Captopril Combined with Thiazide Lowers Renin Substrate Concentration: Implications for Methodology in Renin Assays

1981 ◽  
Vol 60 (5) ◽  
pp. 591-593 ◽  
Author(s):  
S. Rasmussen ◽  
M. Damkjaer Nielsen ◽  
J. Giese
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Substrate Concentration ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Renin Substrate ◽  
Activity Measurements ◽  
Captopril Treatment

1. We have measured plasma concentrations of renin, renin substrate and angiotensins I and II as well as plasma renin activity in nine patients with severe or malignant hypertension during treatment with captopril, hydrochlorothiazide and propranolol. 2. On captopril and hydrochlorothiazide the plasma concentrations of renin substrate and angiotensin II decreased markedly, while renin and angiotensin I levels were increased. 3. The changes in renin substrate concentration suggest a consumption of substrate induced by an increased renin release. Further, the positive feedback of angiotensin II on hepatic renin substrate synthesis may be inhibited. 4. The sequential changes in renin release during captopril treatment should be monitored by measuring plasma renin concentration since plasma renin activity measurements will be profoundly influenced by the marked changes in plasma renin substrate concentration.

Hormonal and renal responses to converting enzyme inhibition during maximal exercise

1987 ◽  
Vol 63 (5) ◽  
pp. 1796-1800 ◽  
Author(s):  
C. E. Wade ◽  
S. R. Ramee ◽  
M. M. Hunt ◽  
C. J. White
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Maximal Exercise ◽  
Plasma Renin ◽  
Renin Activity ◽  
Converting Enzyme ◽  
Renal Handling ◽  
Renal Responses ◽  
Captopril Treatment

The role of angiotensin II in the hormonal and renal responses to maximal exercise was investigated by using the angiotensin-converting enzyme inhibitor captopril. Nine male subjects performed a standardized maximal treadmill test with and without acute captopril treatment (25 mg orally). At rest, captopril elevated plasma renin activity and lowered aldosterone levels. With maximal exercise, captopril treatment reduced the increase in mean arterial blood pressure by 8 mmHg and the increase in plasma renin activity by 3.0 ng ANG I.ml-1.h-1. The responses of adrenocorticotropin (ACTH), cortisol, and vasopressin to maximal exercise were not altered by captopril treatment. Although aldosterone levels were reduced at rest with captopril, during maximal exercise no difference was noted between treatments. Captopril treatment had no effects on the renal handling of salts or water during exercise. In conclusion, angiotensin II plays a role in the increase in mean blood pressure during maximal exercise in normal subjects but has no effect on the exercise responses of ACTH, vasopressin, and aldosterone or on the renal handling of salts and water.

Biological activity of des-asp-,des-arg-angiotensin II in man

1982 ◽  
Vol 99 (4) ◽  
pp. 577-584 ◽  
Author(s):  
Tsuyoshi Kono ◽  
Fumitake Ikeda ◽  
Fumimaro Oseko ◽  
Yoshiaki Ohmori ◽  
Ryuichi Nakano ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Biological Activity ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Renin Release ◽  
Direct Inhibition ◽  
Normal Men

Abstract. The biololgical activity of des-asp1-,des-arg2-angiotensin II (3-8AII) was studied in man. When 3-8AII was infused iv at rates of 22 and 308 pmol (17.5 and 250 ng)/kg · min separately into 5 normal men each for 120 min, blood pressure showed no change, plasma renin activity (PRA) decreased gradually and plasma aldosterone showed a gradual slight increase. The lower dose of 3-8AII partially inhibited captopril-induced PRA increase and plasma aldosterone decrease in the same 5 normal men and the higher dose of the hexapeptide completely abolished them. In one of the 5 normal men blood pressure rose in response to doses of 3-8AII greater than 2220 pmol (1750 ng)/kg · min. When 3-8AII was infused iv at 308 pmol/kg · min into 2 patients with Bartter's syndrome for 60 min, it caused marked decreases in PRA and plasma aldosterone but no change in blood pressure. This decrease in plasma aldosterone is thought to be secondary to the decrease in PRA. From these results it is evident that 3-8AII has a minimal pressor action, a weak aldosterone-stimulating action and a significant renin-suppressing action in man and this PRA-lowering action is thought to be due to direct inhibition of renin release by its whole molecule or a smaller part of the molecule.

