Effects of psychosocial stimuli on plasma renin activity in rats

1976 ◽  
Vol 231 (4) ◽  
pp. 1290-1294 ◽  
Author(s):  
DM Clamage ◽  
CS Sanford ◽  
AJ Vander ◽  
DR Mouw

The effects of two types of psychosocial stimuli on plasma renin activity (PRA) were studied in unanesthetized rats, blood being collected by decapitation. Thirty minutes of exposure to a novel environment ("open field") produced statistically significant increases of PRA in rats maintained on either a standard (1% NaCl) or sodium-free diet. No change in plasma renin substrate occurred. Prior treatment with propranolol (approximately 2 mg/kg) reduced the renin response by approximately 50% but did not completely abolish it. Plasma renin activity was also increased significantly by exposure of caged rats to the presence of a hungry cat for 30 min. We conclude that psychosocial stimuli can produce significant increases in renin secretion and that this response is mediated, at least in part, by the sympathetic nervous system.

1984 ◽  
Vol 35 (6) ◽  
pp. 782-787 ◽  
Author(s):  
Nicolas D Vlachakis ◽  
John Barr ◽  
Manuel Velasquez ◽  
Natalie Alexander ◽  
Robert Maronde

Author(s):  
Mohammed Siddiqui ◽  
Eric K. Judd ◽  
Bin Zhang ◽  
Tanja Dudenbostel ◽  
Robert M. Carey ◽  
...  

Masked uncontrolled hypertension (MUCH) in treated patients is defined as controlled office blood pressure (BP) but uncontrolled out-of-clinic ambulatory BP. Previously, we have shown that patients with MUCH have evidence of heightened out-of-clinic sympathetic nervous system activity. The aim is to test the hypothesis that MUCH patients have higher aldosterone secretion compared with patients with true controlled hypertension. Two hundred twenty-two patients were recruited after having controlled office BP readings at ≥3 clinic visits. Patients taking MR (mineralocorticoid receptor) antagonists and epithelial sodium channel blockers were excluded. All patients were evaluated by clinic automated office BP and morning serum aldosterone and plasma renin activity. Out-of-clinic ambulatory BP monitoring and 24-hour urinary aldosterone, catecholamines, and metanephrines were also measured. Sixty-four patients had MUCH, and the remaining 48 patients had true controlled hypertension. MUCH patients had significantly higher out-of-clinic levels of 24-hour urinary aldosterone, catecholamines, and metanephrines compared with true controlled hypertension. The 2 groups did not differ in serum aldosterone, plasma renin activity, or aldosterone-renin ratio collected in clinic. In addition, 32.8% of MUCH patients had high out-of-clinic 24-hour urinary aldosterone (≥12 µg) but normal clinic serum aldosterone (<15 ng/dL) and aldosterone-renin ratio (<20). Further, in correlation matrix analysis, higher 24-hour urinary catecholamines and metanephrines were associated with higher 24-hour urinary aldosterone and plasma renin activity levels in MUCH patients. Patients with MUCH have higher out-of-clinic urinary aldosterone levels compared with patients with true controlled hypertension. This study suggests that patients with MUCH likely have higher out-of-clinic sympathetic nervous system tone increases aldosterone secretion mediated by increased renin release that may contribute to their higher out-of-clinic BP.


1976 ◽  
Vol 51 (s3) ◽  
pp. 477s-480s
Author(s):  
A. Fournier ◽  
J. M. Hardin ◽  
J. M. Alexandre ◽  
M. Lombaert ◽  
G. Ronco ◽  
...  

1. Acebutolol, a β1-receptor blocker, has, at a daily dose of 800 mg, a mild but significant anti-hypertensive effect in moderate sustained essential hypertension with normal or low plasma renin activity. 2. Prediction of its anti-hypertensive effect is better based on the evaluation of the sympathetic nervous system responsiveness to head-up tilt than on the evaluation of plasma renin activity or dopamine-β-hydroxylase. 3. The anti-hypertensive effect of acebutolol is better explained on the basis of inhibition of the sympathetic nervous system activity than on the basis of suppression of plasma renin activity. 4. A positive correlation between plasma renin activity and dopamine-β-hydroxylase in patients on diuretics suggests the common dependence of these two variables on sympathetic overactivity.


1981 ◽  
Vol 61 (1) ◽  
pp. 69-73 ◽  
Author(s):  
J. Cunningham ◽  
M. J. Vandenburg ◽  
J. M. P. Holly ◽  
F. J. Goodwin

1. Changes in plasma renin activity, plasma noradrenaline, pulse rate and blood pressure after tilting were measured in normal subjects and in patients with renal transplants. 2. There was a marked difference between the renin responses in the two groups, the increases in plasma renin activity in the control subjects being much greater than those in the transplanted patients. 3. Activation of the sympathetic nervous system after tilting, as indicated by changes in pulse rate, blood pressure and plasma noradrenaline, was similar in the two groups. 4. We conclude that the ability of the transplanted kidney to increase plasma renin activity after tilting is impaired, probably as a result of sympathetic denervation of the kidney during transplantation. The results suggest a dominant role of the sympathetic nervous system in the mediation of renin release after tilting.


