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.

Clinical Significance of Plasma Renin Activity in Human Renovascular Hypertension

1976 ◽  
Vol 51 (s3) ◽  
pp. 239s-242s
Author(s):  
A. Salvetti ◽  
F. Arzilli ◽  
P. Sassano ◽  
L. Poli ◽  
A. Pesola
Keyword(s):  
Plasma Renin Activity ◽  
Renovascular Hypertension ◽  
Venous Blood ◽  
Plasma Renin ◽  
Renin Secretion ◽  
Renin Activity ◽  
Diagnostic Significance ◽  
Receptor Blocking ◽  
Contralateral Kidney ◽  
Β Receptor

1. Plasma renin activity (PRA) in peripheral venous blood of patients with renovascular hypertension was found to be high (thirty-five), normal (twenty-one) and low (three). Twenty-one patients with high PRA were cured or improved after successful surgery, as were eight of eleven with normal PRA and one with a low PRA. After surgery high PRA values became normal or low. 2. A β-receptor-blocking agent (oxprenolol) decreased PRA in twenty-eight patients (responders) and it either did not modify or increased PRA in the other fifteen (non-responders). All fourteen non-responders were cured by surgery, as were thirteen out of fifteen responders; ten non-responders became responders after surgery. Oxprenolol suppressed renin secretion of both kidneys of two patients with essential hypertension, and it either decreased (six) or did not modify (four) renin secretion from the ischaemic kidney. 3. PRA measurement in renal veins of twenty-six patients with renovascular hypertension showed that only the ischaemic kidney contributes to the peripheral PRA, renin secretion being suppressed in the contralateral kidney. The suppression of renin secretion from the ischaemic kidney produced either by nephrectomy (nine) or by aortorenal by-pass (six) normalized blood pressure. 4. Peripheral PRA values are of poor diagnostic significance and PRA unresponsiveness to a β-receptor-blocking drug and the suppression of renin secretion from the ischaemic kidney are characteristic findings of renovascular hypertension curable by appropriate surgery.

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 in dogs with acute and chronic renovascular hypertension

1981 ◽  
Vol 240 (4) ◽  
pp. H533-H538
Author(s):  
J. R. Dietz ◽  
J. O. Davis ◽  
J. M. DeForrest ◽  
R. H. Freeman ◽  
S. F. Echtenkamp ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Renovascular Hypertension ◽  
Acute Phase ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Renin Activity ◽  
Arterial Blood ◽  
Renal Prostaglandins ◽  
High Level ◽  
Vascular Receptor

This study examines the role that prostaglandins play in both the developmental and chronic phases of renovascular hypertension. Two 5-mg/kg doses of indomethacin were given to conscious dogs with renal denervation and receiving propranolol during the acute and chronic phases of one-kidney (1-KHT) and the acute phase of two-kidney (2-KHT) renovascular hypertension. Indomethacin produced striking reductions in plasma renin activity from the high level observed during the acute phase of both 1-KHT and 2-KHT. However, plasma renin activity failed to return to normal, and the hypertensive level of pressure decreased only slightly. In the chronic 1-KHT dogs, indomethacin did not lower plasma renin activity or mean arterial blood pressure unless plasma renin activity was elevated above the normal level. Also, indomethacin failed to alter renal function during the acute phase of 1-KHT but effective renal plasma flow fell during chronic 1-KHT. These results suggest that, in the dog, renal prostaglandins are involved in the pathogenesis of both acute 1-KHT and 2-KHT, whereas the role of renal prostaglandins in the regulation of arterial pressure appears to be negligible in chronic 1-KHT except during superimposed sodium depletion or severe hypertension. The data indicate that prostaglandins are involved in renovascular hypertension in the dog only under conditions where plasma renin activity is elevated. It is suggested that the release of renin after renal artery constriction is mediated by the vascular receptor that is at least partially independent of renal prostaglandin synthesis.

Role of macula densa cyclooxygenase-2 in renovascular hypertension

2003 ◽  
Vol 284 (3) ◽  
pp. F498-F502 ◽  
Author(s):  
Andrea Hartner ◽  
Nada Cordasic ◽  
Margarete Goppelt-Struebe ◽  
Roland Veelken ◽  
Karl F. Hilgers
Keyword(s):  
Plasma Renin Activity ◽  
Renovascular Hypertension ◽  
Plasma Renin ◽  
Juxtaglomerular Apparatus ◽  
Macula Densa ◽  
Renin Activity ◽  
Disease States ◽  
Renin Synthesis ◽  
Cox 2

