Coordination of mammary metabolism and blood flow after refeeding in rats.

The production of milk is closely linked to nutritional state in many mammalian species, but the mechanisms by which changes in nutritional state are signaled to the mammary glands are poorly understood. Simultaneous measurements of mammary blood flow and glucose arterio-venous difference were made across the inguinal mammary glands of anesthetized, lactating rats. Blood flow to the mammary glands of previously fed rats was 0.48 mL/min per gram of mammary tissue. Glucose supply was 1.7 mumol/min per gram and 28% was extracted by the mammary glands. After food deprivation for 18 h, mammary blood flow decreased 48%, glucose arterio-venous difference decreased 72%, and hematocrit increased 7%, resulting in a 60% decrease in glucose supply and an 88% decrease in glucose uptake. After 1 h of refeeding, glucose supply had returned to a similar level to that of normally fed animals, but glucose uptake was 60% higher than in the normally fed state. Mammary glucose uptake was not closely linked to either blood flow or glucose supply, suggesting that substrate supply was not the primary determinant of mammary metabolism. Denervation experiments showed that the mammary metabolic response to altered nutritional state was also unlikely to be closely controlled by neural pathways. Severance of the cutaneous branch of the posterior division of the femoral nerve innervating the inguinal mammary glands did not reduce the high glucose uptake by mammary glands of either fed or refed rats, nor did denervation change the low glucose uptake by mammary glands of food-deprived rats. Denervation reduced blood flow in the associated mammary gland, however, indicating that neural pathways may play a role in supporting mammary blood flow when food is available. In in vitro experiments, the rate of glucose uptake was 35% lower in mammary acini from food-deprived rats than in fed rats 2.5 h after tissue removal, indicating some persistence of the food deprivation-induced suppression of mammary metabolism. Administration of insulin increased glucose uptake in acini from both fed and food-deprived rats, indicating that insulin may be involved in signaling the mammary gland of the restoration of nutrient supply when food-deprived rats are refed. The effects of administration of a gut extract in vivo and in vitro are discussed.

The drumming of Isoperla pallida Aubert and Guadalgenus franzi (Aubert) (Plecoptera, Perlodidae), and review and evolutionary considerations of Southern Iberian Peninsula Perlodidae.

The drumming calls of two perlodid species from Southern Spain (Sierra Morena, Jaén) are analyzed and described. Nineteen calls from one male of Guadalgenus franzi were recorded, showing a simple call pattern composed of two beats with an average duration between them of 184.32 msec (range: 165-227). This is the simplest call pattern yet discovered in the Plecoptera. The female of this species also presented a simple call consisting of only one beat. The male of Isoperla pallida showed an ancestral call pattern, more simple than the other Iberian Isoperla species (I. grammatica, I. nevada or I. curtata, all of them with multiphasic drumming calls or I. bipartita with a notably different model consisting of rubbing). Calls from six different males (the female did not drum) consisted of an average of 65.94 beats (range: 25-83) with a duration average of 1462.69 msec (range: 548-1835), regularly repeated with intervals with a duration average of 22.27 msec (range: 17-30). With this study, the vibrational calls of all the Perlodid species from the Southern Iberian Peninsula, except Perlodes microcephalus and Besdolus bicolor, are known. Moreover, it presents the first record and description of the call of the monospecific genus Guadalgenus. An evolutionary approach to the vibrational communication diversification in the perlodids of the Southern Iberian Peninsula is presented, showing a complexity graduation from the more simple drumming calls (shown by Hemimelaena flaviventris and G. franzi) to the rubbing call of I. bipartita and intermediate drumming calls of other Isoperla species, consistent with the drumming evolution paradigm of Stewart (2001).

A new mechanism for spin--lattice relaxation of heavy nuclei in the solid state: 207Pb relaxation in lead nitrate.

A detailed investigation of the spin-lattice relaxation time, T1, for 207Pb in solid lead nitrate has been undertaken in an effort to understand the mechanism of relaxation. The results show that the 207Pb T1 is independent of magnetic field strength and inversely proportional to the square of the temperature. These are signatures of relaxation by a spin-phonon Raman scattering mechanism. Nuclear spin-lattice relaxation in solid lead salts is more efficient for sites with smaller magnetic shielding anisotropy. A coupling mechanism is proposed whereby phonons create a local magnetic field by modulating the valence electron shell motion relative to the nuclear/electron core. Literature data suggest that spin-phonon scattering is a common relaxation pathway for other spin-1/2 heavy nuclei in solids.

