A Correlation Between Plasma Renin Activity and the Pressor Response to Angiotensin II.

1974 ◽  
Vol 29 (5) ◽  
pp. 304-312
Author(s):  
J. Deheneffe ◽  
A. Bernard
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Pressor Response ◽  
Plasma Renin ◽  
Renin Activity

The Pressor Response to Intravenously Infused Angiotensin II: Correlation with Plasma Renin Activity

1974 ◽  
Vol 46 (2) ◽  
pp. 149-161 ◽  
Author(s):  
J. Deheneffe ◽  
A. Bernard
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Dose Response ◽  
Pressor Response ◽  
Plasma Renin ◽  
Renin Activity ◽  
Response Curves ◽  
Basal Plasma ◽  
Dose Response Curves ◽  
The Individual

1. When angiotensin II was infused into forty unselected subjects a linear relationship was found between the increment of diastolic blood pressure and the logarithm of the rate of infusion of angiotensin II. 2. The slope of this line was very reproducible on repeated determinations in the same subject. 3. When the correlations between pre-infusion plasma renin activity and various functions derived from dose—response curves were determined, it was observed that: (i) the significance of the correlation became progressively stronger when increasing thresholds of the pressor response to angiotensin II were considered; (ii) the best correlation was achieved when the slopes of the individual dose—response curves were plotted against the logarithm of corresponding plasma renin activities. 4. These results suggest that the slope of the pressor dose—response curve is the most reliable index of responsiveness to intravenously infused angiotensin II and that it may provide a satisfactory guide to the basal plasma renin activity.

The Immediate Pressor Response to Saralasin in Man: Evidence against Sympathetic Activation and for Intrinsic Angiotensin II-Like Myotropism

1984 ◽  
Vol 66 (5) ◽  
pp. 517-524 ◽  
Author(s):  
C. J. Mathias ◽  
R. J. Unwin ◽  
F. A. Pike ◽  
H. L. Frankel ◽  
P. S. Sever ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Cervical Spinal Cord ◽  
Pressor Response ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Renin Activity ◽  
Sympathetic Activation ◽  
Basal Plasma ◽  
Dose Dependent

1. The cardiovascular and hormonal effects of intravenous saralasin (0.5, 1 and 5 μg min−1 kg−1) were assessed in nine tetraplegic patients (with complete cervical spinal cord transaction above the sympathetic outflow) and in six normal subjects. 2. In the tetraplegic patients, saralasin caused an immediate transient pressor response which was not dose-dependent and substantially greater than the pressor response in normal subjects. The pressor response in the tetraplegic patients was not accompanied by a rise in levels of plasma noradrenaline. 3. In the tetraplegic patients, after α-adrenoceptor blockade with thymoxamine (1 mg kg−1 h−1), twice the dose of intravenous noradrenaline was needed to induce the same pressor response. The pressor response to saralasin (5 μg kg−1 min−1), however, was unaffected by thymoxamine. 4. Saralasin caused minimal changes in levels of plasma renin activity and plasma aldosterone in both groups. There was no relationship between basal plasma renin activity and the pressor response in either group. 5. We therefore conclude that the immediate transient pressor response to saralasin in man is not due to central sympathetic stimulation, is unlikely to be due to peripheral sympathetic activation and is probably the result of intrinsic angiotensin II-like myotropism.

Plasma Renin Activity and Adrenal Angiotensin II Receptors in Fetal, Newborn, Adult and Pregnant Rabbits

Neonatology ◽  
1979 ◽  
Vol 36 (3-4) ◽  
pp. 119-127 ◽  
Author(s):  
M.G. Pernollet ◽  
M.A. Devynck ◽  
G.J. Macdonald ◽  
P. Meyer
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Angiotensin Ii Receptors

Effect of enalapril (MK-421), an orally active angiotensin I converting enzyme inhibitor, on blood pressure, active and inactive plasma renin, urinary prostaglandin E2, and kallikrein excretion in conscious rats

