BROMOCRIPTINE-INDUCED MODULATION OF PLASMA ALDOSTERONE RESPONSE TO ACUTE STIMULATIONS

1979 ◽  
Vol 91 (2) ◽  
pp. 294-302 ◽  
Author(s):  
M. Birkhäuser ◽  
A. Riondel ◽  
M. B. Vallotton
Keyword(s):  
Angiotensin Ii ◽  
Dopaminergic System ◽  
Plasma Aldosterone ◽  
Normal Male ◽  
Upright Posture ◽  
Physiological Control ◽  
Male Volunteers ◽  
Basal Plasma ◽  
Dopaminergic Agent

ABSTRACT The influence of the dopaminergic agent 2-bromoergocryptine on plasma aldosterone response to acute stimulations was assessed in 14 normal male volunteers. Without modifying basal plasma aldosterone levels or urinary aldosterone excretion, bromocriptine retarded and diminished significantly the plasma aldosterone response to angiotensin II or ACTH, but did not alter the response to upright posture. These results point to a bromocriptineinduced modulation of the plasma aldosterone response to direct stimulations at the adrenal level. The present work brings further evidence for an effect of the dopaminergic system on the physiological control of aldosterone.

EFFECT OF TWO CONSECUTIVE ACUTE STIMULI ON PLASMA ALDOSTERONE

1972 ◽  
Vol 71 (1) ◽  
pp. 153-159 ◽  
Author(s):  
Fred H. Katz ◽  
Peggy Romfh ◽  
Judith A. Smith
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Adrenal Cortex ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Upright Posture ◽  
Aldosterone Secretion ◽  
Stimulation Of

ABSTRACT The increase in plasma aldosterone and reduction in plasma renin activity induced by 30 to 60 minutes of mildly pressor angiotensin II infusion in man can be largely abolished when recent prior stimulation of the adrenal cortex by upright posture has been applied. A similar prevention of the ACTH-induced increase in plasma aldosterone can be achieved by previous upright ambulation. These results indicate the intermittent refractoriness of aldosterone secretion and that care must be exerted in the timing of any tests of aldosterone stimulation.

Effect of age on plasma aldosterone response to exogenous angiotensin II in normotensive subjects

1980 ◽  
Vol 94 (4) ◽  
pp. 552-558 ◽  
Author(s):  
Ryoyu Takeda ◽  
Shinpei Morimoto ◽  
Kenzo Uchida ◽  
Isamu Miyamori ◽  
Tetsuji Hashiba
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Sodium Intake ◽  
Plasma Renin ◽  
The Elderly ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Middle Aged ◽  
Basal Plasma ◽  
Normotensive Subjects

Abstract. The plasma aldosterone response to angiotensin II (10 ng/kg/min for 30 min, iv) under conditions of varied sodium intake was studied in 10 young subjects (20 to 35 years), 9 middle-aged (41 to 56 years) and 11 elderly (66 to 73 years) normotensive subjects. Basal plasma renin activity, basal plasma level and urinary excretion of aldosterone were significantly lower in the elderly than in the young and middle-aged groups on both 130 and 25 mEq sodium intakes. When sodium intake was reduced to 25 mEq for 3 days, the weight loss was significantly greater in the elderly than in the young and middle-aged groups. No significant differences in blood pressure and serum electrolytes were found between the three groups. Angiotensin II infusion caused significant increases in the mean blood pressure in all the three groups, but to a greater extent in the elderly group. Plasma aldosterone level and its absolute increment, but not its per cent increment, after angiotensin II infusion were significantly lower in the elderly than in the young and middle-aged groups. In combined young, middleaged and elderly subjects, the absolute plasma aldosterone increment correlated positively with basal plasma aldosterone and plasma renin activity levels on a 25 mEq sodium intake, and with plasma renin response to sodium restriction. These results suggest that ageing may cause a lesser plasma aldosterone response to angiotensin II with a decrease in basal plasma aldosterone, in parallel with a decrease in plasma renin activity, under condition of low sodium diet.

Effect of Immunization against Angiotensin II on Blood Pressure and on Plasma Aldosterone in the Rabbit

1975 ◽  
Vol 48 (5) ◽  
pp. 413-420
Author(s):  
R. Beckerhoff ◽  
M. Kappeler ◽  
W. Vetter ◽  
H. Armbruster ◽  
W. Siegenthaler
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Aldosterone ◽  
Plasma Aldosterone Concentration ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Arterial Blood ◽  
Significant Difference ◽  
Basal Plasma ◽  
Clear Increase

1. Rabbits were actively immunized against angiotensin II (AII). 2. Basal plasma aldosterone concentration was 0.058 ±0.027 pmol/ml (20.7±9.6 pg/ml) (mean±SD) in immunized and 0.056±0.021 pmol/ml (20.2±7.5 pg/ml) in control animals during suppression of adrenocorticotrophic hormone by dexamethasone. When the endogenous formation of AII was stimulated by frusemide, by haemorrhage or by feeding with low sodium diet, a significant increase of plasma aldosterone was observed with no difference between immunized and non-immunized animals. 3. In non-immune rabbits, the average mean arterial blood pressure rose 13 mmHg during the infusion of AII (5 pmol min−1 kg−1) and 27 mmHg during the infusion of 50 pmol min−1 kg−1. In contrast, there was no clear increase in blood pressure in the immunized animals. The blood pressure rose in immune animals (15 mmHg) and in non-immune animals (36 mmHg) during the infusion of 200 pmol min−1 kg−1 AII. Plasma aldosterone rose in all animals in response to each of the three infusions with no significant difference between the two groups. 4. It is concluded that the immunization against AII blocked only the pressor effect of the peptide but had no clear influence on the response of plasma aldosterone to increased AII. Differences between the affinities of the adrenal and vascular AII receptors may explain these findings.

