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.

Effects of indomethacin on plasma renin activity in the conscious rat

1981 ◽  
Vol 240 (3) ◽  
pp. E286-E289 ◽  
Author(s):  
S. Suzuki ◽  
R. Franco-Saenz ◽  
S. Y. Tan ◽  
P. J. Mulrow
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Sodium Retention ◽  
Conscious Rat ◽  
Basal Plasma ◽  
Inhibition Of Prostaglandin Synthesis

The role of prostaglandins in the control of renin release in vivo was evaluated in the conscious rat. Indomethacin suppressed urinary prostaglandin E2 (PGE2) excretion from 5.3 +/- 0.5 to 2.6 +/- 0.5 ng/3 h (P less than 0.001). Basal plasma renin activity (PRA) fell from 6.20 +/- 1.07 to 2.98 +/- 0.45 ng . ml-1 . h-1 (P less than 0.02). Indomethacin suppressed PRA stimulated by furosemide, insulin-induced hypoglycemia, hydralazine, isoproterenol, arachidonic acid, and sodium-free diet, whereas PRA stimulated by PGE2 was not suppressed by indomethacin. The suppression of PRA by indomethacin in the sodium-deplete state rules out sodium retention as the mechanism of action of indomethacin. These results indicate that inhibition of prostaglandin synthesis by indomethacin partially blocks the renin response to several of the known stimulators, suggesting that prostaglandins may play a pivotal role in the control of renin release.

Renal sodium handling in normal humans subjected to low, normal, and extremely high sodium supplies

1985 ◽  
Vol 249 (6) ◽  
pp. F941-F947 ◽  
Author(s):  
J. C. Roos ◽  
H. A. Koomans ◽  
E. J. Dorhout Mees ◽  
I. M. Delawi
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Sodium Intake ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Renin Activity ◽  
Sodium Reabsorption ◽  
Lithium Clearance ◽  
Renal Sodium Handling ◽  
Sodium Handling

We studied renal sodium handling, extracellular fluid volume (ECFV), plasma renin activity, aldosterone and norepinephrine, and blood pressure in eight healthy volunteers after equilibration on intakes of 20, 200, and 1,128 +/- 141 meq sodium, respectively. Renal sodium handling was assessed by means of clearance studies during maximal water diuresis and lithium clearance. Urinary sodium excretions were 22 +/- 4, 202 +/- 19, and 1,052 +/- 86 meq/day. From the lower to the upper sodium intake level, 24-h creatinine clearance rose from 111 +/- 7 to 136 +/- 11 ml/min and inulin clearance from 103 +/- 9 to 129 +/- 9 ml/min, whereas proximal and distal fractional sodium reabsorption (FSRprox and FSRdist, respectively) fell from 86.8 +/- 1.3 to 79.0 +/- 2.7% and from 96.5 +/- 0.5 to 76.0 +/- 1.9%, respectively. During the normal sodium intake (200 meq), intermediate values were recorded. The changes in fractional lithium clearance were less consistent but correlated with FSRprox (r = 0.78, P less than 0.001) and not with FSRdist. Major changes in plasma renin activity, aldosterone, and, to a lesser extent, norepinephrine accompanied these changes in kidney function, displaying inverse and exponential correlations with daily sodium excretion and ECFV. No consistent rise in blood pressure was detected. These observations indicate that in healthy humans renal adaptation to vast variations in sodium intake includes resetting of glomerular filtration rate, FSRprox, and, in particular, FSRdist. Alterations in neurohumoral factors may play a dominant role in this adaptation.

scholarly journals Renin Activity in Heart Failure with Reduced Systolic Function—New Insights

2019 ◽  
Vol 20 (13) ◽  
pp. 3182 ◽  
Author(s):  
Ryan D. Sullivan ◽  
Radhika M. Mehta ◽  
Ranjana Tripathi ◽  
Guy L. Reed ◽  
Inna P. Gladysheva
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Plasma Renin Activity ◽  
Systolic Function ◽  
Companion Animals ◽  
Experimental Studies ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Renin Activity ◽  
Reduced Ejection Fraction

Regardless of the cause, symptomatic heart failure (HF) with reduced ejection fraction (rEF) is characterized by pathological activation of the renin–angiotensin–aldosterone system (RAAS) with sodium retention and extracellular fluid expansion (edema). Here, we review the role of active renin, a crucial, upstream enzymatic regulator of the RAAS, as a prognostic and diagnostic plasma biomarker of heart failure with reduced ejection fraction (HFrEF) progression; we also discuss its potential as a pharmacological bio-target in HF therapy. Clinical and experimental studies indicate that plasma renin activity is elevated with symptomatic HFrEF with edema in patients, as well as in companion animals and experimental models of HF. Plasma renin activity levels are also reported to be elevated in patients and animals with rEF before the development of symptomatic HF. Modulation of renin activity in experimental HF significantly reduces edema formation and the progression of systolic dysfunction and improves survival. Thus, specific assessment and targeting of elevated renin activity may enhance diagnostic and therapeutic precision to improve outcomes in appropriate patients with HFrEF.

