Effect of volume expansion on pressor response to angiotensin II in pregnant ewes

Vascular refractoriness to infused angiotensin II (AII) characterizes normal human and ovine pregnancy. To ascertain whether the refractoriness in the gravid ewe is mediated by either endogenous plasma concentrations of renin and AII or vasomotor reflexes, effects of acute volume expansion (VE) on the pressor response to AII were studied in chronically instrumented nonpregnant and near-term pregnant sheep. Dose-response curves describing the pressor response (delta BP) were determined before and after infusions of 1.0 1 of isotonic saline (NS) or 0.5 1 of 10% dextran (D). In nonpregnant sheep, hematocrit (Hct) and plasma renin activity (PRA) fell in all animals after NS (n = 7) and D (n = 6) (P less than 0.005). After VE with NS and D, delta BP increased at each dose of AII (P less than 0.05). The pressor response to AII in pregnant sheep was not altered by NS although decreases in Hct and PRA were comparable to those in nonpregnant sheep. Baroreceptor responses were not altered. Vascular refractoriness to infused AII in pregnant sheep is not due primarily to changes in plasma concentrations of renin-AII but more likely to another factor, vessel wall refractoriness. In this respect, the ewe is similar to the human.

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Metabolic clearance of angiotensin II in pregnant and nonpregnant sheep

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1985.249.1.e49 ◽

1985 ◽

Vol 249 (1) ◽

pp. E49-E55 ◽

Cited By ~ 8

Author(s):

R. P. Naden ◽

S. Coultrup ◽

B. S. Arant ◽

C. R. Rosenfeld

Keyword(s):

Angiotensin Ii ◽

Pressor Response ◽

Plasma Concentrations ◽

Metabolic Clearance ◽

Ang Ii ◽

Pressor Responses ◽

Pregnant Sheep ◽

Vascular Responsiveness ◽

Arterial Plasma ◽

In Pregnancy

Reduced vascular responsiveness to infused angiotensin II (ANG II) has been observed during pregnancy. It has been proposed that infusions produce lower circulating concentrations of ANG II in pregnancy, due to an increase in the metabolic clearance rate of ANG II (MCRangii). We have evaluated the MCRangii and the arterial plasma concentrations of ANG II during constant infusions of 1.15 micrograms ANG II/min into chronically instrumented pregnant (n = 6) and nonpregnant (n = 9) sheep. Although the pressor responses were significantly less in the pregnant than in the nonpregnant sheep (17.5 +/- 0.5 vs. 34.9 +/- 3.2 mmHg, P less than 0.001), the values for MCRangii were not different: 56.2 +/- 6.3 ml X min-1 X kg-1 in nonpregnant and 55.9 +/- 4.3 ml X min-1 X kg-1 in pregnant sheep. The steady-state plasma ANG II concentrations during the infusions were slightly less in pregnant than in nonpregnant sheep (388 +/- 36 vs. 454 +/- 36 pg/ml); however, this difference would be responsible for only a 2-mmHg reduction in the pressor response. We conclude that the reduced pressor response to infused ANG II in pregnancy is not due to an increase in MCRangii nor to lower plasma ANG II concentrations.

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Pressor Responsiveness to Angiotensin in Renovascular and Steroid Hypertension

Clinical Science ◽

10.1042/cs057047s ◽

1979 ◽

Vol 57 (s5) ◽

pp. 47s-50s ◽

Cited By ~ 3

Author(s):

E. S. Marks ◽

H. Thurston ◽

R. F. Bing ◽

J. D. Swales

Keyword(s):

Angiotensin Ii ◽

Pressor Response ◽

Plasma Renin ◽

Receptor Occupancy ◽

Bilateral Nephrectomy ◽

Hypertensive Rats ◽

Response Curves ◽

Pressor Responses ◽

Salt Hypertension ◽

Converting Enzyme Inhibition

1. The pressor response to angiotensin II was reduced in rats with early (<6 weeks) and chronic (>4 months) Goldblatt two-kidney, one-clip hypertension and enhanced in DOCA—salt hypertension. 2. Converting enzyme inhibition with captopril brought the angiotensin pressor response curves into closer proximity although the DOCA hypertensive rats were minimally hyper-responsive and rats with early and chronic renovascular hypertension showed slightly reduced responsiveness. 3. After bilateral nephrectomy the pressor responses to angiotensin were similar. 4. The pressor response to angiotensin II in these animals was inversely related to plasma renin concentration and therefore largely dependent upon receptor occupancy by endogenous angiotensin II. There is no evidence for enhanced pressor responsiveness to angiotensin in either renovascular or DOCA hypertension.

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

Clinical Science ◽

10.1042/cs0460149 ◽

1974 ◽

Vol 46 (2) ◽

pp. 149-161 ◽

Cited By ~ 1

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.