1973 ◽  
Vol 44 (3) ◽  
pp. 243-251 ◽  
Author(s):  
Dr T. A. Kotchen ◽  
R. P. Hogan ◽  
A. E. Boyd ◽  
T.-K. Li ◽  
Helen C. Sing ◽  
...  

1. Plasma renin activity, plasma adrenaline and noradrenaline concentrations, and urinary adrenaline and noradrenaline excretion rates were measured in ten subjects during 3 days of exposure to a simulated altitude of 12 000 ft. 2. In both the supine and standing positions, renin activities were suppressed during all 3 days at altitude. 3. Plasma noradrenaline and adrenaline concentrations were significantly increased by the third day at altitude. 4. Urinary adrenaline excretion tended to be increased during the entire 3 days at altitude, with no significant change between the first and third day. Noradrenaline excretion was significantly increased on the third day. 5. The finding of decreased renin levels suggests that the enhanced activity of the sympathetic nervous system at high altitude does not stimulate renin release.


1979 ◽  
Vol 57 (s5) ◽  
pp. 149s-152s ◽  
Author(s):  
A. Morganti ◽  
T. G. Pickering ◽  
J. Lopez-Ovejero ◽  
J. H. Laragh

1. To evaluate the effects of converting-enzyme inhibition on the sympathetic nervous system, on renin and on the other known regulators of aldosterone secretion, we measured blood pressure, heart rate, plasma noradrenaline, adrenaline, renin activity, aldosterone, cortisol and serum potassium in 15 sodium-repleted hypertensive patients in supine position and during 30 min of 65° head-up tilt before and during treatment with SQ 14 225. 2. SQ 14 225 produced significant decreases in supine blood pressure and plasma aldosterone and significant increments in plasma renin activity and potassium; in contrast, heart rate, noradrenaline, adrenaline and cortisol were unchanged. 3. While in control tilt studies blood pressure was always maintained, during treatment three of 15 patients had vasovagal syncopes. In the remaining 12 blood pressure was maintained during tilt on SQ 14 225; however, while the tilt-induced responses in heart rate and adrenaline were as in control studies, the 30 min increments in noradrenaline were significantly higher. 4. Both before and during treatment the responses of plasma renin activity and aldosterone to tilt were parallel, and correlated with each other, and cortisol and potassium changed only slightly. 5. It is concluded that the SQ 14 225-induced fall in blood pressure occurs without a concomitant rise in sympathetic nervous activity; thus the increase in supine plasma renin activity, being a reflection of the interruption of the angiotensin feedback mechanism on renin release, indicates an effective suppression of angiotensin II formation. 6. During SQ 14 225 the persistence of aldosterone response to tilt and its relationship with renin activity suggest that the enzymatic blockade is over-ridden; however, in the presence of a reduced formation of angiotensin II a more pronounced response of the sympathetic nervous system is required to defend blood pressure against postural changes.


1988 ◽  
Vol 255 (5) ◽  
pp. R794-R798 ◽  
Author(s):  
N. M. Rawashdeh ◽  
J. C. Rose ◽  
N. D. Ray

To study the functional maturity of beta-receptor-mediated responses, seven chronically catheterized lamb fetuses, 93-107 days of gestation, and seven fetuses, 116-134 days of gestation, received intravenous randomly sequenced infusions of isoproterenol (ISO) 0.03, 0.06, and 0.125 micrograms.kg-1.min-1 for 10 min separated by 45-min intervals or two saline infusions followed by 0.125 micrograms.kg-1.min-1 ISO after treatment with 0.5 mg/kg propranolol (PRO). Each fetus received the two treatments 24-48 h apart. In immature fetuses, plasma renin activity (PRA) of 2.0 +/- 0.7 ng.ml-1.h-1 did not change with either protocol. In mature fetuses, PRA of 7.5 +/- 2.5 ng.ml-1.h-1 increased two- to three-fold after the infusion of the highest two doses of ISO (P less than 0.003). Propranolol blocked this response. No significant changes were observed after the infusions of the lowest dose of ISO or saline. Both groups showed significant heart rate increases with all doses of ISO. Propranolol injection decreased heart rate significantly and blocked responses to ISO. We conclude that although a cardiac beta-receptor-mediated response is present by 93 days of gestation in the lamb fetus, a renal beta-receptor-mediated response, renin secretion, is absent.


1991 ◽  
Vol 37 (10) ◽  
pp. 1811-1819 ◽  
Author(s):  
J E Sealey

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.


1973 ◽  
Vol 45 (s1) ◽  
pp. 295s-299s ◽  
Author(s):  
L. R. Krakoff ◽  
M. Mendlowitz

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.


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