Increase In Plasma Vasopressin Concentration Research Articles

Carotid arterial control of vasopressin secretion in sheep.

The purpose of this study was to test the role of carotid arterial mechanoreceptors in the control of vasopressin secretion in conscious 6- to 7-wk-old lambs. Bilateral carotid occlusion decreased lingual arterial pressure and stimulated reflex increases in heart rate and femoral arterial blood pressure but did not significantly alter plasma concentrations of vasopressin. Acute vagosympathetic blockade, produced by injection of 2% lidocaine onto the vagosympathetic trunks, did not significantly alter heart rate or blood pressure but did stimulate a slow increase in plasma vasopressin concentration, suggesting that afferent vagal fibers tonically inhibit vasopressin secretion. Bilateral carotid occlusion after vagosympathetic blockade stimulated a brisk increase in plasma vasopressin that was larger than the response to vagosympathetic blockade alone. These results suggest that vasopressin secretion in lambs is partially controlled by arterial mechanoreceptors in the carotid sinus and by extracarotid receptors with vagosympathetic afferent fibers.

Antidiuresis and vasopressin release with hypoxemia and hypercapnia in conscious dogs.

To determine the effects of acute blood gas derangements on renal water and solute excretion and vasopressin secretion, six unanesthetized mongrel dogs were studied during 1) combined acute hypoxemia and hypercapnic acidosis [arterial O2 partial pressure (PaO2) 36 +/- 1 Torr, arterial CO2 partial pressure (PaCO2) 54 +/- 2 Torr, pH 7.18 +/- 0.01], 2) acute hypoxemia (PaO2 33 +/- 2 Torr, PaCO2 33 +/- 1 Torr, pH 7.34 +/- 0.01), and 3) acute hypercapnic acidosis (PaO2 83 +/- 3 Torr, PaCO2 53 +/- 1 Torr, pH 7.19 +/- 0.02). Combined acute hypoxemia and hypercapnic acidosis increased (P less than 0.05) mean arterial pressure, but renal hemodynamic function deteriorated with decreased (P less than 0.05) glomerular filtration rate and increased (P less than 0.05) renal vascular resistance. Moreover free water clearance became more negative (P less than 0.05) and urine osmolality increased (P less than 0.05). During acute hypoxemia or acute hypercapnic acidosis alone, mean arterial pressure and renal hemodynamic function were unchanged but free water clearance became more negative (P less than 0.05). During acute hypoxemia, urine osmolality increased (P less than 0.05) comparably with values observed during combined acute hypoxemia and hypercapnic acidosis. Plasma vasopressin concentrations increased profoundly (P less than 0.05) during combined hypoxemia and hypercapnic acidosis and during acute hypoxemia alone and were significantly elevated (P less than 0.05) above the increased plasma vasopressin concentrations observed during acute hypercapnic acidosis. We conclude that acute hypoxemia and hypercapnic acidosis result in impairment of renal water excretion, probably mediated through vasopressin secretion.

Localization and actions of cholecystokinin in the rat pituitary neurointermediate lobe.

Rat pituitary neural lobe contained high concentrations of cholecystokinin-like immunoreactivity (CCK-LI). Section of the pituitary stalk resulted in loss of CCK-LI, and both lactation and replacement of drinking water with 2% saline resulted in marked depletion of CCK-LI. Rats with congenital diabetes insipidus (Brattleboro strain) had a 73% reduction in CCK-LI below the levels of hooded Long-Evans controls, where as levels in the brain were unchanged. Release of CCK-LI, labeled dopamine, and gamma-amino butyric acid in response to potassium depolarization was studied. There was a low fractional release of CCK-LI. Addition of sulfated CCK-8 (CCK-8s) to the medium enhanced the calcium-dependent potassium-stimulated release of dopamine, but basal release was unaffected. gamma-Amino butyric acid release was only poorly calcium dependent and not effected by extracellular CCK-8s. Vasopressin and oxytocin release were stimulated by electrical stimulation of the pituitary stalk, and were unaffected by the addition of CCK-8s to the medium. In vivo, however, the injection of 5 micrograms CCK-8s into the third ventricle resulted in increased plasma vasopressin concentrations.

