Systolic pressure predicts plasma vasopressin responses to hemorrhage and vena caval constriction in dogs.

We have proposed that the reflex increase in arginine vasopressin (AVP) secretion in response to hypovolemia is due to arterial baroreceptor unloading. If arterial pressure is the key to the mechanism, the slope relating plasma AVP to arterial pressure should be the same in response to hemorrhage, a model of true hypovolemia, and in response to thoracic inferior vena caval constriction (IVCC), a model of central hypovolemia. We tested this hypothesis in conscious, chronically instrumented dogs (n = 8). The mean coefficient of determination (r(2)) values obtained from the individual regressions of log AVP onto systolic pressure (SP) and mean arterial pressure (MAP) in response to hemorrhage were 0.953 +/- 0.009 and 0.845 +/- 0.047, respectively. Paired comparisons indicated a significant difference between the means (P < 0.05), hence, SP was used in subsequent analyses. The mean slopes relating the log of plasma AVP to SP in response to hemorrhage and IVCC were -0.034 +/- 0.003 and -0.032 +/- 0.002, respectively, and the means were not significantly different (P = 0.7). The slopes were not altered when the experiments were repeated during acute blockade of cardiac receptors by intrapericardial procaine. Finally, sinoaortic denervation (n = 4) markedly reduced the slope in both the hemorrhage and IVCC treatments. We conclude that baroreceptors monitoring arterial pressure provide the principal reflex control of AVP secretion in response to hypovolemia.

Arterial baroreceptors control plasma vasopressin responses to graded hypotension in conscious dogs.

We studied the role of cardiac and arterial baroreceptors in the reflex control of arginine vasopressin (AVP) and renin secretion during graded hypotension in conscious dogs. The dogs were prepared with Silastic cuffs on the thoracic inferior vena cava and catheters in the pericardial space. Each experiment consisted of a control period followed by four periods of inferior vena caval constriction, during which mean arterial pressure (MAP) was reduced in increments of approximately 10 mmHg. The hormonal responses were measured in five dogs under four treatment conditions: 1) intact, 2) acute cardiac denervation (CD) by intrapericardial infusion of procaine, 3) after sinoaortic denervation (SAD), and 4) during combined SAD+CD. The individual slopes relating MAP to plasma AVP and plasma renin activity (PRA) were used to compare the treatment effects using a 2 x 2 factorial analysis. There was a significant (P < 0.01) effect of SAD on the slope relating plasma AVP to MAP but no effect of CD and no SAD x CD interaction. In contrast, the slope relating PRA and MAP was increased (P < 0.05) by SAD but was not affected by CD. These results support the hypothesis that stimulation of AVP secretion in response to graded hypotension is primarily driven by unloading arterial baroreceptors in the dog.

Is the Gauer-Henry reflex important for immersion diuresis in men?

BACKGROUND: This study examines the relationship between the threshold for plasma vasopressin concentration [PVP] responses and diuresis (Gauer-Henry reflex), and tests the hypothesis that water intake would not influence diuresis. METHODS: Eight men (19-25 yr) underwent four treatments: euhydration in air (Eu-air), euhydration in water immersion (Eu-H2O), and with prior 3.6% hypohydration in air (Hypo-air), and hypohydration in immersion (Hypo-H2O). Ad libitum drinking was allowed during the 3-h experimental and 1-h recovery periods. RESULTS: Drinking was greatest during the first 10 min: 3.5 ml x kg(-1) with Hypo-air (450 ml x 3 h(-1)) and only 1.7 ml x kg(-1) (p < 0.05) with Hypo-H2O (235 ml x 3 h(-1)). At 1 h, concomitant [PVP] decreased from a control level of 6.6+/-1.5 to 4.0+/-1 .0 pg x ml(-1) (delta = 2.6 pg x ml(-1), p < 0.05) with Hypo-air, and from 5.9+/-0.6 to 2.3+/-0.2 pg x ml(-1) (delta = 3.6 pg x ml(-1), p < 0.05) with Hypo-H2O. Urine flow was unchanged from control level (<1.0 ml x min(-1)) with Hypo-air, Hypo-H2O, and Eu-air, but increased to 4-5 ml x min(-1) with Eu-H2O. Neither water intake volume nor urine flow was related to the magnitude of [PVP] depression. Regression of Uosm/Posm ratio on [PVP] and urine flow indicated that [PVP] above 2 pg x ml(-1) did not affect urine flow. Thus, ad libitum water intake in previously hypohydrated subjects did not affect urine flow or the decrease in [PVP]. The threshold [PVP] to initiate significant diuresis was about 2 pg x ml(-1), and significant diuresis can occur with no change in [PVP] maintained at about 1 pg x ml(-1) during immersion in euhydrated subjects. CONCLUSIONS: Thus, it appears that the Gauer-Henry reflex is not the major mechanism for immersion-induced diuresis. Clearly, other diuretic factors are also involved.