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.

Effect of elevated atrial pressure on plasma renin activity in hypotensive fetal lambs

1993 ◽  
Vol 265 (1) ◽  
pp. R76-R81
Author(s):  
A. U. Sheikh ◽  
L. K. Washburn ◽  
R. K. Jaekle ◽  
J. C. Rose
Keyword(s):  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Block Design ◽  
Plasma Renin ◽  
Late Gestation ◽  
Renin Secretion ◽  
Renin Activity ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure

In adults, renin secretion is stimulated by reductions in arterial pressure and inhibited by increases in atrial pressure. In the late gestation fetus, a fall in arterial pressure stimulates renin secretion, but it is unknown whether elevation of atrial pressure will alter such an increase. Therefore we studied the effect of elevated atrial pressure on renin secretion in the presence of nitroprusside-induced arterial hypotension. Thirteen fetal lambs at 127.9 +/- 0.9 days of gestation were prepared 5 days before study with inflatable pulmonary artery occluders and right atrial, vascular, and amniotic catheters. Each fetus underwent two protocols (hypotension and hypotension with occlusion) using a randomized block design. Nitroprusside reduced arterial pressure by 34% in both groups. Right atrial pressure during the course of hypotension was significantly higher in the occlusion group (F = 14.2, P = 0.001). Plasma renin activity increased similarly in both groups during hypotension (F = 6.0, P = 0.003). Elevated right atrial pressure did not alter hypotension-induced renin secretion in the fetus.

Effect of Volume Depletion and Subsequent Propranolol Treatment on Blood Pressure and Plasma Renin Activity in Patients with Essential and with Renovascular Hypertension

1974 ◽  
Vol 48 (s2) ◽  
pp. 69s-71s
Author(s):  
G. G. Geyskes ◽  
P. Boer ◽  
F. H. H. Leenen ◽  
E. J. Dorhout Mees
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Plasma Volume ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Extracellular Fluid Volume ◽  
Renin Activity

1. In nineteen patients, five with unilateral renal artery stenosis and fourteen with essential hypertension (WHO grades I–II), blood pressure, plasma and extracellular fluid volumes and plasma renin activity were studied at the end of three sequential periods: (a) after at least 3 days on a 60 mmol Na+ diet; (b) after 3 days of salt depletion induced with a diuretic and sustained on a 20 mmol Na+ diet; (c) after 3 days during which the 20 mmol Na+ diet was continued and beta-receptor blockade was induced by increasing dosages of propranolol up to 320 mg daily. 2. After sodium depletion extracellular fluid volume and plasma volume decreased and plasma renin activity increased; blood pressure did not change significantly. 3. After adding propranolol, plasma volume and extracellular fluid volume remained low, and there was a significant decrease in plasma renin activity and blood pressure. 4. No correlation could be demonstrated between changes of blood pressure and plasma renin activity. 5. When the responses of the five patients with renal artery stenosis were compared with those of the fourteen patients with essential hypertension, no significant differences were found. 6. Propranolol has a strong anti-hypertensive effect after Na+ depletion, irrespective of the absolute activities of plasma renin.

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.

Fibrinolytic and Renin Activity in Renal Vein Blood of Patients with Renovascular Hypertension

1969 ◽  
Vol 21 (01) ◽  
pp. 012-019
Author(s):  
A Nowak ◽  
F Kokot ◽  
Z Czekała ◽  
J Dosiak ◽  
J Kuska
Keyword(s):  
Plasma Renin Activity ◽  
Renovascular Hypertension ◽  
Fibrinolytic Activity ◽  
Inferior Vena ◽  
Venous Blood ◽  
Vena Cava ◽  
Plasma Renin ◽  
Fibrinolytic System ◽  
Renin Activity ◽  
Hepatic Venous Blood

SummaryThe fibrinolytic system has been studied in 20 patients with renovascular hypertension.Renal and hepatic venous blood was drawn by selective cathetherisations, while peripheral blood was obtained from the inferior vena cava above the bifurcation. In all blood samples the euglobulin fibrinolysis, antiplasmin, plasminogen, fibrinogen, and plasma renin activity were determined.Samples were taken at recumbency and after tilting to 80° for 30 min. In contradistinction to plasma renin activity no differences of the fibrinolytic activity between renal and peripheral venous blood even in that obtained from ischemic kidneys were proved.No diminished secretion of plasminogen activator by ischemic kidneys in man was stated.In the light of the data obtained the participation of fibrinolytic system in the pathogenesis of renovascular hypertension is doubtfal.

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