Angiotensin II-induced thirst and vasopressin release in man

1985 ◽  
Vol 68 (6) ◽  
pp. 669-674 ◽  
Author(s):  
P. A. Phillips ◽  
B. J. Rolls ◽  
J. G. G. Ledingham ◽  
J. J. Morton ◽  
M. L. Forsling
Keyword(s):  
Angiotensin Ii ◽  
Water Deprivation ◽  
Vasopressin Release ◽  
Physiological Conditions ◽  
Physiological Range ◽  
Pathological Conditions ◽  
Plasma Vasopressin ◽  
Plasma Angiotensin ◽  
Vasopressin Secretion ◽  
Single Blind

1. The thirst and plasma vasopressin responses to single-blind controlled intravenous angiotensin II infusions (2-16 ng min−1 kg−1) were investigated in ten healthy young men. 2. Thirst and vasopressin secretion were stimulated in four out of ten subjects. These effects occurred at plasma angiotensin concentrations well above those measured under physiological conditions associated with thirst and vasopressin secretion such as water deprivation. 3. Further studies are needed to define why only certain individuals respond to intravenous angiotensin II infusions and to determine whether potentiation of angiotensin-induced thirst and vasopressin secretion by other stimuli (e.g. hypovolaemia and hypertonicity) might occur in man, in particular under pathological conditions when plasma angiotensin levels are above the physiological range.

Chemoreflex and endocrine components of cardiovascular responses to acute hypoxemia in the llama fetus

1996 ◽  
Vol 271 (1) ◽  
pp. R73-R83 ◽  
Author(s):  
D. A. Giussani ◽  
R. A. Riquelme ◽  
F. A. Moraga ◽  
H. H. McGarrigle ◽  
C. R. Gaete ◽  
...  
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
High Altitude ◽  
Chronic Exposure ◽  
Perfusion Pressure ◽  
Carotid Sinus ◽  
Cardiovascular Responses ◽  
Pronounced Increase ◽  
Plasma Vasopressin ◽  
Plasma Angiotensin

We tested the hypothesis that the llama fetus has a blunted cardiovascular chemoreflex response to hypoxemia by investigating the effects of acute hypoxemia on perfusion pressure, heart rate, and the distribution of the combined ventricular output in 10 chronically instrumented fetal llamas at 0.6-0.7 gestation. Four llama fetuses had the carotid sinus nerves sectioned. In the intact fetuses, there was a marked bradycardia, an increase in perfusion pressure, and a pronounced peripheral vasoconstriction during hypoxemia. These cardiovascular responses during hypoxemia in intact fetuses were accompanied by a pronounced increase in plasma vasopressin, but not in plasma angiotensin II concentrations. Carotid denervation prevented the bradycardia at the onset of hypoxemia, but it did not affect the intense vasoconstriction during hypoxemia. Plasma vasopressin and angiotensin II levels were not measured in carotid-denervated fetuses. Our results do not support the hypothesis that the carotid chemoreflex during hypoxemia is blunted in the llama fetus. However, they emphasize that other mechanisms, such as increased vasopressin concentrations, operate to produce an intense vasoconstriction in hypoxemia. This intense vasoconstriction in the llama fetus during hypoxemia may reflect the influence of chronic exposure to the hypoxia of high altitude on the magnitude and gain of fetal cardiovascular responses to a superimposed acute episode of hypoxemia.

Interactions between brain acetylcholine and prostaglandins in control of vasopressin release

1991 ◽  
Vol 261 (2) ◽  
pp. R420-R426
Author(s):  
M. Inoue ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Stimulation Of

We have examined in conscious rats the interaction between centrally acting prostanoids and acetylcholine in the stimulation of vasopressin secretion. The intracerebroventricular (icv) administration of carbachol (25 ng) resulted in marked transient increases in the plasma vasopressin concentration and mean arterial blood pressure and a transient reduction in heart rate. Central cyclooxygenase blockade by pretreatment icv with either meclofenamate (100 micrograms) or indomethacin (100 micrograms) virtually completely blocked these responses. Prostaglandin (PG) D2 (20 micrograms icv) caused transient increases in the plasma vasopressin concentration (much smaller than after carbachol) and heart rate, whereas mean arterial blood pressure rose gradually during the 15-min course of the experiment. Pretreatment with the muscarinic antagonist atropine (10 micrograms icv) decreased the peak vasopressin response to icv PGD2 by approximately one-third but had no effect on the cardiovascular responses. We conclude that the stimulation of vasopressin release by centrally acting acetylcholine is dependent on increased prostanoid biosynthesis. On the other hand, stimulation of vasopressin release by icv PGD2 is partially dependent on activation of a cholinergic pathway.

