Effect of hypophysectomy on dipsogenic stimuli: evidence for angiotensin supersensitivity

1986 ◽  
Vol 251 (1) ◽  
pp. R53-R58
Author(s):  
R. H. Alper ◽  
C. F. Deschepper ◽  
W. F. Ganong
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Hypertonic Saline ◽  
Water Deprivation ◽  
Plasma Renin ◽  
Circumventricular Organs ◽  
Renin Activity ◽  
Male Rats ◽  
Plasma Renin Concentration ◽  
Hypophysectomized Rats

The effects of long-term hypophysectomy on renin secretion and the renin and drinking responses to isoproterenol were investigated in male rats. Drinking responses to angiotensin II, hypertonic saline, and water deprivation for 24 h were also measured. Plasma renin activity and plasma angiotensin II were variably lower in rats that had been hypophysectomized for 21 days than in intact controls. Angiotensinogen was also reduced, but plasma renin concentration was not. Isoproterenol produced a smaller increase in plasma renin activity in hypophysectomized rats than it did in controls, but with the one dose of isoproterenol that was tested, the increase in plasma renin concentration was comparable in the two groups. However, the drinking responses to isoproterenol were greater in the hypophysectomized rats. The drinking responses produced by infusion of angiotensin II were also greater, but the responses to infusion of hypertonic saline and to 24 h of water deprivation were not. The data suggest that in rats hypophysectomized for 21 days the circumventricular organs that mediate thirst are hyperresponsive to circulating angiotensin II, possibly because the relatively low circulating angiotensin II levels permit the upregulation of angiotensin II receptors in these structures.

Water deprivation-induced drinking in rats: role of angiotensin II

1983 ◽  
Vol 244 (2) ◽  
pp. R244-R248 ◽  
Author(s):  
C. C. Barney ◽  
R. M. Threatte ◽  
M. J. Fregly
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Water Intake ◽  
Water Deprivation ◽  
Plasma Renin ◽  
Sodium Concentration ◽  
Renin Activity ◽  
Deprivation Period ◽  
Dependent Component

The role of angiotensin II in the control of water intake following deprivation of water for varying lengths of time was studied. Male rats were deprived of water for 0, 12, 24, 36, or 48 h. Water intakes were measured with and without pretreatment with the angiotensin I-converting enzyme inhibitor, captopril (50 mg/kg, ip). Captopril had no significant effect on water intake following either 0 or 12 h of water deprivation. However, captopril significantly attenuated water intake following 24-48 h of water deprivation with the magnitude of the attenuation increasing as the length of the period of water deprivation increased. Plasma renin activity was significantly increased over control levels after 24-48 h of water deprivation but not after 12 h of water deprivation. Plasma renin activity tended to increase as the length of the water-deprivation period increased. Serum osmolality and sodium concentration were significantly increased over control levels following 12-48 h of water deprivation. Serum osmolality and sodium concentration failed to show any further increases with increasing length of water deprivation beyond the increases following 12 h of water deprivation. The data indicate that the water intake of water-deprived rats can be divided into an angiotensin II-dependent component and angiotensin II-independent component. The angiotensin II-independent component appears to be more important in the early stages of water deprivation whereas the angiotensin II-dependent component becomes more important as the length of the water-deprivation period increases.

Plasma Renin Activity and Adrenal Angiotensin II Receptors in Fetal, Newborn, Adult and Pregnant Rabbits

Neonatology ◽  
1979 ◽  
Vol 36 (3-4) ◽  
pp. 119-127 ◽  
Author(s):  
M.G. Pernollet ◽  
M.A. Devynck ◽  
G.J. Macdonald ◽  
P. Meyer
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Angiotensin Ii Receptors

Effect of enalapril (MK-421), an orally active angiotensin I converting enzyme inhibitor, on blood pressure, active and inactive plasma renin, urinary prostaglandin E2, and kallikrein excretion in conscious rats

1984 ◽  
Vol 62 (1) ◽  
pp. 116-123 ◽  
Author(s):  
Ernesto L. Schiffrin ◽  
Jolanta Gutkowska ◽  
Gaétan Thibault ◽  
Jacques Genest
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Ace Inhibition ◽  
Renin Activity ◽  
Prostaglandin E ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Angiotensin I Converting Enzyme