1984 ◽  
Vol 62 (1) ◽  
pp. 116-123 ◽  
Author(s):  
Ernesto L. Schiffrin ◽  
Jolanta Gutkowska ◽  
Gaétan Thibault ◽  
Jacques Genest
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Ace Inhibition ◽  
Renin Activity ◽  
Prostaglandin E ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Angiotensin I Converting Enzyme

The angiotensin I converting enzyme (ACE) inhibitor enalapril (MK-421), at a dose of 1 mg/kg or more by gavage twice daily, effectively inhibited the pressor response to angiotensin I for more than 12 h and less than 24 h. Plasma renin activity (PRA) did not change after 2 or 4 days of treatment at 1 mg/kg twice daily despite effective ACE inhibition, whereas it rose significantly at 10 mg/kg twice daily. Blood pressure fell significantly and heart rate increased in rats treated with 10 mg/kg of enalapril twice daily, a response which was abolished by concomitant angiotensin II infusion. However, infusion of angiotensin II did not prevent the rise in plasma renin. Enalapril treatment did not change urinary immunorcactive prostaglandin E2 (PGE2) excretion and indomethacin did not modify plasma renin activity of enalapril-treated rats. Propranolol significantly reduced the rise in plasma renin in rats receiving enalapril. None of these findings could be explained by changes in the ratio of active and inactive renin. Water diuresis, without natriuresis and with a decrease in potassium urinary excretion, occurred with the higher dose of enalapril. Enalapril did not potentiate the elevation of PRA in two-kidney one-clip Goldblatt hypertensive rats. In conclusion, enalapril produced renin secretion, which was in part β-adrenergically mediated. The negative short feedback loop of angiotensin II and prostaglandins did not appear to be involved. A vasodilator effect, apparently independent of ACE inhibition, was found in intact conscious sodium-replete rats.

L-arginine analogues inhibit aldosterone secretion in rats

1995 ◽  
Vol 268 (5) ◽  
pp. R1137-R1142 ◽  
Author(s):  
J. C. Simmons ◽  
R. H. Freeman
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Methyl Ester ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Bilateral Nephrectomy ◽  
Aldosterone Secretion ◽  
Series Of Experiments

L-Arginine analogues, e.g., NG-nitro-L-arginine methyl ester (L-NAME), increase arterial pressure and suppress renin release in the rat. On the basis of these observations, it was hypothesized that L-arginine analogues also would attenuate aldosterone secretion. This hypothesis was tested in anesthetized rats treated with L-NAME or NG-nitro-L-arginine (L-NNA, 185 mumol/kg ip). The aldosterone secretion rate, plasma renin activity, and adrenal blood flow were attenuated in rats treated with L-NAME and L-NNA compared with control animals. Similar experiments were performed in anephric rats to examine the effects of L-NAME on aldosterone secretion independent of the circulating reninangiotensin system. The administration of L-NAME reduced adrenal blood flow but failed to reduce aldosterone secretion in these anephric rats. Bilateral nephrectomy reduced plasma renin activity essentially to undetectable levels in these animals. In a third series of experiments, two groups of anephric rats were infused with angiotensin II (3 micrograms/kg body wt iv) to provide a stimulus for aldosterone secretion. Aldosterone secretion and adrenal blood flow were markedly reduced in angiotensin II-infused rats pretreated with L-NAME compared with the control anephric animals infused with angiotensin II. Overall these results suggest that L-arginine analogues attenuate aldosterone secretion by inhibiting the adrenal steroidogenic effects of endogenous or exogenous angiotensin II and/or by reducing plasma levels of renin/angiotensin.