Plasma aldosterone response to acute stimulation in panhypopituitarism

1981 ◽  
Vol 97 (4) ◽  
pp. 514-521 ◽  
Author(s):  
M. Birkhäuser ◽  
A. M. Rionde ◽  
R. Gaillard ◽  
F. Mantero ◽  
M. B. Vallotton
Keyword(s):  
Angiotensin Ii ◽  
Anterior Pituitary ◽  
Plasma Aldosterone ◽  
Pituitary Hormone ◽  
Upright Posture ◽  
Healthy Controls ◽  
Lower Plasma ◽  
Aldosterone Secretion ◽  
Anterior Pituitary Hormone

Abstract. The influence of acute stimulation by ACTH, upright posture and angiotensin II on plasma aldosterone levels was assessed in human panhypopituitarism. While stimulation by ACTH in hypopituitary patients induced a plasma aldosterone increase similar to that observed in healthy controls, stimulation by upright posture or by infusion of angiotensin II resulted in a lower plasma aldosterone response than in controls in most of the patients. These results suggest that the presence of an anterior pituitary hormone, most likely ACTH, directly or indirectly exerts a permissive action on aldosterone secretion in man.

Effect of Changes in Sodium Balance on Potassium/Aldosterone Dose-Response Curves in the Dog

1982 ◽  
Vol 62 (4) ◽  
pp. 373-380 ◽  
Author(s):  
M. G. Nicholls ◽  
M. Tree ◽  
J. H. Livesey ◽  
R. Fraser ◽  
J. J. Morton ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Dose Response ◽  
Plasma Potassium ◽  
Plasma Aldosterone ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Sodium Depletion ◽  
Beagle Dogs ◽  
Response Curves ◽  
Dose Response Curves

1. Potassium was infused intravenously in an incremental fashion and the plasma aldosterone responses were measured in conscious beagle dogs at five different intakes of dietary sodium. 2. Potassium/aldosterone dose—response curves were constructed for each dietary sodium regimen. 3. The rate of increase of plasma potassium during graded potassium infusion became progressively greater with increasing sodium depletion. 4. Regression lines of plasma aldosterone on plasma potassium were progressively elevated and steepened with increasing sodium depletion. 5. The alteration of these dose-response curves could in part have been the result of chronic elevation of plasma potassium and angiotensin II, and depression of plasma sodium, with sodium deprivation. 6. By contrast, acute changes in plasma angiotensin II or sodium concentrations across incremental infusions of potassium did not explain the progressive changes in the potassium/aldosterone dose—response curves. 7. The steepest part of the plasma aldosterone response curve was in the plasma potassium range 4–6 mmol/l. 8. Maximum achieved aldosterone levels were similar to or greater than those attained during angiotensin II infusion in previous studies in beagle dogs. 9. Potassium, like angiotensin II and adrenocorticotropic hormone, becomes a more effective stimulus to aldosterone with sodium depletion, thereby facilitating the preservation of sodium homoeostasis.

Effects of angiotensin II and atrial natriuretic peptide alone and in combination on urinary water and electrolyte excretion in man

1988 ◽  
Vol 74 (4) ◽  
pp. 419-425 ◽  
Author(s):  
J. McMurray ◽  
A. D. Struthers
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Normal Male ◽  
Urinary Flow ◽  
Ang Ii ◽  
Electrolyte Excretion ◽  
Water Excretion ◽  
Background Infusion ◽  
Atrial Natriuretic

1. Atrial natriuretic peptide (ANP) has previously been shown to inhibit the renin–angiotensin–aldosterone system (RAAS) at several different levels. We have now investigated a further non-endocrine, renal interaction between ANP and the RAAS. 2. The effects of ANP and angiotensin II (ANG II) alone, and in combination, on urinary electrolyte and water excretion were studied in eight normal male subjects undergoing maximal water diuresis. 3. ANP caused a significant increase in urine flow and sodium excretion. ANG II alone was antidiuretic, antinatriuretic and antikaliuretic. When ANP was given against a background infusion of ANG II, urinary flow rate and electrolyte excretion increased from a new lower level to reach a value intermediate between that found with ANG II alone and ANP alone. 4. It is concluded that the renal effects of ANP are modified in the presence of simultaneously elevated levels of ANG II and that net water and electrolyte excretion reflect the sum of the opposing influences of each peptide. While this interplay may be non-specific, it is possible that ANP may exert some of its actions by specifically inhibiting the intrarenal effects of ANG II.

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.

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