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.

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.

The Effect of Dietary Sodium Intake on the Blood Pressure and Cardiac Output Responses to Angiotensin II in Unanaesthetized Rats

1977 ◽  
Vol 52 (6) ◽  
pp. 571-576
Author(s):  
Barbara L. Slack ◽  
J. M. Ledingham
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Dose Response ◽  
Sodium Intake ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Response Curves ◽  
Low Sodium ◽  
Dose Response Curves

1. Dose—response curves for the pressor activity of angiotensin II have been determined in unanaesthetized rats receiving diets containing 2·5% (w/w) or 0·007% (w/w) sodium and administered in various sequences. 2. Dose—response curves were shifted to the left in rats on a high-, compared with a low-, sodium intake. This response was maintained for 7 days on changing from high to low sodium. 3. There was no difference in the relation between the fall of cardiac output and the rise of blood pressure in any of the experimental groups. 4. Dose—response curves for peripheral resistance showed the same directional change as seen for the pressor response in rats on high- and low-sodium diets. Since depression of cardiac output was proportional to the pressure rise, the absolute change in peripheral resistance was greater than the blood pressure response. The proportional changes were similar. 5. It is concluded that alterations in the pressor response to angiotensin caused by changes in sodium loading are attributable to changes in peripheral resistance and not to changes in the cardiac output response to the acute rise in blood pressure.

Influence of right atrial stretch on plasma renin activity in the conscious rat

1987 ◽  
Vol 65 (2) ◽  
pp. 257-259 ◽  
Author(s):  
Susan Kaufman
Keyword(s):  
Plasma Renin Activity ◽  
Superior Vena ◽  
Vena Cava ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Renin Activity ◽  
Right Atrial ◽  
Balloon Inflation ◽  
Conscious Rat ◽  
Basal Plasma

Rats were prepared with inflatable balloons at the superior vena cava – right atrium junction. After recovery 1 week later, when blood was taken from conscious, normovolaemic animals plasma renin activity was found not to be influenced by right atrial stretch. Plasma renin activity was then measured in rats in which an extracellular fluid deficit had been produced by peritoneal dialysis against a hyperoncotic, isotonic solution. Although basal plasma renin activity was elevated (6.8 ± 0.9 from 1.5 ± 0.2 ng∙mL∙h, n = 19), no depression was observed in the experimental group after 15 or 90 min of balloon inflation. In rats pretreated with isoprenaline (10 μg/kg body wt.) plasma renin activity was also increased over basal levels, but again balloon inflation caused no reduction in plasma renin activity. It would appear that right atrial stretch has little, if any, influence on renin release in the conscious rat.

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.

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.

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.

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