Arterial baroreceptors control blood pressure and vasopressin responses to hemorrhage in conscious dogs.

The goal of this study was to determine the role of arterial baroreceptors in the reflex control of arginine vasopressin (AVP), renin, and cortisol secretion in response to a 30-ml/kg hemorrhage in conscious dogs. The hormonal responses were measured in six dogs under four treatment conditions: 1) intact, 2) acute cardiac denervation (CD) by intrapericardial infusion of procaine, 3) after sinoaortic denervation (SAD), and 4) during combined SAD + CD. In the intact condition, mean arterial pressure (MAP) was maintained at control levels until blood loss reached 20 ml/kg and the absolute magnitude of the fall at 30 ml/kg was 35 +/- 10 mmHg. Similar responses were obtained during acute CD. In contrast, MAP fell earlier (at 5 ml/kg, P < 0.05) and to much lower levels in both the SAD and SAD + CD conditions. The individual slopes relating systolic pressure to plasma AVP, renin activity (PRA), and cortisol were used to compare the treatment effects using a 2 x 2 factorial analysis. There was a significant (P < 0.01) effect of SAD on the slope relating AVP to systolic pressure but no effect of CD and no SAD x CD interaction. In contrast, there was no effect of either SAD or CD on the relationship between PRA or plasma cortisol and systolic pressure. These results indicate that maintenance of blood pressure and the normal pattern of AVP secretion during hemorrhage depend on intact arterial baroreceptor reflexes.

Hemodynamic and hormonal responses to hemorrhage in conscious rabbits at mid- and late gestation.

This study tests the hypothesis that conscious rabbits late in pregnancy (P), but not at midgestation (MP), are less able to maintain arterial pressure during hemorrhage. Blood volume (BV) was elevated (P < 0.05) by an average of 13 +/- 4 (MP) and 35 +/- 3% (P). Rabbits were bled in both the nonpregnant (NP) and P state at 2% of the initial BV per minute. The hemorrhage was stopped after arterial pressure decreased. In NP rabbits, arterial pressure was well maintained near control pressures of 70 +/- 2 mmHg until 38 +/- 2% of the initial BV was removed and then rapidly fell to reach a nadir at 35 +/- 2 mmHg. In contrast, in P rabbits, basal arterial pressure was lower (61 +/- 2 mmHg; P < 0.05) and gradually decreased to below control after <25% of the initial BV was removed. Moreover, the rapid hypotensive phase was triggered with a lower percent BV removal (33 +/- 2%; P < 0.05). Basal heart rate was higher during P (149 +/- 5 vs. 189 +/- 9 beats/min; P < 0.05), and reflex increases were delayed. The slope of the relationship between arterial pressure and vasopressin was not modified during P, although the line was shifted to a lower pressure (P < 0.05). Larger increases in plasma renin activity and ANG II concentration were produced during hemorrhage in P rabbits. In contrast, no differences in the changes in arterial pressure, heart rate, and vasopressin were found between NP and MP rabbits during hemorrhage, although increases in renin and ANG II were greater at MP (P < 0.05). In summary, although P conscious rabbits are less able to maintain blood pressure during hemorrhage, this change is not evident at MP. These data suggest that the factors that mediate the P-induced alterations in arterial pressure regulation are not operative until late in gestation.