Plasma Renin Activity, Renin Substrate and Angiotensin II in the Isolated Dog Kidney Preparation

1978 ◽  
Vol 1 (5) ◽  
pp. 241-246 ◽  
Author(s):  
M. Staroukine ◽  
J.L. Vanherweghem ◽  
J. Ducobu ◽  
A. d’Hollander ◽  
A. Verniory
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Substrate ◽  
Dog Kidney ◽  
Isolated Dog Kidney

Renin activity in aortic tissue of rats

1969 ◽  
Vol 47 (1) ◽  
pp. 53-56 ◽  
Author(s):  
J. Rosenthal ◽  
R. Boucher ◽  
J. M. Rojo-Ortega ◽  
J. Genest
Keyword(s):  
Plasma Renin Activity ◽  
Substrate Concentration ◽  
Plasma Renin ◽  
Bilateral Adrenalectomy ◽  
Renin Activity ◽  
Aortic Tissue ◽  
Renin Substrate ◽  
Purina Chow ◽  
Low Levels ◽  
Parallel Fashion

Plasma renin activity, aortic tissue renin, and plasma renin substrate concentrations were measured simultaneously and sequentially in groups of rats after (1) bilateral nephrectomy, (2) water deprivation, and (3) bilateral adrenalectomy. Following nephrectomy, plasma renin activity and aortic tissue renin fell in parallel fashion to undetectable or very low levels after 18 h, whereas the substrate concentration in plasma increased markedly. Rats deprived of water for 3 days, but receiving Purina Chow, showed a significant increase in plasma renin activity and in aortic tissue renin and a marked decrease in plasma substrate concentration. Bilateral adrenalectomy resulted in a. very marked augmentation of plasma renin activity and of aortic tissue renin with a concomitant suppression of plasma substrate concentration. These findings suggest that arterial tissue renin reacts to the same stimuli which modify renin activity in plasma.

Elevation of plasma renin activity during avoidance performance in baboons

1976 ◽  
Vol 231 (3) ◽  
pp. 772-776 ◽  
Author(s):  
ML Blair ◽  
EO Feigl ◽  
OA Smith
Keyword(s):  
Plasma Renin Activity ◽  
Substrate Concentration ◽  
Avoidance Performance ◽  
Plasma Renin ◽  
Renin Activity ◽  
Sidman Avoidance ◽  
Papio Cynocephalus ◽  
Plasma Samples ◽  
Renin Substrate ◽  
Lever Pressing

The effect of a 3-h Sidman avoidance operant conditioning schedule (liver pressing to avoid an electric shock) on plasma renin activity and renin substrate concentration was examined in baboons (Papio cynocephalus). Plasma samples were drawn over a 24-h period on both the control and test days, and the avoidance session was presented on the morning of the test day. Plasma renin activity was significantly higher on the test day than at the corresponding hours of the control day at 1, 2, and 3 h after onset of the avoidance test and 30 min after its termination (P = .032). The magnitude of the increase in plasma renin activity was not correlated with either the rate of lever pressing or the number of shocks received. Renin substrate concentration was not changed during or after the avoidance session. These data demostrate that plasma renin activity can be increased by a psychological stimulus.

Angiotensin II receptor subtypes in renal cortex of rats and rhesus monkeys

1991 ◽  
Vol 261 (3) ◽  
pp. F512-F518 ◽  
Author(s):  
R. E. Gibson ◽  
H. H. Thorpe ◽  
M. E. Cartwright ◽  
J. D. Frank ◽  
T. W. Schorn ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Rhesus Monkeys ◽  
Renal Cortex ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Receptor Subtypes ◽  
Ang Ii ◽  
At2 Receptors

The angiotensin II (ANG II) receptor has recently been shown to exhibit subtypes with respect to antagonist binding. Of particular interest are the potent nonpeptide antagonists, DUP 753 and PD 121981, which exhibit selectivity for the subtype 1 (AT1) and subtype 2 (AT2) receptors, respectively. We used these high-affinity antagonists in competition with 125I-[Sar1,Ile8]ANG II to determine autoradiographically the distribution of these ANG II-receptor subtypes in the renal cortex of rats and rhesus monkeys. Binding of the radioligand to receptor in sections of rat renal cortex was inhibited by DUP 753; inhibition by PD 121981 was not detected. By contrast, AT1 and AT2 receptors are present in the renal cortex of rhesus monkeys in regionally distinct structures. DUP 753 inhibited binding to the ANG II receptor in glomeruli. PD 121981 inhibited binding to arterial smooth muscle and the juxtaglomerular (JG) apparatus. The JG apparatus also exhibits radioligand binding, which is inhibited by DUP 753. The effect of DUP 753 and PD 123177 (a more water-soluble analogue of PD 121981) on changes in plasma renin activity was examined to determine if one or both of these subtypes participate in the ANG II-mediated negative feedback of control of renin release. Although DUP 753 increased plasma renin activity to the same extent as the angiotensin-converting enzyme inhibitor, enalaprilat, in rats and rhesus monkeys, the AT2 antagonists did not affect renin release in either species. Thus both subtypes of ANG II receptor are present in rhesus monkey cortex, but a function for only the AT1 subtype was demonstrated.

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