Increased Plasma Vasopressin and Serum Uric Acid in the Low Renin Type of Essential Hypertension

In 22 50-year-old men with long-standing, untreated essential hypertension of the low renin type, venous plasma vasopressin concentrations were about three times those of 15 matched normotensive control subjects (p less than 0.005). These patients also had increased arterial concentrations of noradrenaline and adrenaline (p less than 0.05) but there was no direct association between these two catecholamines and vasopressin. On the other hand, adrenergic beta-receptor blockade with oxprenolol reduced both blood pressure and plasma vasopressin (p less than 0.01) while venous plasma dopamine concentrations significantly increased. In addition, the hypertensives had highly significantly increased serum uric acid (p less than 0.001) that correlated positively with venous vasopressin concentrations (p less than 0.05). According to these data, patients with the volume-sustained low renin type of essential hypertension have increased plasma vasopressin concentrations that probably are inversely related to dopaminergic nervous activity. The data also indicate that increased plasma vasopressin correlates with serum uric acid, most probably through increased tubular reabsorption of this acid.

Effect of angiotensin II on vasopressin in plasma and platelets in SH and WKY rats.

A study was carried out of the effects of iv angiotensin II on vasopressin release and the distribution of vasopressin between platelets and plasma in 12 week old conscious unrestrained SH and WKY rats. Angiotensin II was infused at rates of 31.25 to 500 ng/kg X min for 20 min. There was an enhanced pressor responsiveness to angiotensin II in the SH rats. Angiotensin II caused a moderate increase in plasma vasopressin concentrations, but only at doses which produced maximal pressor responses (250 to 500 ng/kg X min). There were no significant differences in vasopressin responses to angiotensin II in SH compared to WKY rats. Approximately 30% of circulating immunoreactive vasopressin was found in platelets in both SH and WKY rats, and this distribution was not greatly affected by the iv infusion of angiotensin II.

Role of the renin-angiotensin system in the control of vasopressin and ACTH secretion during the development of renal hypertension in dogs.

Experiments were performed to determine if the activation of the renin-angiotensin system that occurs during the development of two-kidney, one clip Goldblatt hypertension in dogs is accompanied by increases in vasopressin and adrenocorticotrophic hormone (ACTH) secretion. Following renal artery constriction, there were marked increases in arterial blood pressure, plasma renin activity (PRA), and plasma angiotensin II (AII) concentration. These changes were accompanied by an increase in plasma vasopressin concentration during the second week following constriction, and there were significant correlations between plasma vasopressin concentration and PRA (r = 0.57, p less than 0.001), and between plasma vasopressin concentration and plasma AII concentration (r = 0.59, p less than 0.001). In contrast, plasma corticosteroid concentration, used as an index of changes in ACTH secretion, did not change significantly. Acute blockade of the renin-angiotensin system with captopril or saralasin produced the expected changes in blood pressure, PRA, and plasma AII concentration but did not decrease plasma vasopressin or corticosteroid concentrations. These results indicate that during the development of renal hypertension in dogs, there may be an interaction between the renin-angiotensin system and vasopressin, but not between the renin-angiotensin system and the pituitary-adrenal axis. They also show that the antihypertensive action of captopril in this experimental model is not mediated via suppression of vasopressin, ACTH, or corticosteroid secretion.

Cardiovascular response to vasopressin vasopressor antagonist administration during water deprivation in the rat.

The cardiovascular effects of intracerebroventricular (i.c.v.) and intravenous (i.v.) injection of a selective vasopressin vasopressor antagonist, [1-beta-mercapto-beta, beta-cyclopentamethylenepropionic acid-2-(0-methyl)tyrosine]arginine vasopressin (TMe-AVP) were examined in conscious rats under basal conditions and following 48 h of water deprivation. Pressor responses to i.v. vasopressin (50 ng/kg) were not blunted by i.c.v. treatment with either vehicle or 0.5 microgram/kg TMe-AVP. A dose of 5.0 microgram/kg TMe-AVP (i.c.v.) did reduce the pressor response to vasopressin, indicating peripheral leakage of the antagonist. Water deprivation for 48 h increased plasma vasopressin concentrations from 0.7 +/- 0.1 to 2.8 +/- 0.1 microU/ml and increased blood pressure from 112 +/- 2 to 123 +/- 1 mm Hg. No effect of the vasopressin antagonist on blood pressure could be detected following either i.c.v. (0.5 microgram/kg) or i.v. (5.0 micrograms/kg) treatment in water-deprived animals. However, a significant increase in heart rate was observed in water-deprived rats following i.v. injection of 5.0 micrograms/kg of TMe-AVP. Central vasopressin vasopressor receptor blockade appears to exert little effect on blood pressure either under basal conditions or during water deprivation. The data further delineate the relationship of plasma vasopressin concentrations to cardiovascular homeostasis.