Plasma volume expansion with oral fluids in hypohydrated men at rest and during exercise.

BACKGROUND: The purpose for this study was to evaluate various carbohydrate (CHO)-electrolyte fluid formulations for consumption by astronauts to maintain or restore their plasma volume (PV) and total body water (TBW) during and after extravehicular activity (exercise experiment, EE) and for a few hours before reentry and immediately after landing (rest experiment RE). HYPOTHESIS: That fluid formulation electrolyte content would be more important than osmotic (Osm) content for increasing or maintaining PV during the RE and EE. METHODS: In the RE, 5 healthy men (23-44 yr), previously dehydrated for 24 h, drank 6 fluid formulations (Water, 19.6 Na, 157 Na, 19.6 Na + glucose, and the prepared drinks Performances and Power)--one each at weekly intervals, and then sat for 70 min. In the EE, four healthy 24-h dehydrated men (30-46 yr) exercised for 70 min supine on a cycle ergometer (load = 71 +/- 1% peak VO2). RESULTS: Rest: Subjects who consumed formulations with total Osm concentrations nearer the normal range (157 Na - 270 mOsm x kg(-1), Performance with 19.6 mEq x L(-1) Na - 380 mOsm, and to some extent Power with 23.5 mEq x L(-1) Na - 390 mOsm) had the greater increases in PV; intake of drink 157 Na, with the largest Na content, induced the greatest hypervolemia of 7.6% (p < 0.05). The various additional ions, in addition to 19.6 Na, probably contributed to the 4.6% (p < 0.05) hypervolemia with Performance. Water was not effective. Exercise: Stabilization of PV between 15-70 min was not related to drink total CHO, Na or Osm content. Performance and 157 Na were no more effective than 19.6 Na or 19.6 Na + glu for PV stabilization. Water was the least effective. Regulatory mechanisms controlling PV during exercise appear to be independent of oral fluid formulation Osm-electrolyte content. CONCLUSIONS: Drink cation (sodium) content is more important that its total osmotic content for increasing plasma volume at rest. Fluid formulations with greater hypervolemic action in resting subjects may not be as effective during exercise; therefore different formulations for use during exercise appear to be necessary.

Reduction of pituitary AVP and OT contents in rats following spaceflight.

BACKGROUND: Responses of pituitary concentrations of vasopressin (AVP) and oxytocin (OT) during spaceflight have been variable, possibly due to differences in flight conditions or in age and strain of flight animals. METHODS: We reviewed findings of three space-flights of varying flight and recovery durations in which rats of different ages and strains were used. Male rats ranging in weight from 248-396 g were flown in space for 7-14 d. Flight animals were then compared with vivarium controls and synchronous controls. Parallel ground-based studies (hypergravity and simulated hypogravity) were conducted. RESULTS: Pituitary content of AVP was significantly (p < or = 0.05) decreased by spaceflight (6.3 +/- 0.3 micrograms.mg-1 protein in flight vs. 8.3 +/- 0.5 micrograms.mg-1 protein in vivarium). OT content was also reduced during spaceflight (4.3 +/- 0.2 micrograms.mg-1 protein in flight vs. 6.1 +/- 0.3 micrograms.mg-1 protein in vivarium). Vivarium and synchronous control rats showed no difference in pituitary contents. Flight duration or recovery times did not appear to influence pituitary hormone contents. Strain of rat had an effect on content but not on responses to spaceflight. Age of animals confounded the response to spaceflight: pituitary contents of AVP and OT were not altered in young animals (< or = 60 d old). Hindlimb suspended animals showed no difference in AVP but OT content was decreased. Ground-based exposure to hypergravity (2 G) did not alter content of AVP or OT in young animals. CONCLUSIONS: Decreases in pituitary content of AVP and OT with spaceflight may be due to a variety of factors unique to the microgravity environment. Differences between studies may be due in part to differences in size and age of rats used.

