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.

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.

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.

Plasma renin activity and plasma prorenin assays

1991 ◽  
Vol 37 (10) ◽  
pp. 1811-1819 ◽  
Author(s):  
J E Sealey
Keyword(s):  
Plasma Renin Activity ◽  
Sodium Intake ◽  
Vascular Complications ◽  
Plasma Renin ◽  
Renin Activity ◽  
Blood Collection ◽  
Kinetic Assay ◽  
Renin Substrate ◽  
Patients With Diabetes ◽  
Commercial Kits

Abstract Sensitivity and accuracy are essential features of an assay of plasma renin activity (PRA) because the normal concentration of PRA is only 1 pmol/L, and subnormal concentrations have diagnostic relevance. Conditions for blood collection need to be standardized but the conditions are not difficult for outpatients. For routine diagnostic purposes blood should be collected from ambulatory (ideally, untreated) patients on moderate sodium intake. To avoid irreversible cryoactivation of plasma prorenin (which is present in 10-fold greater concentrations than renin), samples should be processed at room temperature and stored completely frozen. Cryoactivation occurs when plasma is liquid at temperatures less than 6 degrees C. PRA is commonly measured with an enzyme kinetic assay in which angiotensin I (Ang I) is formed by the reaction of plasma renin with endogenous renin substrate (angiotensinogen). The Ang I so formed is measured by RIA; results are expressed as an hourly rate (micrograms/L formed per hour). This method, which is provided by most commercial kits, has the potential for unlimited sensitivity because the step for Ang I generation can be prolonged as long as necessary, so that enough Ang I forms to be measured accurately. Unfortunately, that sensitivity is not always exploited. Dilution of plasma during pH adjustment should be kept to a minimum. The Ang I generation step should last at least 3 h. The step should last 18 h for samples with PRA less than 1.0 micrograms/L per hour, to eliminate the errors inherent in the measurement and subtraction of immunoreactive Ang I in the untreated plasma (blank subtraction). These changes actually simplify PRA measurements because they eliminate the need for ice in the clinic and reduce by almost half the number of samples to be assayed by RIA. I also describe the method for measurement of plasma prorenin, which may be an important marker for patients with diabetes mellitus who subsequently develop vascular complications.

Plasma Renin Activity and Plasma Renin Substrate in Hypertension Associated with Steroid Excess

1973 ◽  
Vol 45 (s1) ◽  
pp. 295s-299s ◽  
Author(s):  
L. R. Krakoff ◽  
M. Mendlowitz
Keyword(s):  
Oral Contraceptive ◽  
Plasma Renin Activity ◽  
Cushing’S Syndrome ◽  
Plasma Renin ◽  
Cushing's Syndrome ◽  
Glucocorticoid Therapy ◽  
Renin Activity ◽  
Angiotensin I ◽  
Renin Substrate ◽  
Contraceptive Agents

1. Plasma renin activity and plasma renin substrate were measured by radioimmunoassay of generated angiotensin I in patients with steroid excess syndromes. Significant increases in substrate were observed in patients with Cushing's syndrome, during glucocorticoid therapy and on oral contraceptive agents. Suppression of plasma renin activity occurred only in primary aldosteronism. 2. The Michaelis constant (Km) for the reaction between renin and substrate in plasma at physiological pH (7.4) was also determined. The extent to which elevated plasma renin substrate increases the velocity of angiotensin I formation was then calculated. 3. In patients with Cushing's syndrome, glucocorticoid therapy or oral contraceptive use, elevated renin substrate coupled with failure of suppression of circulating renin results in increased angiotensin I formation.

Effects of Sex Hormones on the Renal Pressor System

1971 ◽  
Vol 49 (4) ◽  
pp. 292-301 ◽  
Author(s):  
Alberto Nasjletti ◽  
Masato Matsunaga ◽  
Georges M. C. Masson
Keyword(s):  
Plasma Renin Activity ◽  
Sex Hormones ◽  
Negative Feedback ◽  
Substrate Concentration ◽  
Renal Hypertension ◽  
Plasma Renin ◽  
Renin Activity ◽  
High Substrate Concentration ◽  
High Substrate ◽  
Constant Dose

The effects of sex and sex hormones on angiotensinogen, renin activity, and renin concentration in plasma and on renal renin were investigated in rats. During estrus there was a significant increase in angiotensinogen, which was suppressed by ovariectomy. In males, castration had no effect. Administration of stilbestrol caused a rapid increase in angiotensinogen. Renal renin and plasma renin concentration decreased while plasma renin activity remained near normal levels. Following addition of a constant dose of rat renin, plasma from estrogen-treated rats released angiotensin at a faster rate than normal plasma; this increased reactivity is attributed to the high substrate concentration and not to the lack of an inhibitor, to the presence of an activator, or of a more reactive substrate. These changes were not modified by progesterone or testosterone. Progesterone alone caused a significant increase in renal renin. Estrogens did not elicit hypertension nor modify a preexisting renal hypertension. These observations support the hypothesis that the primary effect of estrogens is an increased angiotensinogen formation, and that the resulting enhancement in plasma reactivity to renin causes an increase in angiotensin which acts as a negative feedback on renin production.

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