Vasopressin release during nonhypotensive hemorrhage and angiotensin II infusion

1975 ◽  
Vol 228 (1) ◽  
pp. 149-154 ◽  
Author(s):  
RE Shade ◽  
L Share
Keyword(s):  
Angiotensin Ii ◽  
Carotid Artery ◽  
Common Carotid Artery ◽  
Volume Control ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Arterial Plasma ◽  
Carotid Arterial

These experiments were designed to determine whether angiotensin II (AII) could potentiate the increase in plasma vasopressin (ADH) concentration produced by continuous, nonhypotensive hemorrhage in nephrectomized dogs. Infusion of AII (10 ng/kg.min) into a common carotid artery in nonbled dogs did not increase plasma ADH levels, suggesting that increases in carotid arterial plasma AII concentration alone do not stimulate an increase in ADH release. Subsequently, nephrectomized dogs subjected to nonhypotensive hemorrhage (0.44 ml/kg.min) were infused as follows: 0.9% saline intravenously, AII (10 ng/kg.min) intravenously, or AII (10 ng/kg.min) into the carotid. The Plasma ADH concentration increased in all three groups of dogs during hemorrhage. Although the AII-infused dogs demonstrated significant increases in plasma ADH levels earlier during hemorrhage, these changes were small; there were no statistically significant differences in plasma ADH concentrations among the three groups. These results suggest that increases in plasma AII concentration have little or no significant effect on the volume control of ADH release.

Ventricular receptors stimulate vasopressin release during hemorrhage

1988 ◽  
Vol 254 (2) ◽  
pp. R204-R211 ◽  
Author(s):  
B. C. Wang ◽  
G. Flora-Ginter ◽  
R. J. Leadley ◽  
K. L. Goetz
Keyword(s):  
Left Atrial ◽  
Heart Rate Response ◽  
Venous Pressure ◽  
Control Level ◽  
Conscious Dogs ◽  
Central Venous ◽  
Vasopressin Release ◽  
Cardiac Denervation ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion

These experiments were designed to investigate whether a reflex arising from ventricular receptors is capable of stimulating vasopressin secretion during hemorrhage. Three groups of conscious dogs (sham operated, cardiac denervated, and ventricular denervated) were hemorrhaged slowly until 30 ml blood/kg body wt had been removed. Hemorrhage produced comparable decreases in stroke volume, central venous pressure, and left atrial pressure in each group of dogs but produced a different pattern of heart rate response in each group. Plasma vasopressin concentrations before hemorrhage did not differ in the three groups of dogs. In sham-operated dogs plasma vasopressin increased from a control level of 2.4 +/- 0.3 to 6.2 +/- 1.7, 200.0 +/- 65.4, and 991.3 +/- 220.9 pg/ml after 10, 20, and 30 ml/kg of blood had been removed, respectively. In contrast, plasma vasopressin did not increase in either cardiac-denervated or ventricular-denervated dogs after 10 ml/kg of blood had been removed, and the increases in circulating vasopressin after 20 and 30 ml/kg hemorrhage were markedly attenuated by cardiac denervation and by ventricular denervation. The magnitude of the increase in plasma vasopressin in the cardiac-denervated and ventricular-denervated dogs did not differ significantly at comparable levels of hemorrhage. The results are consistent with the possibility that a reflex initiated by ventricular receptors is primarily responsible for stimulating the secretion of vasopressin during hemorrhage in conscious dogs.

Effect of blood glucose concentration on osmoregulation in diabetes mellitus

1989 ◽  
Vol 256 (3) ◽  
pp. R597-R604 ◽  
Author(s):  
C. J. Thompson ◽  
S. N. Davis ◽  
P. H. Baylis
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Blood Glucose Concentration ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Plasma Sodium ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Insulin Dependent ◽  
Vasopressin Secretion

Poorly controlled insulin-dependent diabetes mellitus is associated with considerable elevations of plasma vasopressin concentrations, although well-controlled diabetics have normal osmoregulated thirst and vasopressin release. We studied the effect of blood glucose concentration on osmoregulated thirst and vasopressin secretion in insulin-dependent diabetes mellitus. Blood glucose was maintained overnight, and for the duration of the study, in either the euglycemic (4-5 mmol/l) or hyperglycemic (10-12 mmol/l) range, and patients underwent infusion of hypertonic (855 mmol/l) sodium chloride solution. Plasma sodium was lower during the hyperglycemic study, but elevation in plasma sodium concentration by infusion of saline caused progressive linear increases in both thirst and plasma vasopressin concentrations in both studies. Linear regression analysis defined lowered plasma sodium thresholds for both thirst appreciation and vasopressin release during the hyperglycemic study, although the sensitivity of the osmoreceptors remained unchanged. Analysis of the data in terms of plasma osmolality, corrected for the increase in blood glucose in the hyperglycemic study, revealed no differences in the osmotic thresholds for thirst or vasopressin release; sensitivity of the osmoreceptors also remained the same. Drinking abolished thirst and lowered plasma vasopressin concentrations before major changes in plasma sodium were observed. These results show that insulin-dependent diabetic patients osmoregulate appropriately when moderately hyperglycemic but that the threshold plasma sodium for vasopressin secretion and thirst appreciation is lowered by an unknown mechanism.

