Role of the pituitary in the effects of tonin on adrenal secretion of the rat

1983 ◽  
Vol 61 (3) ◽  
pp. 201-206 ◽  
Author(s):  
Ernesto L. Schiffrin ◽  
Raul Garcia ◽  
Jolanta Gutkowska ◽  
Jacques Genest
Keyword(s):  
Plasma Renin ◽  
Plasma Corticosterone ◽  
Plasma Aldosterone ◽  
High Rate ◽  
Pituitary Hormone ◽  
Plasma Aldosterone Concentration ◽  
Plasma Angiotensin ◽  
Hypophysectomized Rats ◽  
Adrenal Secretion

Chronically catheterized conscious rats were infused intravenously with tonin at 2.4 and 12 μg∙kg−1∙min−1 for 2 h. Plasma aldosterone concentration (PAC) at the end of the experiment was 11.2 ± 2.4 ng% in controls, 8.5 ± 2.8 ng% in rats infused with tonin at the lower rate, and 26.2 ± 3.6 ng% (p < 0.01 vs. controls) in rats infused at the higher rate. Plasma corticosterone (PC) was significantly higher (p < 0.05) in the group infused at the high rate while plasma renin activity (PRA) was significantly reduced in this group of rats. Plasma angiotensin II (AII) concentration was similar in all three groups. PAC was elevated after tonin infusion in the presence of AII blockade. PAC in conscious sodium-depleted rats infused with tonin was not significantly changed, but PRA was significantly reduced (p < 0.01). In chronically hypophysectomized rats, PAC remained unchanged by tonin infusion. The failure of tonin to stimulate aldosterone in hypophysectomized animals indicates a role of a pituitary hormone (probably ACTH) in the effect of tonin on adrenal secretion.

The Hypotensive Effect of Propranolol in Captopril-Treated Patients Does Not Involve the Plasma Renin—Angiotensin—Aldosterone System

1981 ◽  
Vol 61 (s7) ◽  
pp. 441s-444s ◽  
Author(s):  
J. Staessen ◽  
R. Fagard ◽  
P. Lijnen ◽  
L. J. Verschueren ◽  
A. Amery
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Serum Potassium ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Placebo Treatment ◽  
Plasma Aldosterone ◽  
Double Blind ◽  
Plasma Aldosterone Concentration ◽  
Plasma Angiotensin

1. With a double-blind cross-over protocol, 20 hypertensive captopril-treated patients were studied by adding in a variable sequence a placebo and propranolol (80 mg three times a day) to their captopril regimen (200 mg three times a day), during periods each lasting 1 month. During captopril—placebo treatment their diastolic blood pressure remained elevated between 90 and 114 mmHg. 2. The additional administration of propranolol produced a significant hypotensive effect, but no alterations of the plasma angiotensin II and aldosterone concentrations and of the urinary aldosterone excretion occurred. The present data indicate that in captopril-treated patients the hypotensive effect of propranolol is achieved independently of changes in the plasma angiotensin II and aldosterone concentration. 3. The additional administration of propranolol also produced an increase in the serum potassium levels in the absence of any change in the plasma aldosterone concentration or in the urinary aldosterone excretion.

Blood pressure and renal function during chronic changes in sodium intake: role of angiotensin

1980 ◽  
Vol 239 (3) ◽  
pp. F271-F280 ◽  
Author(s):  
J. E. Hall ◽  
A. C. Guyton ◽  
M. J. Smith ◽  
T. G. Coleman
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Filtration Fraction ◽  
Plasma Aldosterone Concentration ◽  
Angiotensin System