The hemodynamic effects of prostacyclin infusions in normotensive and ACTH induced hypertensive conscious sheep.

The aim of this study was to determine the effect of ACTH-induced hypertension on the hemodynamic dose-response curves to intravenous infusion of prostacyclin (PGI2) in conscious sheep. PGI2 was infused for 10 minutes at doses of 0.05-0.50 micrograms/kg per min and hemodynamic dose-response curves were performed before, during and after ACTH-induced hypertension. Prior to ACTH administration prostacyclin infusions produced dose dependent decreases in mean arterial pressure (MAP), calculated total peripheral resistance (CTPR) and stroke volume (SV). These changes were accompanied by an increase in cardiac rate (CR) and cardiac output (CO). After five days of ACTH treatment MAP had risen from 72 +/- 1 to 91 +/- 2 mm Hg and infusions of PGI2 produced similar effects on MAP to those seen prior to ACTH. However the effects on CTPR, CO, SV and CR were all potentiated relative to normotensive animals. Three days after ACTH administration had ceased and basal pressure had returned to normotensive levels, the responses of CR, CO and SV to PGI2 infusions were similar to those seen prior to ACTH. However the exaggerated fall in CTPR seen during ACTH treatment was still present and this resulted in a very large decrease in MAP. These studies suggest that in this model of steroid-induced hypertension the resistance vessels are more sensitive to PGI2 and that the blood pressure response to PGI2 is regulated by different mechanisms to those seen prior to ACTH.

A comparison of the haemodynamic effects of dietary sodium restriction and acute sodium depletion in the conscious sheep.

The use of a low Na, low K sorghum grain diet supplemented with intraruminal electrolyte infusions has enabled dietary manipulation of sodium status to be studied in the sheep. Dietary sodium restriction reduced urinary sodium excretion within 24 h with maximal retention after 3 days. There were no other substantial metabolic or haemodynamic changes. A more severe form of sodium deficiency produced by parotid salivary drainage resulted after only 2 days in a sodium deficit 3-4 times that seen with 14 days of sodium restriction. Extracellular fluid volume and cardiac output decreased. Blood pressure was unchanged but there was an increase in peripheral resistance and plasma renin concentration.

Effect of potassium, angiotensin II and ACTH on blood aldosterone and cortisol in sheep on different dietary potassium and sodium intakes.

The short term aldosterone response to manipulations of potassium (K), angiotensin II (AII) and ACTH were examined in sheep on a variety of chronic electrolyte regimes. Reduction in Na intake increased blood aldosterone to a greater extent on 100 mmol/day K than a K-free diet. Aldosterone increased in response to AII under conditions of chronic dietary Na restriction, in contrast to acute Na depletion. The effects of K, AII, and ACTH on aldosterone concentrations in sheep on varying intakes of Na and K are similar to that reported for other species.

Inter-relationships between sodium and potassium intake and the blood pressure effects of ACTH in sheep.

These studies examine the effect of sodium (Na) and potassium (K) intake on the pressor and metabolic actions of ACTH (20 micrograms/kg/day) in sheep. After 21 days on each of five regimens in which Na and K intake varied from 0 to 100 mmol/day, no simple relationship between Na and K intake and blood pressure was found. After five days of ACTH treatment, mean arterial pressure (MAP) rose + 5 mmHg in sheep on 0 mmol Na, 0 mmol K (expressed as 0 Na 0 K); + 13 mmHg on 10 Na 100 K; + 5 mmHg on 0 Na 100 K; + 20 mmHg on 100 Na 0 K and + 24 mmHg on 100 Na 100 K. Plasma [K] was unchanged by ACTH on 0 Na 0 K but fell in sheep on the other electrolyte regimens. Water intake increased with ACTH on all regimens except 100 Na 0 K. Blood aldosterone concentration was high in sheep maintained on 0 Na regimens but lower after five days of ACTH treatment in all groups. Blood cortisol and corticosterone concentrations increased with ACTH on all regimens studied.

The baroreceptor-heart rate reflex in ACTH hypertension in sheep.