Effects of intraventricular injection of Sar1-Ala8-angiotensin II on plasma vasopressin level increased by angiotensin II and by water deprivation in conscious rats

1980 ◽  
Vol 93 (4) ◽  
pp. 407-412 ◽  
Author(s):  
K. Yamaguchi ◽  
H. Hama ◽  
T. Sakaguchi ◽  
H. Negoro ◽  
K. Kamoi
Keyword(s):  
Angiotensin Ii ◽  
Water Deprivation ◽  
Plasma Osmolality ◽  
Male Rats ◽  
Intraventricular Injection ◽  
Plasma Vasopressin ◽  
Significant Difference ◽  
Median Plasma ◽  
Specific Antagonist ◽  
The Brain

Abstract. The effects of intraventricular injection of Sar1-Ala8-angiotensin II (a specific antagonist of angiotensin II) on the plasma vasopressin level increased by intraventricular injection of angiotensin II and by water deprivation (46 h) were examined in conscious male rats with an indwelling cannula in the third cerebral ventricle. Blood samplings were made by decapitation and the plasma level of vasopressin was determined by radioimmunoassay. Twenty-five, 50 or 100 ng of angiotensin II produced significant (P<0.05) increase in plasma vasopressin level 90 sec after the injection. The effect of 50 ng of angiotensin II was inhibited significantly (P<0.05) at least with 100 ng of Sar1-Ala8-angiotensin II given 2 min before the injection of angiotensin II. The dehydrated rats to which 1000 ng of Sar1-Ala8-angiotensin II was given 5 min before the decapitation showed the significantly (P<0.05) lower median plasma vasopressin level than that of the dehydrated controls. No significant difference in plasma osmolality was noted between them. These results suggest that the plasma vasopressin response to intraventricular angiotensin II is produced via angiotensin II receptors in the brain and that Sar1-Ala8-angiotensin II inhibits the effect of endogenous angiotensin II on plasma vasopressin level under dehydration.

Central cholinergic control of vasopressin release in conscious rats

1986 ◽  
Vol 251 (2) ◽  
pp. E146-E150 ◽  
Author(s):  
K. Iitake ◽  
L. Share ◽  
Y. Ouchi ◽  
J. T. Crofton ◽  
D. P. Brooks
Keyword(s):  
Blood Pressure ◽  
Muscarinic Receptors ◽  
Dependent Manner ◽  
Conscious Rat ◽  
Vasopressin Release ◽  
Conscious Rats ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Dose Dependent ◽  
Stimulation Of

Intracerebroventricular (icv) administration of carbachol into conscious rats evoked a substantial increase in vasopressin secretion and blood pressure in a dose-dependent manner. These effects were blocked by pretreatment with the muscarinic blocker, atropine (10 micrograms icv), but not by the nicotinic blocker, hexamethonium (10 micrograms icv). Hexamethonium did, however, block the increase in blood pressure, the decrease in heart rate, and the very small elevation in the plasma vasopressin concentration induced by nicotine (10 micrograms icv). These results indicate that stimulation of either central nicotinic or muscarinic receptors can affect the cardiovascular system and suggest that the cholinergic stimulation of vasopressin secretion may involve primarily muscarinic receptors in the conscious rat.