Homeostatic responses to water deprivation or hemorrhage in lactating and non-lactating bedouin goats

1. 1. Three lactating and three non-lactating black Bedouin goats were subjected to four days of water deprivation or to hemorrhage. 2. 2. Four days of water deprivation caused body wt losses of 32 and 23% and plasma volume losses of 30 and 34% in lactating and non-lactating goats respectively. 3. 3.Plasma osmolality increased 17 and 15% in lactating and non-lactating goats. Plasma arginine vasopressin concentration rose from about 5 pg/ml to a mean of 36 pg/ml. Plasma renin activity increased from about 0.7 ng/ml/hr to a mean of 3.45 ng/ml/hr in lactating and to 3.15 ng/ml/hr in non-lactating goats. 4. 4. At 4.5 hr post-rehydration plasma osmolality and plasma vasopressin concentration were back to normal in non-lactating, but still elevated in lactating goats. Plasma renin activity increased after rehydration. 5. 5. Rapid blood volume loss of 21–28% increased plasma vasopressin concentration to 16–35 pg/ml in non-lactating and to 70 or > 500 pg/ml in lactating goats. 6. 6. It is concluded that black Bedouin goats are well adapted to endure severe dehydration and rapid rehydration, but that they (especially lactating animals) react strongly to rapid volume depletion.

Hypothalamic integration of dopaminergic and opiate pathways controlling vasopressin secretion.

Lesions of the circumventricular organs were produced by administration of monosodium-L-glutamate to neonatal rats. At 16 weeks of age these rats were given different stimuli to vasopressin release. In control rats, morphine (50 micrograms) injected into the third ventricle resulted in a rapid increase in plasma vasopressin concentrations at 10 min, followed by a reduction at 20 min. The circumventricular organ-lesioned rats, however, showed a pronounced fall in vasopressin secretion both at 10 and 20 min after 50 micrograms morphine. A similar abolition of the morphine-elicited rise in plasma vasopressin could also be achieved by the iv infusion of small doses of dopamine in normal rats. Hypoxic stimuli, which result in a marked rise in vasopressin in normal rats, failed to elicit any increase in circumventricular organ-lesioned animals. Vasopressin release after stimulation with 9% saline, however, was augmented in the lesioned animals. These results suggest that circumventricular organs have an important role in controlling neurohypophyseal secretion and that they differentially control different stimuli to vasopressin release via dopaminergic and opiate pathways.

Effects of nonhypotensive hemorrhage on renal organ and urinary clearances of vasopressin in the dog.

A study was undertaken to investigate the effects of moderate nonhypotensive hemorrhage on the renal organ and urinary clearances of vasopressin in anesthetized dogs. A nonhypotensive hemorrhage was conducted in nine dogs by withdrawal of 12 ml/kg arterial blood over 10 min. This reduction in blood volume increased the plasma vasopressin concentration from a prehemorrhage value of 4.3 +/- 0.5 to 12.5 +/- 3.4 microU/ml (P less than 0.01) in the 15-min period immediately after hemorrhage and to 8.1 +/- 1.4 microU/ml (P less than 0.01) in the 45- to 60-min period after hemorrhage. The increased plasma vasopressin concentration was not associated with changes in either plasma osmolality or mean arterial blood pressure. The urinary excretion of vasopressin increased significantly after hemorrhage (P less than 0.01, 0-15 min after hemorrhage; P less than 0.05, 45-60 min after hemorrhage) and correlated significantly with the plasma vasopressin concentration (r = 0.92; P less than 0.001). However, this moderate nonhypotensive hemorrhage did not change the renal vasopressin extraction ratio or the renal organ and urinary clearances of vasopressin from their prehemorrhage values of 0.27 +/- 0.02, 2.00 +/- 0.20 ml/min X kg, and 1.43 +/- 0.13 ml/min X kg, respectively. At no time were these values different from those in nine time control dogs. Thus, changes in the renal handling of vasopressin do not contribute to the increase in the plasma vasopressin concentration after moderate nonhypotensive hemorrhage.

Role of vasopressin in blood pressure regulation during adrenal insufficiency.