Mechanisms for vasopressin effects on intraocular pressure in anesthetized rats.

Continuous intracameral infusions of a balanced salt solution (0.175 microliter min-1) have been reported to raise intraocular pressure (IOP) in anesthetized rats. Palm et al. (1995) previously reported that this effect was attenuated significantly by inclusion of arginine-vasopressin (AVP, 10 ng 0.175 microliter-1) in the infusate. This study used experimental and computer simulation methods to investigate factors underlying these changes in IOP. First, constant intracameral infusions of artificial cerebrospinal fluid (aCSF) at different fixed rates (0.049-0.35 microliter min-1) were used to estimate the outflow resistance. Secondly, IOP responses were measured during an 2 hr intracameral infusion of either aCSF or AVP that was the sum of a small constant component (0.05 microliter min-1) and a larger periodic component (0.25 microliter min-1, cycling for 4 min on, then 4 min off); the mean infusion rate was 0.175 microliter min-1. As shown previously for 0.175 microliter min-1 constant infusions, the periodic aCSF infusion induced a significant rise in IOP that was attenuated by AVP administration. Complex demodulation analysis and the estimated gain parameter of a second order transfer function fit to the periodic responses indicated that outflow resistance increased significantly during the infusions in both aCSF and AVP groups, but that the indices of resistance did not differ significantly between aCSF and AVP infused eyes. This finding implies that changes in outflow resistance do not explain the difference in IOP responses to intracameral aCSF and AVP. The two responses differed significantly, though, in damping factors, such that the aCSF responses were considerably more underdamped than the AVP responses. It is hypothesized that aCSF-induced increase in IOP reflects both (1) a small component reflecting increased outflow resistance and (2) a larger non-resistive component. Since the non-resistive component is insensitive to pretreatment with acetazolamide, it is suggested that the aCSF-induced elevation in IOP reflects primarily vascular perfusion changes that are reduced by local vasoconstrictor actions of AVP. The latter mechanism likely maintains vascular perfusion of the globe when intraocular hypertension develops.

Drinking-induced plasma vasopressin and norepinephrine changes in dehydrated humans.

After 24-h water deprivation, five men (23-41 yr; 78 +/- 3.6 kg) consumed, within 4.0-6.2 min, 12 mL/kg of one of six fluid formulations (16.5 C) once a week over a period of 6 weeks: water, hypotonic saline (0.045% Na+), isotonic saline (0.36% Na+), hypertonic glucose (9.7% glucose), and two commercial mildly hypertonic 9.7% carbohydrate drinks. Blood samples were drawn 5 min before and 3, 9, 15, 30, and 70 min after completion of drinking. Ingestion induced no significant change in plasma Na+, K+, osmotic, or protein concentrations; blood pressure; or heart rate. Plasma volume (PV) was increased (P < 0.05) between 30-70 min with isotonic saline and the two commercial drinks. Ingestion induced a decrease in plasma AVP (PAVP) at 3 min, which was maximal (P < 0.05) at 15 min with all drinks. Thus, the act of drinking, independent of the composition or osmolality of the fluid absorbed, leads to a prompt inhibition of PAVP secretion in man. With the exception of rehydration with isotonic saline, this prompt response was followed by a long lasting inhibition of PAVP. There was no change in PRA, plasma aldosterone, atrial natriuretic peptide, or epinephrine, but an increase in plasma norepinephrine occurred immediately after ingestion, which suggests, like that for PAVP depression, a drinking-stimulated neural mechanism.