Water deprivation-induced drinking in rats: role of angiotensin II

1983 ◽  
Vol 244 (2) ◽  
pp. R244-R248 ◽  
Author(s):  
C. C. Barney ◽  
R. M. Threatte ◽  
M. J. Fregly
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Water Intake ◽  
Water Deprivation ◽  
Plasma Renin ◽  
Sodium Concentration ◽  
Renin Activity ◽  
Deprivation Period ◽  
Dependent Component

The role of angiotensin II in the control of water intake following deprivation of water for varying lengths of time was studied. Male rats were deprived of water for 0, 12, 24, 36, or 48 h. Water intakes were measured with and without pretreatment with the angiotensin I-converting enzyme inhibitor, captopril (50 mg/kg, ip). Captopril had no significant effect on water intake following either 0 or 12 h of water deprivation. However, captopril significantly attenuated water intake following 24-48 h of water deprivation with the magnitude of the attenuation increasing as the length of the period of water deprivation increased. Plasma renin activity was significantly increased over control levels after 24-48 h of water deprivation but not after 12 h of water deprivation. Plasma renin activity tended to increase as the length of the water-deprivation period increased. Serum osmolality and sodium concentration were significantly increased over control levels following 12-48 h of water deprivation. Serum osmolality and sodium concentration failed to show any further increases with increasing length of water deprivation beyond the increases following 12 h of water deprivation. The data indicate that the water intake of water-deprived rats can be divided into an angiotensin II-dependent component and angiotensin II-independent component. The angiotensin II-independent component appears to be more important in the early stages of water deprivation whereas the angiotensin II-dependent component becomes more important as the length of the water-deprivation period increases.

scholarly journals Effects of Ramipril on the Aldosterone/Renin Ratio and the Aldosterone/Angiotensin II Ratio in Patients With Primary Aldosteronism

Hypertension ◽  
2020 ◽  
Vol 76 (2) ◽  
pp. 488-496 ◽  
Author(s):  
Zeng Guo ◽  
Marko Poglitsch ◽  
Diane Cowley ◽  
Oliver Domenig ◽  
Brett C. McWhinney ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Ace Inhibitors ◽  
Primary Aldosteronism ◽  
Characteristic Curve ◽  
False Negative ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Plasma Aldosterone Concentration

The aldosterone/renin ratio (ARR) is currently considered the most reliable approach for case detection of primary aldosteronism (PA). ACE (Angiotensin-converting enzyme) inhibitors are known to raise renin and lower aldosterone levels, thereby causing false-negative ARR results. Because ACE inhibitors lower angiotensin II levels, we hypothesized that the aldosterone/equilibrium angiotensin II (eqAngII) ratio (AA2R) would remain elevated in PA. Receiver operating characteristic curve analysis involving 60 patients with PA and 40 patients without PA revealed that the AA2R was not inferior to the ARR in screening for PA. When using liquid chromatography-tandem mass spectrometry to measure plasma aldosterone concentration, the predicted optimal AA2R cutoff for PA screening was 8.3 (pmol/L)/(pmol/L). We then compared the diagnostic performance of the AA2R with the ARR among 25 patients with PA administered ramipril (5 mg/day) for 2 weeks. Compared with basally, plasma levels of equilibrium angiotensin I (eqAngI) and direct renin concentration increased significantly ( P <0.01 or P <0.05) after ramipril treatment, whereas eqAngII and ACE activity (eqAngII/eqAngI) decreased significantly ( P <0.01). The changes of plasma renin activity and plasma aldosterone concentration in the current study were not significant. On day 14, 4 patients displayed false-negative results using ARR_direct renin concentration (plasma aldosterone concentration/direct renin concentration), 3 of whom also showed false-negative ARR_plasma renin activity (plasma aldosterone concentration/plasma renin activity). On day 15, 2 patients still demonstrated false-negative ARR_plasma renin activity, one of whom also showed a false-negative ARR_direct renin concentration. No false-negative AA2R results were observed on either day 14 or 15. In conclusion, compared with ARR which can be affected by ACE inhibitors causing false-negative screening results, the AA2R seems to be superior in detecting PA among subjects receiving ACE inhibitors.

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