema mediates part of the long-term hypotensive effects of AT1 receptor blockade in the conscious rat.

Intragastric hypertonic saline increases vasopressin and central Fos immunoreactivity in conscious rats.

Although experimental evidence supports peripheral osmoreceptor modulation of arginine vasopressin (AVP) release, a local osmotic signal required for osmoreceptor activation has yet to be identified using physiological sodium loads. Additionally, the central pathway involved in peripheral control of AVP has not been clearly established. Experiments were conducted to examine the effect of intragastric saline on portal venous osmolarity, plasma AVP (P(AVP)), and Fos immunoreactivity. In anesthetized rats, intragastric infusion (2.9 ml) of hypertonic (600 mosM) saline significantly increased portal venous osmolarity while systemic blood osmolarity remained constant. In conscious rats, intragastric hypertonic saline significantly elevated P(AVP) (3.6 +/- 1.3 to 5.8 +/- 1.9 pg/ml), whereas no changes were observed in plasma osmolarity in either the isotonic (296.2 +/- 1.4 to 297.6 +/- 1.1 mosM) or hypertonic (291.7 +/- 1.7 to 291.4 +/- 1.8 mosM) group. Finally, intragastric hypertonic saline significantly increased Fos immunoreactivity in the nucleus of the solitary tract (NTS), area postrema (AP), lateral parabrachial nucleus (LPBN), supraoptic nucleus (SON), and paraventricular nucleus (PVN). These results indicate that intragastric hypertonic saline produces a portal venous osmotic signal that triggers peripheral osmoreceptors to stimulate AVP release while activating the NTS, AP, and LPBN in addition to the SON and PVN.

The sympathetic nervous system and long-term regulation of arterial pressure: what are the critical questions?

1. The role of the sympathetic nervous system in long-term control of arterial pressure remains unclear despite decades of intense research. 2. Previous studies have shown that denervation of arterial baroreceptors does not chronically increase arterial pressure. As baroreceptors are thought to provide the primary 'error signal' to the autonomic nervous system, this has been interpreted as evidence against neural control of arterial pressure over long periods of time. 3. The possibility that other 'error signals' are important in the long-term control of sympathetic activity (and arterial pressure) is introduced. 4. The following 'Critical Questions' are presented for subsequent discussion: (i) is the sympathetic nervous system a 'major player' in the long-term control of arterial pressure; (ii) why doesn't arterial pressure remain at hypertensive levels after arterial baroreceptor denervation; and (iii) which 'error signals' are most important in the long-term control of sympathetic outflow?

Hormones as long-term error signals for the sympathetic nervous system: importance of a new perspective.

1. A hormonal-sympathetic reflex model for long-term control of arterial pressure is presented. It is hypothesized that the hormonal-sympathetic reflex regulates arterial pressure during chronic dietary salt loading by decreasing sympathetic tone. This sympathetic response is mediated by an increase in plasma vasopressin (AVP) and a decrease in plasma angiotensin (AngII). 2. Three new models of neurogenic salt-dependent hypertension are presented. All models are theoretically based on an impaired hormonal-sympathetic reflex. 3. In the first model, sympathetic responsiveness is 'clamped' by long-term alpha-adrenergic blockade with prazosin. Prazosin treated rats exhibit marked salt-dependent hypertension despite normal suppression of the renin-angiotensin system. 4. In the second model, the ability of the central nervous system to respond to salt-induced changes in AVP and AngII concentrations was prevented by long-term administration of antagonists selective for the AVP-V1 and AT1. This 'clamp' of the afferent hormonal signal resulted in salt-dependent hypertension identical in magnitude to that observed in prazosin treated rats. 5. In the third model, the long-term arterial pressure responses to increasing dietary salt were examined in sino-aortic denervated (SAD) rats. SAD rats exhibited salt-dependent hypertension, of lesser magnitude than that observed with 'clamped' afferent and efferent pathways of the hormonal-sympathetic reflex. 6. A primary role for hormonal 'error signals' is presented and the impact this perspective has on past and future investigations of central mechanisms of long-term arterial pressure regulation is discussed.

Effect of jaw opening on the direction and magnitude of human incisal bite forces.

The maximum bite force (MBF) appears to be different when measured at different jaw openings (e.g., Manns et al., 1979; Mackenna and Turker, 1983; Lindauer et al., 1993). However, the change could be related to a change in the bite direction. We have measured the MBF on incisors and its direction in three dimensions for different jaw openings in ten subjects. Surface electromyography (EMG) of anterior temporalis and masseter muscles on both sides was recorded simultaneously. The results showed that: (1) the average %MBF increased as the jaw was opened, reached a plateau between 14 and 28 mm of incisal separation, and then decreased at wider jaw openings; (2) the initial forward bite direction with respect to the mandibular occlusal plane shifted backwards during jaw opening; and (3) the activity of the masseter muscles declined and that of the temporalis muscles was largely unchanged, resulting in an increase of the ratio between the activity in temporalis and masseter muscles (T/M). There was a significant correlation between bite direction and jaw opening (r = 0.51, p < 0.001) and between T/M ratio and jaw opening (r = 0.56, p < 0.001). Based on comparative data, we have calculated sarcomere lengths while the jaw is opened and hypothesize that the average %MBF reaches its maximum when the sarcomeres in the masseter muscle achieve their optimum length. A plateau continues during further jaw opening, until those of temporalis reach their optimum length while those of masseter lengthen beyond their optimum length. The change in bite direction was attributed to either a change in the relation between upper and lower bite points as the jaw was opened or the gradual decline of masseter activity at larger openings.