Effects of angiotensin, vasopressin and atrial natriuretic peptide on intraocular pressure in anesthetized rats.

The effects of atrial natriuretic peptide (ANP), vasopressin (AVP) and angiotensin (ANG) on blood and intraocular pressures of pentobarbital anesthetized rats were evaluated following intravenous, intracerebroventricular or anterior chamber routes of administration. Central injections did not affect intraocular pressure. Equipressor intravenous infusions of ANG raised, whereas AVP decreased, intraocular pressure. Direct infusions of a balanced salt solution (0.175 microliter/min) raised intraocular pressure between 30 and 60 min. Adding ANG or ANP slightly reduced this solvent effect but AVP was markedly inhibitory. An AVP-V1 receptor antagonist reversed the blunting of the solvent-induced rise by the peptide, indicating receptor specificity. Acetazolamide pretreatment lowered intraocular pressure, but the solvent-induced rise in intraocular pressure and inhibition by AVP still occurred without altering the temporal pattern. Thus, these effects appear unrelated to aqueous humor synthesis rate. The data support the possibility of intraocular pressure regulation by peptides acting from the blood and aqueous humor.

Vasopressin effects on lung liquid volume in fetal sheep.

The normal switch from placental to pulmonary gas exchange at birth requires rapid removal of liquid from the lungs. Previous reports contend that vasopressin may be important in regulating this process, but this notion derives from studies in which fetal sheep received very large doses of vasopressin that yielded plasma concentrations at least 10 times greater than those that have been measured during normal labor. To study the physiologic effects of vasopressin on lung liquid volume in fetal sheep, we made three sets of experiments. First, we measured plasma vasopressin concentrations [VP] in 15 late-gestation fetal sheep, five of which were at various stages of spontaneous labor. [VP] in these fetuses ranged from < 1 (prelabor) to 31 (during labor) microU/mL; postmortem extravascular lung water (EVLW) ranged from 4.5 to 14.5 g/g dry lung tissue. In a second series of studies, we measured EVLW in five sets of near-term (138 +/- 1 d, term = 147 d) twin fetal sheep that received an 8-h i.v. infusion of either isotonic saline (control twin) or AVP (AVP-treated twin) at a rate of approximately 1 (mU/kg)/min. This dose was chosen to mimic [VP] measured in fetuses that had been studied during labor. [VP] did not change in the control twins, whereas [VP] increased from 1.8 +/- 1.0 to 27.7 +/- 3.5 microU/mL in treated twins. There was a small, statistically significant difference in EVLW between twins that received AVP and untreated twins (11.9 +/- 1.8 versus 14.6 +/- 2.8 g/g dry lung).(ABSTRACT TRUNCATED AT 250 WORDS)

Intrapericardial denervation: responses to water immersion in rhesus monkeys.

Eleven anesthetized rhesus monkeys were used to study cardiovascular, renal, and endocrine alterations associated with 120 min of head-out water immersion. Five animals underwent complete intrapericardial denervation using the Randall technique, while the remaining six monkeys served as intact controls. Each animal was chronically instrumented with an electromagnetic flow probe on the ascending aorta, a strain gauge pressure transducer implanted in the apex of the left ventricle (LV), and electrocardiogram leads anchored to the chest wall and LV. During immersion, LV end-diastolic pressure, urine flow, glomerular filtration rate, sodium excretion, and circulating atrial natriuretic peptide (ANP) each increased (P < 0.05) for intact and denervated monkeys. There were no alterations in free water clearance in either group during immersion, yet fractional excretion of free water increased (P < 0.05) in the intact monkeys. Plasma renin activity (PRA) decreased (P < 0.05) during immersion in intact monkeys but not the denervated animals. Plasma vasopressin (PVP) concentration decreased (P < 0.05) during the first 30 min of immersion in both groups but was not distinguishable from control by 60 min of immersion in denervated monkeys. These data demonstrate that complete cardiac denervation does not block the rise in plasma ANP or prevent the natriuresis associated with head-out water immersion. The suppression of PVP during the first minutes of immersion after complete cardiac denervation suggests that extracardiac sensing mechanisms associated with the induced fluid shifts may be responsible for the findings.