The present study was designed to quantitate the role of the renin-angiotensin system (RAS) in determining the chronic relationships between arterial pressure (AP), renal hemodynamics, and Na excretion. In six control dogs, Na balance was achieved during chronic step increases in Na intake from 5 to 500 meq/day with small increases in AP (<7 mmHg), moderate increases in GFR (19%), and decreases in filtration fraction (FF) and plasma renin activity. Similar increases in Na intake in six dogs with angiotensin II (AII) fixed, due to constant intravenous infusion of 5 ng . kg-1 . min-1 AII, caused large increases in AP (42%), GFR (31%) FF, and calculated renal Na reabsorption (TNa) above control. In six dogs with AII formation blocked with SQ 14,225, Na balance at intakes of 5-80 meq/day occurred at reduced AP, GFR, FF, and TNa, although plasma aldosterone concentration (PAC) was not substantially different from that in control dogs. At Na intakes above 240 meq/day, AP was not altered by SQ 14,225. These data indicate that during chronic changes in Na intake the RAS plays a major role, independent of changes in PAC, in allowing Na balance without large changes in GFR or AP. The mechanism whereby AII conserves Na chronically is through increased TNa, since steady-state TNa was increased by AII and decreased by SQ 14,225.

Effect of Spironolactone on Aldosterone Regulation in Man

1980 ◽  
Vol 58 (3) ◽  
pp. 227-233 ◽  
Author(s):  
R. C. Gaillard ◽  
A. M. Riondel ◽  
P. Chabert ◽  
M. B. Vallotton
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Plasma Corticosterone ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Minor Role ◽  
Corticosterone Concentration ◽  
Plasma Aldosterone Concentration ◽  
Normal Men

1. The action of spironolactone, a well-known antagonist of mineralocorticoids, on aldosterone regulation was investigated in normal young men to see whether it also acted as an inhibitor of biosynthesis in the adrenal gland. 2. The action of spironolactone was studied under three different conditions: (a) during 3 days of treatment with spironolactone; (b) during 1 day of combined administration with long acting adrenocorticotropic hormone (ACTH); (c) in the course of a continuous infusion of angiotensin II. 3. Spironolactone did not alter the metabolism of aldosterone or cortisol. 4. Spironolactone administration produced: (a) a marked increase in both aldosterone secretion and plasma renin activity, but no change in the plasma aldosterone/plasma renin activity ratio, the cortisol secretion rate or the plasma corticosterone concentration; (b) no blunting in the response of aldosterone to stimulation by ACTH; (c) no decrease in plasma aldosterone concentration when changes of the endogenous renin activity were prevented by an infusion of angiotensin II. 5. These results do not confirm the considerable inhibition of aldosterone excretion found by others after spironolactone administration to normal men. We observed no inhibition of aldosterone biosynthesis by spironolactone. However, a minimal, short-lived inhibition of biosynthesis cannot be excluded, but this possible action of spironolactone plays at best a minor role in the action of this drug.

Renin, aldosterone, electrolyte, and cortisol responses to hypoxic decompression

1977 ◽  
Vol 43 (3) ◽  
pp. 421-424 ◽  
Author(s):  
J. R. Sutton ◽  
G. W. Viol ◽  
G. W. Gray ◽  
M. McFadden ◽  
P. M. Keane
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Cortisol ◽  
Acute Mountain Sickness ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Plasma Aldosterone Concentration ◽  
Urinary Potassium ◽  
Mountain Sickness

Responses of plasma renin activity, plasma aldosterone, plasma cortisol, and plasma electrolyte concentration and urinary electrolyte and aldosterone excretion were studied in four men during hypoxic decompression to a stimulated altitude of 4,760 m in a pressure chamber. Three of the four subjects developed significant acute mountain sickness. Plasma sodium and potassium concentrations were unchanged. No significant change in plasma renin activity was observed, but values tended to fall. Plasma aldosterone concentration was depressed while plasma cortisol was elevated and diurnal variation lost. Urinary sodium excretion was unchanged, but urinary potassium and aldosterone excretion were decreased. The decrease in plasma and urinary aldosterone and urinary potassium in the absence of change in plasma renin activity or plasma potassium is of uncertain origin. It is unlikely to be due to a decrease in adrenocorticotropin secretion since plasma cortisol rose during the same time. None of the changes could be causally implicated in the development of acute mountain sickness although the increase in plasma cortisol was greatest in the most ill.