The effect of adrenal insufficiency on the plasma concentrations of two vasoactive hormones, vasopressin and angiotensin II, was studied in conscious dogs. In addition the role of vasopressin in the maintenance of blood pressure during adrenal insufficiency was studied using [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid),2-(O-methyl)tyrosine]arginine vasopressin, a specific antagonist of the vasoconstrictor action of vasopressin. Dogs were bilaterally adrenalectomized and maintained on daily cortisol and deoxycorticosterone acetate injections. Withdrawal of steroids for 4 days resulted in a 4-fold increase in plasma vasopressin concentration (P less than 0.05) and a 3-fold increase in plasma angiotensin II concentration (P less than 0.001); mean arterial pressure did not change significantly. Administration of the vasopressin antagonist in adrenalectomized dogs maintained on steroids had no effect on blood pressure. In marked contrast, vasopressin blockade in dogs with adrenal insufficiency decreased mean arterial pressure by 22 +/- 5 mm Hg (P less than 0.001). These results demonstrate the plasma angiotensin II and vasopressin concentrations increase during adrenal insufficiency in conscious dogs, and that vasopressin plays an important role in blood pressure regulation in this hypovolemic state.

Age-related vasopressin changes in rat plasma and the hypothalamo-hypophyseal system

Immunoreactive vasopressin (VP) was measured in the plasma, neurohypophysis (NH) and hypothalamus (HT) of young (3 months), adult (12 months), and old (30 months) Sprague-Dawley male rats, both intact and anesthetized with halothane. VP content in the HT of the old rats was about half that of young and adultsrats. Total VP content in the NH increased with age, reflecting large glandular size in the old rats. However, VP content was similar in all three groups, when expressed per mg of wet tissue. Plasma VP concentration was undetectable in the old intact rats and it rose to the levels of intact young or adult rats during halothane anesthesia. The anesthesia-related increase in plasma VP concentration was statistically significant in young but not in adult rats. These results suggest that in the intact rats during aging: (1) the synthesis of VP in the HT may be reduced; (2) the storage of VP in the NH is not impaired; and (3) the undetectable plasma VP concentration may reflect either reduced VP release or increased degradation.

Arginine vasopressin response to insulin-induced hypoglycemia in man.

Insulin-induced hypoglycemia causes an increase in plasma vasopressin concentration in man and rat. To assess the mechanism by which this occurs, the effect of hypoglycemia was studied in healthy adults. After insulin injection, a 7-fold rise in plasma immunoreactive arginine vasopressin to 8.2 +/- 3.6 pg/ml was observed in 10 normal subjects. This was associated with a rise in plasma sodium of 2 meq/liter, but no significant change in mean arterial pressure or hematocrit was observed. The significance of the plasma sodium rise was assessed by observing the vasopressin response to hypoglycemia in a patient shown previously to have a selective loss of the vasopressin response to osmotic stimulation. His plasma vasopressin rose from 1.6 to 12.5 pg/ml with no fall in blood pressure or volume. beta-Adrenergic blockade with propranolol before repeat insulin-induced hypoglycemia did not reduce the vasopressin response (peak plasma vasopressin, 8.1 +/- 1.7 pg/ml), despite suppression of PRA. Linear regression analysis showed that the rise in plasma vasopressin and the percentage decline in plasma glucose correlated significantly (r = 0.57, P less than 0.001). In conclusion, hypoglycemia releases vasopressin nonosmotically by a mechanism that appears to be independent of factors currently known to effect vasopressin secretion.

Inhibition by β-endorphin of isoprenaline-induced vasopressin release and its reversal by naloxone

The effect of β-endorphin on isoprenaline-induced vasopressin release was investigated in rats. β-Endorphin (0.29 nmol i.c.v. or 2.9 nmol i.v.) suppressed markedly the increase in plasma vasopressin concentrations in response to isoprenaline without altering the concomitant increase in plasma renin concentration or fall in mean arterial blood pressure. Naloxone (1 mg/kg) prevented this inhibition as did chronic morphine pretreatment. These results show that β-endorphin can inhibit isoprenaline-induced vasopressin release by acting on opiate receptors.