Upregulation of the inducible cyclooxygenase (COX-2) in the macula densa accompanies the activation of the juxtaglomerular apparatus in many high-renin conditions. The functional role of COX-2 in these disease states is poorly understood. We tested whether COX-2 is required to increase renin in renovascular hypertension. Rats with established two-kidney, one-clip (2K1C) hypertension were treated for 2 wk with two different inhibitors of COX-2, NS-398 and rofecoxib, respectively. Hypertension in 2K1C rats was not affected or slightly enhanced by COX-2 inhibition, as measured intra-arterially in conscious animals. The increase in plasma renin activity was also unchanged by both rofecoxib and NS-398. The number of glomeruli with a renin-positive juxtaglomerular apparatus was elevated in clipped kidneys and decreased in contralateral kidneys of 2K1C rats. This pattern was unaltered by COX-2 inhibition. To test the effects of COX-2 blockade on a primarily macula densa-mediated stimulus, we studied salt depletion for comparison. A low-salt diet induced a significant increase in plasma renin activity, which was partially inhibited by treatment with NS-398. We conclude that inhibition of COX-2 in established renovascular hypertension does not affect renin synthesis or release. Thus either COX-2 is not necessary for the macula densa mechanism or the macula densa is not important for maintaining high renin in renovascular hypertension.

Micro determination of plasma renin activity in normal infants and children on capillary and venous blood

1979 ◽  
Vol 99 (1) ◽  
pp. 93-95 ◽  
Author(s):  
Michéle Dechaux ◽  
Jean-Marie Limal ◽  
Michel Broyer ◽  
Charles Sachs
Keyword(s):  
Plasma Renin Activity ◽  
Venous Blood ◽  
Plasma Renin ◽  
Infants And Children ◽  
Renin Activity

scholarly journals Studies on Plasma Renin Activity in Patients with Renovascular Hypertension

1972 ◽  
Vol 36 (6) ◽  
pp. 617-621 ◽  
Author(s):  
YUKIO MIURA ◽  
TATSUO SATO ◽  
KEISHI ABE ◽  
IWAO ONO ◽  
KAORU YOSHINAGA
Keyword(s):  
Plasma Renin Activity ◽  
Renovascular Hypertension ◽  
Plasma Renin ◽  
Renin Activity

EFFECT OF AGE ON DIAGNOSTIC USEFULNESS OF STIMULATED PLASMA RENIN ACTIVITY AND SARALASIN TEST IN DETECTION OF RENOVASCULAR HYPERTENSION

The Lancet ◽  
1980 ◽  
Vol 316 (8199) ◽  
pp. 821-824 ◽  
Author(s):  
GunnarH. Anderson ◽  
Patricia Randall ◽  
Jay Springer ◽  
DavidH.P. Streeten ◽  
Nancy Blakeman
Keyword(s):  
Plasma Renin Activity ◽  
Renovascular Hypertension ◽  
Plasma Renin ◽  
Renin Activity ◽  
Diagnostic Usefulness ◽  
Effect Of Age

Relationships between Plasma Renin Activity and Urinary and Plasma Catecholamines

1974 ◽  
Vol 48 (s2) ◽  
pp. 287s-290s ◽  
Author(s):  
U. Werner ◽  
H. Günnewig ◽  
K. D. Bock
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Renovascular Hypertension ◽  
Significant Positive Correlation ◽  
Plasma Renin ◽  
Primary Hypertension ◽  
Renin Activity ◽  
Positive Correlation ◽  
Noradrenaline Concentration

1. The relations between the changes in plasma renin activity (PRA) and urinary catecholamine excretion (UCA) or plasma noradrenaline concentration have been investigated (a) in patients with benign primary hypertension, with renovascular hypertension and with idiopathic asympatheticotonic hypotension (ASH), and (b) during orthostasis and after administration of frusemide, of the β-blocking agent tenormin, of clonidine and of dihydralazine. 2. In primary hypertension noradrenaline and mean arterial pressure (Pm) showed a close positive correlation. 3. The mean values of both PRA and UCA were higher in renovascular hypertension than in primary hypertension and extremely low in ASH. The overlap of individual values between the patient groups was markedly reduced by using the quotient PRA/UCA. There was a statistically significant positive correlation between PRA and UCA in primary hypertension and in renovascular hypertension, with a different slope of the regression lines. 4. The increase of PRA and of noradrenaline during orthostasis was closely correlated. Frusemide and β-receptor blockade changed the slope of the regression line by additional stimulation or inhibition respectively of PRA. 5. Clonidine decreased, and dihydralazine increased both PRA and noradrenaline concentration. These changes again showed a significant positive correlation. The fall of mean arterial pressure produced by clonidine was correlated with the decrease of PRA and of noradrenaline concentration.

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