Effect of loading right atrial and ventricular receptors on stimulated AVP, ACTH, and renin secretion in awake dogs.

The goal of this study was to test the hypothesis that increasing or decreasing the load on baroreceptors in the right heart influenced the secretion of arginine vasopressin (AVP), adrenocorticotropic hormone (ACTH), and renin during a state of sustained arterial hypotension. The hypothesis was tested in chronically instrumented conscious dogs prepared with inflatable cuffs around the pulmonary artery (PA) and the thoracic inferior vena cava (IVC). In one protocol (n = 5), mean arterial pressure was reduced 10 or 20% below control by constriction of the PA, a maneuver that caused a fall in left atrial pressure (LAP) and an increase in right atrial pressure (RAP). Plasma AVP, ACTH, atrial natriuretic peptide (ANP), and plasma renin activity (PRA) all increased (P < 0.05) in response to constriction of the PA. Reducing RAP to control by constriction of the IVC during maintained constriction of the PA had no effect on MAP, LAP, plasma AVP, ACTH, or PRA, but plasma ANP fell significantly. In a separate protocol (n = 4), constriction of the IVC was used to reduce MAP 10 or 20% below control, and this led to significant decreases in both LAP and RAP and increases in plasma AVP, ACTH, and PRA. RAP was then increased above control by constriction of the PA without altering either MAP or LAP. Raising RAP from a level that was 6.3 +/- 1.3 mmHg below control to 3.5 +/- 1.0 mmHg above control had no effect on plasma AVP, ACTH, or PRA.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in the baroreflex during pregnancy in conscious dogs: heart rate and hormonal responses.

This study was performed to test the hypothesis that reflex increases in heart rate, PRA, and plasma concentrations of vasopressin, angiotensin-II, ACTH, and cortisol are reduced during pregnancy. The hypothesis was tested by measuring, in pregnant and nonpregnant conscious dogs, changes in arterial and atrial pressures, heart rate, and plasma hormone concentrations during 30-min infusions of three doses of nitroprusside (1, 2, and 4 micrograms/kg.min). Between-group differences were determined by comparing the relationships between arterial or atrial pressure and plasma hormone concentrations. Hypotension-induced increases in heart rate and plasma levels of vasopressin, ACTH, and cortisol were blunted when the dogs were pregnant. In contrast, reflex increases in PRA and angiotensin-II were increased. These results indicate that the activity of the baroreceptor reflex is altered during pregnancy in dogs.

Effect of water temperature on diuresis-natriuresis: AVP, ANP, and urodilatin during immersion in men.

Effects of water temperature on diuresis, natriuresis, and associated endocrine responses during head-out immersion were studied in eight men (23.4 +/- 0.3 yr) during four 5-h experimental conditions: air control at 28 degrees C and immersion at 34.5 degrees C [thermoneutral (Tnt)], 36 degrees C [above Tnt (aTnt)], and 32 degrees C [below Tnt (bTnt)]. Esophageal temperature decreased by approximately 0.4 degrees C in bTnt and increased by approximately 0.5 degrees C in aTnt. Cardiac output increased by approximately 80% in aTnt and approximately 40% in bTnt while thoracic impedance, an index of central blood pooling, decreased by 7.5 omega in bTnt (NS vs. Tnt) and 8.8 omega in aTnt (P < 0.05 vs. Tnt and bTnt). Total peripheral resistance decreased at all temperatures (50% in aTnt, 20% in bTnt). Urine flow and Na+ excretion increased by sixfold in bTnt and Tnt but by only threefold in aTnt. Creatinine clearance was unchanged while osmolal clearance (but not free water clearance) increased two-fold with all immersions. Plasma atrial natriuretic peptide (ANP), urinary urodilatin, and urinary guanosine 3',5'-cyclic monophosphate increased while plasma renin activity, aldosterone, and arginine vasopressin (AVP) decreased similarly at all temperatures. bTnt did not potentiate diuresis by selective attenuation of AVP. The overall natriuretic response exhibited a higher correlation with urodilatin (r = 0.45, P < 0.001) than with ANP (r = 0.26, P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin, vasopressin, and atrial natriuretic peptide in the rat eye.