Effects of centrally administered endogenous opioid peptides on drinking behavior, increased plasma vasopressin concentration and pressor response to hypertonic sodium chloride

Intracerebroventricular (i.v.t.) administration of β-endorphin or leucine 5-enkephalin inhibited drinking behavior, the pressor response and increased plasma vasopressin concentration stimulated by an acute elevation in CSF sodium chloride concentration (10 μl, 1 M NaCl i.v.t.). These effects of endogenous opioid peptides were prevented by naloxone, indicating opiate receptors were required for the biologic response. Drinking behavior associated with regulatory stimuli operant during dehydration was also inhibited by opioid peptides. β-Endorphin (i.v.t.) delayed the onset and/or reduced the volume of water consumed in response to hypertonic sodium chloride (relative cellular dehydration), polyethylene glycol (hypovolemia) and food-associated drinking behavior. Inhibition of drinking did not appear related to sensory-motor dysfunction as another motivated behavior, eating (onset, amount consumed) was unaffected by β-endorphin. It is concluded from these results that centrally administered endogenous opioid peptides inhibit sodium chloride-stimulated cerebral mechanisms affecting blood pressure and hydration.

Effects of increases in plasma vasopressin concentration on plasma renin activity, blood pressure, heart rate, and plasma corticosteroid concentration in conscious dogs.

It is known that vasopressin decreases PRA and heart rate and increases blood pressure and plasma corticosteroid concentration. The purpose of this study was to determine the plasma concentration of vasopressin required to produce these effects. Arginine vasopressin was administered iv to five normal conscious dogs as priming injections of 0.1, 0.5, 1.0, 2.5, 5.0, and 10.0 ng/kg, followed by infusions of 0.01, 0.05, 0.1, 0.25, 0.5, and 1.0 ng/kg x min, respectively, for 30 min. These doses produced increases in the plasma vasopressin concentration (+/- SE) of 1.0 +/- 0.8, 2.1 +/- 4.3, 4.3 +/- 1.8, 11.4 +/- 1.0, 19.7 +/- 6.4, and 30.8 +/- 7.8 pg/ml, respectively, from a basal level of 2.7 +/- 0.2 pg/ml. An increase in the plasma vasopressin concentration of 2.1 +/- 0.3 pg/ml suppressed PRA by 19 +/- 5% (P < 0.02); increases of 4.2 +/- 1.8 pg/ml or more suppressed PRA by 34 +/- 12% (P < 0.005). Only the highest dose of vasopressin produced a significant pressor effect (9 +/- 3 mm Hg; P < 0.05) or lowered the heart rate (18 +/- 4 beats/min; P < 0.005). An increase in plasma vasopressin concentration of 19.7 +/- 6.4 pg/ml was required to increase the plasma corticosteroid concentration (1.2 +/- 0.2 to 2.2 +/- 0.4 microgram/dl; P < 0.01); the largest dose of vasopressin increased the plasma corticosteroid concentration from 1.5 +/- 0.1 to 2.4 +/- 0.6 microgram/dl (P < 0.02). Twenty-four-hour water deprivation in the same dogs increased the plasma vasopressin concentration from 2.5 +/- 0.2 to 7.4 +/- 0.6 pg/ml (P < 0.01). Nonhypotensive hemorrhage in another group of dogs increased the plasma vasopressin concentration from 2.5 +/- 0.2 to 47.4 +/- 16.8 pg/ml (P < 0.05). These data indicate that elevations in the plasma vasopressin concentration within the range observed during 24 h of water deprivation and nonhypotensive hemorrhage produced significant decreases in renin secretion and heart rate and elevations in blood pressure and corticosteroid secretion.

Hemodynamic effects of exogenous and endogenous vasopressin at low plasma concentrations in conscious dogs.

The possibility that vasopressin plays a role in cardiovascular control arouses increasing interest. We studied in unanesthetized dogs the hemodynamic consequences of 1-hour vasopressin infusions that modified plasma concentrations over a range similar to that found in physiological situations. We also examined the cardiovascular events following the stimulation of endogenous vasopressin release by an increase in plasma osmolality. In dogs with baroreceptor reflexes intact, vasopressin infusions which increased plasma vasopressin concentration by 2-20 fmol/ml did not affect mean arterial pressure. However, they significantly decreased cardiac ouput (measured by an electromagnetic flowmeter) and increased total peripheral resistance. After baroreceptor denervation, vasopressin infusion rates as low as 40 fmol/kg per min (0.017 microU/kg per min) led to an increase in mean arterial pressure. Cardiac output was unaffected until much higher infusion rates were used. Changes in total peripheral resistance were very similar to those calculated in dogs with intact baroreceptors. The release of vasopressin following infusions of hypertonic solutions either intravenously or into a carotid artery induced detectable hemodynamic changes which appeared in many respects similar to those following low infusion rates of vasopressin. We conclude that physiological plasma concentrations of vasopressin have hemodynamic effects even though they do not normally modify arterial pressure, presumably because of some particular interaction of vasopressin with the baroreceptor reflex.