Renin, Angiotensin and Aldosterone in Human Pregnancy and the Menstrual Cycle

1971 ◽  
Vol 16 (3) ◽  
pp. 183-196 ◽  
Author(s):  
J. I. S. Robertson ◽  
R. J. Weir ◽  
G. O. Düsterdieck ◽  
R. Fraser ◽  
M. Tree
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin ◽  
Normal Pregnancy ◽  
Maternal Plasma ◽  
Plasma Aldosterone ◽  
Sodium Depletion ◽  
Aldosterone Secretion ◽  
Renin Substrate ◽  
Plasma Aldosterone Concentration ◽  
In Pregnancy

Aldosterone secretion is frequently, although not invariably, increased above the normal non-pregnant range in normal pregnancy. Substantial increases in plasma aldosterone concentration have also been demonstrated as early as the sixteenth week. In pregnancy, aldosterone secretion rate responds in the usual way to changes in sodium intake. Plasma renin concentration is frequently, but not invariably, raised above the normal non-pregnant range. Plasma renin-substrate is consistently raised in pregnancy. Plasma angiotensin II has also been shown usually to be raised in a series of pregnant women. A significant positive correlation has been shown between the maternal plasma aldosterone concentration and the product of the concurrent plasma renin and renin-substrate concentrations. This suggests that the increased plasma aldosterone in pregnancy is the consequence of an increase in circulating angiotensin II, which in turn is related to the level of both renin and its substrate in maternal blood. For these reasons, estimations of renin activity in pregnancy are of dubious value. The increased renin, angiotensin and aldosterone concentrations may represent a tendency to maternal sodium depletion, probably mainly a consequence of the increased glomerular filtration rate. It is possible that the nausea and other symptoms of early pregnancy may be a consequence of this tendency to sodium depletion, with its attendant hormonal changes. In ‘pre-eclampsia’, renin and aldosterone values are generally slightly lower than in normal pregnancy. Human chorion can apparently synthesize renin independently of the kidney. The physiological significance of this remains at present obscure, but it seems unlikely that this source contributes much, if at all, to the often elevated maternal plasma renin. Plasma renin, renin-activity and angiotensin II concentrations, and aldosterone secretion are increased in the luteal phase of the menstrual cycle.

Dissociation in plasma renin and adrenal ANG II and aldosterone responses to sodium restriction in rats

1991 ◽  
Vol 261 (4) ◽  
pp. E487-E494 ◽  
Author(s):  
A. Menachery ◽  
L. M. Braley ◽  
I. Kifor ◽  
R. Gleason ◽  
G. H. Williams
Keyword(s):  
Plasma Renin ◽  
Fold Increase ◽  
Plasma Aldosterone ◽  
Delayed Response ◽  
Ang Ii ◽  
Sodium Restriction ◽  
Sodium Depletion ◽  
Pathway Activity

In rats, plasma renin activity (PRA) increases sharply, reaching a plateau within hours of sodium restriction. Plasma aldosterone increases gradually, not reaching a plateau for 1-2 days. To determine whether this dissociation is secondary to the time needed to modify adrenal sensitivity to angiotensin II (ANG II) and to assess the role of locally produced ANG II in this process, rats were salt restricted for 0-120 h. Plasma hormone levels were assessed, adrenal ANG II was measured, and basal and ANG II (1 x 10(-8) M)-stimulated steroidogenesis were determined in vitro. Although PRA attained an elevated plateau within 8 h, plasma aldosterone did not peak until after 48 h of sodium depletion. The in vitro aldosterone sensitivity to exogenous ANG II was not apparent until rats had been salt restricted for 16 h. A plateau (4-fold increase above the ANG II response on high salt) was achieved between 24 and 48 h. Adrenal ANG II also exhibited a similar delayed response that correlates significantly with changes in aldosterone biosynthesis and late pathway activity. Thus the dissociation between PRA and plasma aldosterone may be secondary to a lag in the zona glomerulosa's (ZG) steroidogenic response to ANG II as well as a parallel lag in tissue ANG II production, suggesting that changes in tissue ANG II may mediate ZG sensitivity to ANG II during sodium deprivation.

scholarly journals Adrenal adaptation in potassium-depleted men: role of progesterone?