Angiotensin (Ang), vasopressin (VP) and atrial natriuretic peptide (ANP) were assayed in the anterior uvea and retina from eyes of decapitated rats and rats perfused through the heart with phosphate buffered saline to remove peptides from blood and ocular fluids. All peptides were detected, and ANP was the most abundant. Uveal content of each peptide was greater than the retina. Perfusion did not affect ANP or VP content, but Ang was eliminated. Washout may explain the lack of immunohistochemical localization in the eye for Ang, but not VP. Also, washout does not account for available immunohistochemical data describing the localization of ANP in ocular tissue.

Dexamethasone and ergonovine effects on cerebrospinal fluid pressure in conscious rats.

Prior work showed that intracerebroventricular (i.c.v.) infusions of artificial cerebrospinal fluid (aCSF), at a rate of 8 microliters/min x 10 min, elevated CSF pressure (CSFp) of conscious rats after a 2-hour delay. The rise was associated with an increased resistance to outflow and decreased intracranial compliance. When maintained by a continuous infusion of 0.25 microliter/min into each lateral ventricle, CSFp recordings can be made for 24 h and a higher CSFp occurs. Here, we pretreated rats with ergonovine or dexamethasone to determine their effects on the delayed CSFp rise. Ergonovine (0.5 mg/kg i.p.) pretreatment, in a 6-hour protocol using only the 10-min infusion, slightly reduced CSFp (p < 0.05, one-tail test) but the time course of the delayed rise in CSFp was unchanged (p > 0.05). Ergonovine increased intracranial compliance (p < 0.05) 20 min after infusion when CSFp was normal, but not when CSFp was elevated at 4 h (p > 0.05). Dexamethasone (40 micrograms i.m.) pretreatment was tested in the 24-hour protocol. It reduced (p < 0.05) normal CSFp during the 2-hour lag after infusion and the CSFp rise was reduced (p < 0.05) for about 8 h. However, the time course and ending CSFp were unchanged (p > 0.05). Thus, prior cerebral vasoconstriction or a steroidal anti-inflammatory drug have partial efficacy in reducing CSFp, but do not prevent the unknown events that precede the delayed CSFp rise after i.c.v. infusions.

Hemorrhage decreases arterial pressure sooner in pregnant compared with nonpregnant dogs: role of baroreflex.

This study was performed to test the hypothesis that smaller reflex increases in vasopressin, cortisol, adrenocorticotropic hormone (ACTH), and angiotensin II (ANG II) concentrations are produced by hemorrhage in pregnant compared with nonpregnant conscious dogs. Equivalent hemorrhages (1% of the initial blood volume per minute) produced larger decreases in arterial pressure [P < 0.01; 107 +/- 6 to 73 +/- 10 mmHg (pregnant); 109 +/- 6 to 90 +/- 5 mmHg (nonpregnant)] but produced similar increases in plasma vasopressin concentration in the pregnant animals. As a result, the slope of the arterial pressure-to-vasopressin relationship was reduced (P < 0.05). During pregnancy, smaller increases in plasma cortisol concentration and heart rate were also produced for a given decrease in arterial pressure, but the relationship between pressure and ACTH was not significantly affected. In contrast, higher levels of plasma renin activity and plasma ANG II concentration were achieved in the pregnant dogs. In general, the relationships between plasma hormone levels and either left or right atrial pressure were not significantly altered. These results indicate that reflex increases in heart rate, vasopressin, and cortisol concentration are attenuated in pregnant dogs and that this attenuation may contribute to the inability of pregnant animals to achieve normal cardiovascular homeostasis during hemorrhage.