ACTH administration in sheep produces an adrenally dependent rise in blood pressure. Cardiac output and heart rate are usually increased. The precise mechanisms involved in the genesis of the hypertension are unclear. This study examines the sensitivity of the baroreflex heart rate response to phenylephrine hydrochloride and sodium nitroprusside before, during and after ACTH administration in sheep. During ACTH administration there was a sustained rise in blood pressure within 24 hours, whereas heart rate rose gradually. There was a sustained fall in baroreflex sensitivity to sodium nitroprusside within 24 hours, whereas baroreflex sensitivity to phenylephrine fell gradually over the first three days. The different time course of the change in sensitivity suggests that two different mechanisms are influenced by ACTH administration, for instance, changes in function in both cardiac vagal efferents and sympathetic pathways.

Effects of converting enzyme inhibition with captopril on renal function in normal and ACTH treated sheep.

1. The effect on renal function in sheep of inhibiting converting enzyme with captopril was examined before and after 5 days ACTH administration. 2. Glomerular filtration rate, effective renal plasma flow, effective renal blood flow, mean arterial pressure and plasma sodium were all significantly increased by ACTH treatment and plasma potassium was decreased. Captopril (20 mg i.v.) had no effect on renal function or blood pressure before or after ACTH treatment, although urinary potassium excretion decreased following captopril on day 6 of ACTH treatment. 3. The increase in glomerular filtration rate and effective renal plasma flow seen with ACTH treatment in sheep does not appear to be mediated by the reninangiotensin system.

A comparison of the effects of two angiotensin converting enzyme inhibitors, SQ 14 225 and MK 422 in Na-restricted sheep.

1. The effects of angiotensin converting enzyme inhibition (CEI) using an intravenous infusion of either SQ 14 225 or MK 422 on blood pressure, plasma renin concentration, blood aldosterone concentration and urinary Na excretion, were studied in sodium-restricted sheep. 2. After 7 days of infusion of either drug mean arterial pressure had decreased and plasma renin concentration had increased. 3. Urinary sodium excretion and blood aldosterone concentration were not altered by infusion of either compound. 4. This study confirms a role for angiotensin II in the control of blood pressure in the Na-restricted sheep but suggests that urinary Na excretion in the sheep is not as dependent on angiotensin II as has been reported in other species.

Effect of angiotensin converting enzyme inhibition with SQ 14 225 on blood pressure in sheep.

The effect of intravenous injection of the angiotensin converting enzyme inhibitor SQ 14 225 on blood pressure, heart rate and plasma renin concentration (PRC) was investigated in 15 intact conscious ewes as follows: sodium replete during angiotensin I infusion (n = 4); sodium replete (n = 6); sodium deplete (n = 5); chronic water deprivation (n = 5); AcTH treated sodium replete (n = 6). Following SQ 14 225 mean arterial pressure fell 5 +/- 1 mmHg in sodium replete, 20 +/- 4 mmHg in acutely sodium deplete, 7 +/- 2 mmHg in chronic water deprivation and 6 +/- 2 mmHg in ACTH treated sodium replete sheep. This suggests that the renin-angiotensin system plays no significant role in maintaining the elevated blood pressure of sheep with ACTH induced hypertension. Heart rate rose in all groups except the water deprived animals following SQ 14 225. PRC rose from 5.1 +/- 2.1 pmo1AI/ml plasma/h. to 12.4 +/- 2.0 in sodium replete sheep, from 11.9 +/- 1.0 to 68 +/- 13 in acutely sodium deficient animals, and from 13.3 +/- 4.3 to 32.9 +/- 0.6 in chronically water deprived animals, but showed little change in ACTH treated sheep, falling from 2.3 +/- 0.5 to 1.7 +/- 0.2 pmo1AI/ml plasma/h.

ACTH hypertension modifies the haemodynamic effects of prostacyclin infusions in sheep.

1. The haemodynamic effects of short-term prostacyclin infusions (0.05-0.50 microgram/kg per min) were investigated in conscious adult sheep. 2. Haemodynamic dose-response curves to prostacyclin were performed before, during and after production of ACTH-induced hypertension. 3. Prior to ACTH administration prostacyclin produced dose-dependent reductions in mean arterial pressure, total peripheral resistance and stroke volume and these were accompanied by increased in heart rate and cardiac output. 4. After 5 days of ACTH-induced hypertension prostacyclin produced similar effects on mean arterial pressure to those seen prior to ACTH but the effects on heart rate, cardiac output, stroke volume and total peripheral resistance were markedly increased. 5. These studies demonstrate that the responsiveness of the circulation to prostacyclin is altered in ACTH-induced hypertension.