EFFECTS OF ANGIOTENSIN II ON ARGININE-VASOPRESSIN IN PHYSIOLOGICAL AND PATHOLOGICAL SITUATIONS IN MAN

1977 ◽  
Vol 74 (2) ◽  
pp. 251-259 ◽  
Author(s):  
P. L. PADFIELD ◽  
J. J. MORTON
Keyword(s):  
Angiotensin Ii ◽  
Arginine Vasopressin ◽  
Plasma Levels ◽  
High Plasma ◽  
Physiological Control ◽  
Vasopressin Release ◽  
Normal Volunteers ◽  
Plasma Angiotensin ◽  
Plasma Arginine ◽  
Acute Changes

Studies were designed to determine whether angiotensin II has a direct stimulatory effect on arginine-vasopressin in man and to determine the role, if any, played by angiotensin II in the control of vasopressin release in physiological and pathological conditions. Acute infusion of angiotensin II in normal volunteers produced small but definite increases in plasma levels of arginine-vasopressin (5·4 ± 0·3 (s.e.m.) to 6·4 ± 0·2 pg/ml) only when plasma angiotensin II levels were supraphysiological. Concurrent measurements of plasma arginine-vasopressin and angiotensin II were made during acute changes in fluid balance and posture in normal volunteers and in clinical conditions characterized by high plasma levels of angiotensin II (Addison's disease and Bartter's syndrome). The results of these studies allow us to conclude that there is little to suggest a direct effect of angiotensin II which is likely to be relevant to the normal physiological control of arginine-vasopressin in man.

Effect of ovarian steroids on vasopressin secretion

1982 ◽  
Vol 95 (1) ◽  
pp. 147-151 ◽  
Author(s):  
Mary L. Forsling ◽  
P. Strömberg ◽  
M. Åkerlund
Keyword(s):  
Postmenopausal Women ◽  
Vasopressin Release ◽  
Ovarian Steroids ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Menstruating Women ◽  
Plasma Oestradiol

In normally menstruating women plasma vasopressin concentrations vary with the stage of the cycle and are highest at the time of ovulation and lowest at the onset of menstruation. To determine whether this is the result of changes in the circulating concentrations of ovarian steroids, vasopressin concentrations were determined in six postmenopausal women given oestrogen and progestogen. An increase in plasma oestradiol concentrations to 299 ± 97·8 pmol/l augmented vasopressin release. Administration of medroxyprogesterone did not influence vasopressin concentrations but when given in combination with oestrogen a fall was observed. Thus it appears that ovarian steroids can modulate vasopressin release.

Osmoregulation of thirst and vasopressin secretion in insulin-dependent diabetes mellitus

1988 ◽  
Vol 74 (6) ◽  
pp. 599-606 ◽  
Author(s):  
C. J. Thompson ◽  
S. N. Davis ◽  
P. C. Butler ◽  
J. A. Charlton ◽  
P. H. Baylis
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Sodium Chloride ◽  
Plasma Osmolality ◽  
Glucose Infusion ◽  
Diabetic Patients ◽  
Healthy Controls ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion

1. Osmotically stimulated thirst and vasopressin release were studied during infusions of hypertonic sodium chloride and hypertonic d-glucose in euglycaemic clamped diabetic patients and healthy controls. 2. Infusion of hypertonic sodium chloride caused similar elevations of plasma osmolality in diabetic patients (288.0 ± 1.0 to 304.1 ± 1.6 mosmol/kg, mean ± sem, P < 0.001) and controls (288.6 ± 0.9 to 305.7 ± 0.6 mosmol/kg, P < 0.001), accompanied by progressive increases in plasma vasopressin (diabetic patients, 0.9 ± 0.3 to 7.7 ± 1.5 pmol/l, P < 0.001; controls 0.5 ± 0.1 to 6.5 ± 1.0 pmol/l, P < 0.001) and thirst ratings (diabetic patients 1.0 ± 0.2 to 7.1 ± 0.5 cm, P < 0.001; controls 1.8 ± 0.4 to 8.0 ± 0.5 cm, P < 0.001) in both groups. 3. Drinking rapidly abolished thirst and vasopressin secretion before major changes in plasma osmolality occurred in both diabetic patients and healthy controls. 4. There were close and significant correlations between plasma vasopressin and plasma osmolality (diabetic patients, r = + 0.89, controls r = + 0.93) and between thirst and plasma osmolality (diabetic patients r = +0.95, controls r = +0.97) in both diabetic patients and healthy controls during hypertonic saline infusion. 5. Hypertonic d-glucose infusion caused similar elevations in blood glucose in diabetic patients (4.0 ± 0.2 to 20.1 ± 1.2 mmol/l, P < 0.001) and healthy controls (4.3 ± 0.1 to 19.3 ± 1.2 mmol/l, P < 0.001) but did not change plasma vasopressin or thirst ratings. There was no correlation between plasma osmolality and either thirst or plasma vasopressin during hypertonic d-glucose infusion. 6. The characteristics of osmoregulated thirst and vasopressin release are similar in health and diabetes mellitus. As hyperglycaemia was not dipsogenic, however, the thirst of poorly controlled diabetes mellitus may be due to hypovolaemia secondary to polyuria rather than hyperosmolality due to elevated blood glucose concentrations.

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