Vasopressin release during cardiac operation

Plasma vasopressin (VP), serum and urine osmolality (Sosm, Uosm), serum and urine electrolytes (Na+, K+), cardiac index, and arterial pressure were studied before, during, and after cardiopulmonary bypass (CPB) in 27 patients. Of these, 13 underwent coronary artery bypass (CAB), seven underwent aortic valve replacement (AVR), and seven underwent mitral valve replacement (MVR). During CPB, plasma VP concentration rose significantly in all three groups. The CAB group showed the highest average increase in plasma VP concentration during CPB over the preinduction values, an increase significantly higher than that in the valve groups (p < 0.05). The average increase was 31.5 ± 6.7 μU/ml in the CAB group, 22.1 ± 3.8 μU/ml in the MVR group, and 14.9 ± 3.1 μU/ml in the AVR group. The first measured elevation occurred 5 to 10 minutes before CPB in CAB patients (28.6 ± 8.1 μU/ml, p < 0.05) and within 5 minutes CPB in the valve groups [33.3 ± 4.7 μU/ml (p < 0.01) in AVR group and 24.5 ± 4.7 μ/ml of starting (p < 0.05) in MVR group]. Serum Na+ and K+ concentrations, Sosm, and urine Na+ concentrations were unchanged. In all groups, Uosm and urine K+ concentration decreased significantly during CPB. Because urine flow increased substantially during CPB, the Na+ excretion increased (p < 0.01) but K+ excretion fell significantly below the prebypass levels (p < 0.05) in all groups. There was no correlation between plasma VP concentration and any hemodynamic or renal parameter in any group. Possible factors associated with elevated plasma VP concentration during CPB and those associated with the difference among the groups are discussed.

Influence of converting enzyme inhibition on the release of vasopressin induced by angiotensin.

1 The effects of intravenous infusion of angiotensin I, II and (des-1-Asp) angiotensin II (angiotensin III) on the plasma vasopressin levels, with and without converting enzyme inhibition, were investigated in conscious rats by use of a specific radioimmunoassay. 2 All three peptides caused a dose-dependent increase in vasopressin release, angiotensin III infusion being less effective than angiotensin I or II. 3 The converting enzyme inhibitor, SQ 20881 (Pyr-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro) (1.0 mg/kg, i.v.), had no effect on the plasma vasopressin concentrations in bilaterally nephrectomized rats, but increased them in intact or sham-operated animals. 4 SQ 20881 potentiated vasopressin release, elicited by angiotensin I, leaving that elicited by angiotensin II unchanged. The receptor antagonist, saralasin, prevented the angiotensin-induced increase in plasma vasopressin concentration, even after pretreatment with SQ 20881. 5 These data support the assumption that the renin-angiotensin system may be involved in the control of vasopressin release, and indicate that in addition to angiotensin II, angiotensin I and III may also contribute, acting in concert.

Mechanism of Suppression of Plasma Renin Activity by Centrally Administered Angiotensin II*

Experiments were performed to determine if the suppression of plasma renin activity (PRA) produced by injection of angiotensin II into the cerebral ventricles is a consequence of the associated increase in plasma vasopressin concentration or arterial blood pressure. The possibility that vasopressin mediates the pressor effect of centrally administered angiotensin II was also investigated. The experiments were performed in pentobarbital- anesthetized dogs with cannulas placed in the third cerebral ventricle. Thirty min after intraventricular injection of angiotensin II (500 ng) in 12 dogs, PRA decreased from 16.0 ± 3.7 to 12.0 ± 3.5 ng/ml-3 h (P < 0.05) in association with an increase in plasma vasopressin concentration from 9.7 ± 1.8 to 20.4 ± 3.6 pg/ml (P < 0.001) and an increase in mean arterial pressure from 124 ± 4 to 136 ± 5 mm Hg (P < 0.001). In 9 acutely hypophysectomized dogs, intraventricular angiotensin II produced no changes in PRA (37.3 ± 8.6 to 35.1 ± 7.4 ng/ml-3 h) or plasma vasopressin conc...