The angiotensin I converting enzyme (ACE) inhibitor enalapril (MK-421), at a dose of 1 mg/kg or more by gavage twice daily, effectively inhibited the pressor response to angiotensin I for more than 12 h and less than 24 h. Plasma renin activity (PRA) did not change after 2 or 4 days of treatment at 1 mg/kg twice daily despite effective ACE inhibition, whereas it rose significantly at 10 mg/kg twice daily. Blood pressure fell significantly and heart rate increased in rats treated with 10 mg/kg of enalapril twice daily, a response which was abolished by concomitant angiotensin II infusion. However, infusion of angiotensin II did not prevent the rise in plasma renin. Enalapril treatment did not change urinary immunorcactive prostaglandin E2 (PGE2) excretion and indomethacin did not modify plasma renin activity of enalapril-treated rats. Propranolol significantly reduced the rise in plasma renin in rats receiving enalapril. None of these findings could be explained by changes in the ratio of active and inactive renin. Water diuresis, without natriuresis and with a decrease in potassium urinary excretion, occurred with the higher dose of enalapril. Enalapril did not potentiate the elevation of PRA in two-kidney one-clip Goldblatt hypertensive rats. In conclusion, enalapril produced renin secretion, which was in part β-adrenergically mediated. The negative short feedback loop of angiotensin II and prostaglandins did not appear to be involved. A vasodilator effect, apparently independent of ACE inhibition, was found in intact conscious sodium-replete rats.

L-arginine analogues inhibit aldosterone secretion in rats

1995 ◽  
Vol 268 (5) ◽  
pp. R1137-R1142 ◽  
Author(s):  
J. C. Simmons ◽  
R. H. Freeman
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Methyl Ester ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Bilateral Nephrectomy ◽  
Aldosterone Secretion ◽  
Series Of Experiments

L-Arginine analogues, e.g., NG-nitro-L-arginine methyl ester (L-NAME), increase arterial pressure and suppress renin release in the rat. On the basis of these observations, it was hypothesized that L-arginine analogues also would attenuate aldosterone secretion. This hypothesis was tested in anesthetized rats treated with L-NAME or NG-nitro-L-arginine (L-NNA, 185 mumol/kg ip). The aldosterone secretion rate, plasma renin activity, and adrenal blood flow were attenuated in rats treated with L-NAME and L-NNA compared with control animals. Similar experiments were performed in anephric rats to examine the effects of L-NAME on aldosterone secretion independent of the circulating reninangiotensin system. The administration of L-NAME reduced adrenal blood flow but failed to reduce aldosterone secretion in these anephric rats. Bilateral nephrectomy reduced plasma renin activity essentially to undetectable levels in these animals. In a third series of experiments, two groups of anephric rats were infused with angiotensin II (3 micrograms/kg body wt iv) to provide a stimulus for aldosterone secretion. Aldosterone secretion and adrenal blood flow were markedly reduced in angiotensin II-infused rats pretreated with L-NAME compared with the control anephric animals infused with angiotensin II. Overall these results suggest that L-arginine analogues attenuate aldosterone secretion by inhibiting the adrenal steroidogenic effects of endogenous or exogenous angiotensin II and/or by reducing plasma levels of renin/angiotensin.

Vasopressin Effects on Plasma Renin Activity in Male and Female Rats

1978 ◽  
Vol 55 (3) ◽  
pp. 301-307 ◽  
Author(s):  
I. W. Henderson ◽  
R. J. Balment ◽  
J. Ann Oliver
Keyword(s):  
Plasma Renin Activity ◽  
Diabetes Insipidus ◽  
Antidiuretic Hormone ◽  
Plasma Renin ◽  
Renin Activity ◽  
Female Rats ◽  
Male Rats ◽  
Adrenergic Blockade ◽  
Male And Female ◽  
Male And Female Rats

1. The influence of gonadal and pituitary factors on the plasma renin response to exogenous vasopressin was examined in anaesthetized rats. 2. Plasma renin activity (PRA) was measured in Brattleboro rats (with and without hypothalamic diabetes insipidus) and Long-Evans male and female rats, before and after single intravenous injection of antidiuretic hormone (ADH) or saline. 3. Control saline injections did not change PRA. ADH reduced PRA in male, but increased PRA in female rats. Rats with diabetes insipidus displayed the greatest changes and were used in subsequent experiments. Extrarenal renin activity (nephrectomized rats) gave qualitatively similar responses to ADH. Plasma renin concentration, which was also measured with PRA in intact and nephrectomized male and female rats with diabetes insipidus, increased in the females and decreased in the males after ADH. 4. Castration, 24 h before study, abolished the ADH-induced fall in PRA, and testosterone implanted before castration did not restore the response. Cyproterone acetate reversed the ADH effect in males, so that PRA then rose after ADH. Hypophysectomized male rats, with depressed basal plasma renin activities, also showed a reduced PRA after ADH. 5. Ovariectomy had little effect on the ADH-induced renin release and the response was similar at oestrus, metoestrus and dioestrus. In hypophysectomized female rats ADH reduced PRA; a male pattern of response was seen in hypophysectomized female rats. 6. In both sexes PRA responses to ADH were blunted but not abolished by β-adrenergic blockade (propranolol). α-Adrenergic blockade (phenoxybenzamine) had little influence on the male response but in females the typical increase disappeared so that ADH reduced PRA. 7. It is concluded that pituitary hormones, including gonadotrophins and gonadal factors as well as adrenal sex steroids, appear to affect significantly the interplay between antidiuretic hormone and the renin—angiotensin system.

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