Renin and vasopressin responses to graded reductions in atrial pressure in conscious dogs.

Hypovolemia activates reflexes that stimulate secretion of renin and arginine vasopressin (AVP). A large body of evidence, obtained mainly in anesthetized preparations, supports the hypothesis that unloading cardiac receptors stimulates increases in plasma AVP and renin activity (PRA). We have observed significant increases in PRA before any change in either mean arterial pressure (MAP) or pulse pressure in conscious dogs undergoing continuous hemorrhage; however, plasma AVP did not change until there was a significant fall in MAP. These results are compatible with the hypothesis that cardiac receptors cause reflex stimulation of renin but not AVP secretion. The aim of the present study was to test the hypothesis that a decrease in atrial pressure alone is sufficient to stimulate an increase in plasma AVP and PRA. Graded thoracic inferior vena caval constriction (TIVCC) was used to reduce atrial pressure in four steps without altering MAP in conscious dogs. In a fifth step, TIVCC was increased to cause a fall in MAP. A reduction in left atrial pressure (LAP) of 4.2 +/- 0.9 mmHg was accompanied by a significant (P < 0.05) increase in PRA from a control value of 0.4 +/- 0.1 ng angiotensin I (ANG I).ml-1.3 h-1 to 1.1 +/- 0.2 ng ANG I.ml-1.3 h-1 but no change in plasma AVP (from 1.0 +/- 0.1 to 1.2 +/- 0.2 pg/ml) or MAP (from 85 +/- 5 mmHg to 86 +/- 4 mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)

Left heart and arterial baroreceptors interact in control of plasma vasopressin, renin, and cortisol in awake dogs.

Arterial hypotension induced by constriction of the ascending aorta (AA) causes increases in left atrial pressure (LAP) and plasma atrial natriuretic peptide (ANP), but no change in plasma arginine vasopressin (AVP), plasma renin activity (PRA), or cortisol. In the present study, we tested the hypothesis that the rise in left heart pressure during constriction of the AA suppressed the stimulation of AVP, renin, and cortisol secretion in response to arterial hypotension. Dogs were prepared with inflatable cuffs around the AA, the pulmonary artery (PA), and the thoracic inferior vena cava (IVC) and with catheters in the left and right atria and abdominal aorta. In one series of experiments, the AA was constricted to lower mean arterial pressure (MAP) 10 or 20% below control for 15 min. Then, either the PA or the IVC was constricted to bring LAP back to control levels but without altering the degree of arterial hypotension. Constriction of the AA alone led to significant increases in LAP and plasma ANP but no change in plasma AVP, cortisol, or PRA. Reducing LAP to control levels by constriction of either the PA or IVC led to significant and similar increases in plasma AVP, cortisol, and PRA. Plasma ANP fell significantly 10 min after LAP was normalized by constriction of the IVC but not when LAP was normalized by constriction of the PA, because PA constriction caused a significant rise in right atrial pressure that stimulated ANP secretion. The increases in plasma AVP and PRA after normalizing LAP by constriction of the PA were compared with the increases obtained during identical falls in MAP induced by constriction of the IVC alone, a maneuver that lowers LAP below control. The increases in plasma AVP in the two conditions were identical, indicating that the stimulation of left heart baroreceptors alone can account for the suppression of AVP secretion in response to unloading arterial baroreceptors. In contrast, there was a greater rise in PRA during hypotension caused by constriction of the IVC alone compared with the condition in which LAP was normalized but plasma ANP remained elevated. This suggests that increased left heart pressure inhibits renin secretion in response to arterial hypotension by reflex mechanisms and by increased plasma ANP concentration.