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Acute saline loading in normal and bilaterally atrial-resected conscious dogs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1988.255.1.h144 ◽

1988 ◽

Vol 255 (1) ◽

pp. H144-H152

Author(s):

A. W. Cowley ◽

P. R. Anderas ◽

M. M. Skelton

Keyword(s):

Arterial Pressure ◽

Volume Expansion ◽

Isotonic Saline ◽

Plasma Renin ◽

Water Excretion ◽

Volume Load ◽

Saline Loading ◽

Before And After ◽

Level 3 ◽

The Central Nervous System

Acute isotonic saline volume loads (400 ml) were intravenously administered to conscious, renal-denervated dogs before and after bilateral removal of the atrial free walls and atrial appendages to determine the role of atrial-mediated hormonal factors in the renal excretory response. In one group of dogs (n = 11), the volume was given in 10 min; in another group (n = 5), the volume was given in 30 min while arginine vasopressin (AVP) was infused to maintain plasma AVP at a fixed, normal level (3 pg/ml). Sodium and water excretion, mean arterial pressure, and plasma hormone levels were determined before and for 5 h after volume loads. Atrial resection resulted in a 40-50% reduction of sodium and water excretion in both groups during the first 2 h after volume expansion. The blunted renal excretory responses could not be explained by differences in arterial pressure, renal sympathetic nerve activity, or by hormonal differences of plasma immunoreactive atrial natriuretic factor (iANP), plasma AVP, plasma renin activity, or plasma aldosterone. Plasma iANP was not significantly increased by the volume load in either the normal or atrial-resected state. Atrial-resected dogs exhibited normal plasma levels of iANP. The data indicate the presence of an unidentified diuretic and natriuretic substance, which is released with volume expansion from either the cardiac atria or via the central nervous system, and that the release of this factor is removed by atrial resection.

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

Acta Clinica Belgica ◽

10.1080/17843286.1974.11716948 ◽

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

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Effects of ouabain, low K+, and aldosterone on hypoxic pressor reactivity of rat lungs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1985.248.1.h55 ◽

1985 ◽

Vol 248 (1) ◽

pp. H55-H60 ◽

Cited By ~ 5

Author(s):

J. Herget ◽

I. F. McMurtry

Keyword(s):

Angiotensin Ii ◽

Energy Metabolism ◽

Atpase Activity ◽

Pressor Response ◽

Hypoxic Pulmonary Vasoconstriction ◽

Response Curves ◽

Hypoxic Response ◽

Rat Lungs ◽

Hypoxic Vasoconstriction ◽

Low K

It can be postulated that inhibition of lung tissue Na+-K+-ATPase might potentiate hypoxic pulmonary vasoconstriction by depolarizing some excitable cell or, in contrast, that it might blunt the hypoxic response by reducing cellular metabolic rate and sensitivity to hypoxia. Thus the purpose of this study was to test in isolated rat lungs whether hypoxic pressor reactivity was related inversely or positively to Na+-K+-ATPase activity. Dose-pressor response curves to hypoxia, angiotensin II, or KCl were measured under control conditions and after exposure either to one of two inhibitors of Na+-K+-ATPase, ouabain, and low-K+ solution or to a stimulator of Na+-K+ pumping, aldosterone. Ouabain and low K+ depressed the response to hypoxia but had little effect on that to angiotensin II. The response to KCl was increased by ouabain. Aldosterone potentiated the hypoxic response. These results do not support the idea that membrane depolarization due to inhibition Na+-K+ pumping is a component of hypoxic vasoconstriction. They do suggest a positive relationship between Na+-K+-ATPase activity and hypoxic pressor reactivity and are consistent with the idea that Na+-K+-ATPase activity might influence hypoxic reactivity indirectly by altering cellular energy metabolism. It is also possible that the results were somehow due to changes in intracellular [Na+] or transmembrane Na+ gradient, rather than to changes in energy metabolism.

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Effect of renal denervation on the suppression of renin secretion by vasopressin in conscious dogs

AJP Renal Physiology ◽

10.1152/ajprenal.1984.247.6.f881 ◽

1984 ◽

Vol 247 (6) ◽

pp. F881-F887 ◽

Cited By ~ 3

Author(s):

L. C. Gregory ◽

I. A. Reid

Keyword(s):