2019 ◽  
Vol 35 (11) ◽  
pp. 1901-1908
Author(s):  
Anne Blanchard ◽  
Sylvie Brailly Tabard ◽  
Antonin Lamaziere ◽  
Damien Bergerot ◽  
Valentina Zhygalina ◽  
...  
Keyword(s):  
Healthy Subjects ◽  
Human Subjects ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Plasma Potassium ◽  
Potassium Depletion ◽  
Healthy Human ◽  
Plasma Aldosterone Concentration ◽  
Tandem Mass Spectroscopy

AbstractBackgroundIn rodents, the stimulation of adrenal progesterone is necessary for renal adaptation under potassium depletion. Here, we sought to determine the role of progesterone in adrenal adaptation in potassium-depleted healthy human volunteers and compared our findings with data collected in patients with Gitelman syndrome (GS), a salt-losing tubulopathy.MethodsTwelve healthy young men were given a potassium-depleted diet for 7 days at a tertiary referral medical centre (NCT02297048). We measured by liquid chromatography coupled to tandem mass spectroscopy plasma steroid concentrations at Days 0 and 7 before and 30 min after treatment with tetracosactide. We compared these data with data collected in 10 GS patients submitted to tetracosactide test.ResultsThe potassium-depleted diet decreased plasma potassium in healthy subjects by 0.3 ± 0.1 mmol/L, decreased plasma aldosterone concentration by 50% (P = 0.0332) and increased plasma 17-hydroxypregnenolone concentration by 45% (P = 0.0232) without affecting other steroids. CYP17 activity, as assessed by 17-hydroxypregnenolone/pregnenolone ratio, increased by 60% (P = 0.0389). As compared with healthy subjects, GS patients had 3-fold higher plasma concentrations of aldosterone, 11-deoxycortisol (+30%) and delta 4-androstenedione (+14%). Their post-tetracosactide progesterone concentration was 2-fold higher than that of healthy subjects and better correlated to plasma potassium than to plasma renin.ConclusionThe increase in 17-hydroxypregnenolone concentration after mild potassium depletion in otherwise healthy human subjects suggests that 17 hydroxylation of pregnenolone prevents the increase in progesterone observed in potassium-depleted mice. The unexpected over-response of non-mineralocorticoid steroids to tetracosactide in GS subjects suggests that the adrenal system not only adapts to sodium depletion but may also respond to hypokalaemia.

scholarly journals Hypertension Accompanied by Hyperaldosteronism, Hyperkalemia, and Hyperchloremic Acidosis: A Case Report and Literature Review

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Yunyun Yang ◽  
Yang Ou ◽  
Yan Ren ◽  
Haoming Tian ◽  
Tao Chen
Keyword(s):  
Metabolic Acidosis ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Heterozygous Mutation ◽  
Plasma Aldosterone Concentration ◽  
First Case ◽  
Whole Exome ◽  
Exon 11 ◽  
Clinical Problems

This study reported on a 24-year-old woman who complained of a paroxysmal headache for six months and elevated blood pressure for four months. Laboratory examination revealed increased serum potassium and chloride levels, metabolic acidosis, suppressed renin activity, and increased plasma aldosterone concentration. Whole-exome sequencing revealed a heterozygous mutation in exon 11 of the KLHL3 gene: c.1298G > A. After treatment with low-dose hydrochlorothiazide, her clinical problems were controlled. This patient is the first case of Gordon syndrome (GS) within the Chinese population caused by a heterozygous KLHL3 mutation. A systematic review of the published literature identified 27 patients with GS caused by a KLHL3 mutation. These patients had a mean age of 28.2 ± 22.0 years; 74.1% presented with hypertension, 76.9% with hyperkalemia, and 59.1% with metabolic acidosis. The patients also had varying levels of plasma renin activity and plasma aldosterone concentrations.

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