Angiotensin Ii ◽

Plasma Renin Activity ◽

Renal Denervation ◽

Plasma Renin ◽

Renin Secretion ◽

Conscious Dogs ◽

Reflex Response ◽

Renal Nerves ◽

Ang Ii ◽

Before And After

Previous studies have shown that the inhibition of renin secretion by vasopressin (AVP) in conscious dogs is related to vasoconstrictor activity and may be a reflex response mediated by the renal nerves. The aim of the present experiments was to determine whether the suppression of plasma renin activity (PRA) by AVP is blocked by renal denervation. AVP and, for comparison, angiotensin II (ANG II) were infused intravenously for 45 min in seven conscious dogs before and after bilateral renal denervation. Before denervation, AVP infusion at 0.2 and 1.0 ng X kg-1 X min-1 suppressed PRA from 7.4 +/- 1.1 to 4.7 +/- 1.0 (P less than 0.01) and from 7.9 +/- 1.8 to 3.8 +/- 0.8 ng X ml-1 X 3 h-1 (P less than 0.01), respectively. ANG II infusion at 5.0 and 10.0 ng X kg-1 X min-1 decreased PRA from 7.5 +/- 2.3 to 2.5 +/- 0.7 (P less than 0.01) and from 6.0 +/- 1.1 to 1.8 +/- 0.4 ng X ml-1 X 3 h-1 (P less than 0.01), respectively. One to three weeks following renal denervation, PRA had decreased from 6.7 +/- 1.3 to 2.9 +/- 0.5 ng X ml-1 X 3 h-1 (P less than 0.01), and renal norepinephrine was undetectable. After denervation, neither AVP infusion at 0.2 (3.0 +/- 0.5 to 2.4 +/- 0.4 ng X ml-1 X 3 h-1) nor 1.0 ng X kg-1 X min-1 (3.1 +/- 0.8 to 2.8 +/- 1.0 ng X ml-1 X 3 h-1) suppressed PRA.(ABSTRACT TRUNCATED AT 250 WORDS)

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Pressor responses of rats to vasopressin: effect of sodium, angiotensin, and catecholamines

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1983.244.2.h253 ◽

1983 ◽

Vol 244 (2) ◽

pp. H253-H258 ◽

Cited By ~ 1

Author(s):

M. Burnier ◽

H. R. Brunner

Keyword(s):

Angiotensin Ii ◽

Sodium Intake ◽

Pressor Response ◽

Response Curves ◽

Ether Anesthesia ◽

Spontaneously Hypertensive ◽

Lysine Vasopressin ◽

Pressor Responses ◽

Wistar Kyoto ◽

The Right

The pressor response to lysine vasopressin was tested in groups of male Wistar, Brattleboro, Wistar-Kyoto, and spontaneously hypertensive rats. Moreover, the influence of sodium intake, angiotensin II, saralasin, captopril, norepinephrine, and isoproterenol on vasopressin pressor responses was evaluated. The right iliac artery and one or both femoral veins of the animals were catheterized under light ether anesthesia. The experiments were carried out following a 2-h stabilization period with the rats awake and semirestrained. Pressor responsiveness was evaluated acutely on the basis of dose-response curves (0.5-4 mU). In the Wistar rats, angiotensin II (10 and 30 ng/min) and isoproterenol (10 ng/min) markedly decreased the response to vasopressin, whereas variations in sodium intake and blood pressure per se did not seem to exert any influence. Norepinephrine (250 ng/min) slightly enhanced the pressor responsiveness to the smaller doses of lysine-vasopressin. Brattleboro rats with congenital diabetes insipidus were less sensitive to vasopressin than the other animals, and neither angiotensin II nor isoproterenol induced any change. In conclusion, the pressor responsiveness to vasopressin can vary considerably depending on several factors. These must be taken into account when evaluating the possible pressor role of vasopressin in experimental and clinical settings.

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Changes in Blood Pressure in Relation to Vascular and Plasma Renin after Renin Injection in Rats

Clinical Science ◽

10.1042/cs063153s ◽

1982 ◽

Vol 63 (s8) ◽

pp. 153s-156s ◽

Cited By ~ 8

Author(s):

M. Loudon ◽

R. F. Bing ◽

J. D. Swales ◽

H. Thurston

Keyword(s):

Blood Pressure ◽

Angiotensin Ii ◽

Pressor Response ◽

Plasma Renin ◽

Aortic Tissue ◽

Relative Importance ◽

Bilateral Nephrectomy ◽

Single Intravenous Injection ◽

Angiotensin Ii Antagonist ◽

Renal Origin

1. To assess the relative importance of vascular as opposed to plasma renin, groups of conscious rats received a single intravenous injection of partially purified rat renin 18 h after bilateral nephrectomy. Blood pressure was monitored continuously and plasma and aortic renin concentrations were determined at 1, 3, 6 or 9 h after injection. In separate groups of rats the effect of the competitive angiotensin II antagonist, saralasin, on blood pressure was measured 3 or 6 h after renin injection. 2. Blood pressure remained elevated for up to 6 h after renin injection, returning to normal by 9 h. Saralasin infusion reversed the rise in blood pressure at both 3 and 6 h after injection. 3. Aortic renin concentration followed the pattern of the pressor response whereas plasma renin concentration had returned to subnormal values by 3 h. 4. Circulating renin of renal origin is taken up by aortic tissue. The pressor response to exogenous renin in rats after bilateral nephrectomy is not related to changes in plasma renin but is similar in duration to the persistence of aortic renin-like activity and can be blocked by saralasin at both 3 and 6 h after injection.

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