Renin-aldosterone system suppression during water immersion in renovascular hypertension

1985 ◽  
Vol 68 (5) ◽  
pp. 609-612 ◽  
Author(s):  
P. Coruzzi ◽  
A. Biggi ◽  
L. Musiari ◽  
C. Ravanetti ◽  
A. Novarini
Keyword(s):  
Plasma Renin Activity ◽  
Renovascular Hypertension ◽  
Water Immersion ◽  
Distal Tubule ◽  
Plasma Renin ◽  
Sodium Concentration ◽  
Renin Secretion ◽  
Renin Activity ◽  
Reflex Control ◽  
Cardiopulmonary Receptors

1. We studied renin-aldosterone system behaviour in five renovascular hypertensive patients during central hypervolaemia by water immersion to the neck. 2. Water immersion significantly suppressed the high peripheral renin levels of the patients despite an autonomic renin secretion from the stenotic kidney, a significant reduction of mean blood pressure and an increase in distal tubule sodium concentration. 3. The effect of immersion on plasma aldosterone appeared to be primarily mediated via suppression of plasma renin activity (PRA). 4. Our data suggest that: (a) the renin secretion is mainly modulated by cardiopulmonary receptors activity; (b) the neurogenic reflex control of plasma renin activity is very effective in renovascular hypertension.

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.

Differential maturation of beta-adrenoceptor-mediated responses in the lamb fetus

1988 ◽  
Vol 255 (5) ◽  
pp. R794-R798 ◽  
Author(s):  
N. M. Rawashdeh ◽  
J. C. Rose ◽  
N. D. Ray
Keyword(s):  
Heart Rate ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Secretion ◽  
Renin Activity ◽  
Functional Maturity ◽  
Beta Adrenoceptor ◽  
Beta Receptor

To study the functional maturity of beta-receptor-mediated responses, seven chronically catheterized lamb fetuses, 93-107 days of gestation, and seven fetuses, 116-134 days of gestation, received intravenous randomly sequenced infusions of isoproterenol (ISO) 0.03, 0.06, and 0.125 micrograms.kg-1.min-1 for 10 min separated by 45-min intervals or two saline infusions followed by 0.125 micrograms.kg-1.min-1 ISO after treatment with 0.5 mg/kg propranolol (PRO). Each fetus received the two treatments 24-48 h apart. In immature fetuses, plasma renin activity (PRA) of 2.0 +/- 0.7 ng.ml-1.h-1 did not change with either protocol. In mature fetuses, PRA of 7.5 +/- 2.5 ng.ml-1.h-1 increased two- to three-fold after the infusion of the highest two doses of ISO (P less than 0.003). Propranolol blocked this response. No significant changes were observed after the infusions of the lowest dose of ISO or saline. Both groups showed significant heart rate increases with all doses of ISO. Propranolol injection decreased heart rate significantly and blocked responses to ISO. We conclude that although a cardiac beta-receptor-mediated response is present by 93 days of gestation in the lamb fetus, a renal beta-receptor-mediated response, renin secretion, is absent.

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.

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.

Dissociation of Renin-Aldosterone and Renal Prostaglandin E during Volume Expansion Induced by Immersion in Normal Man

1980 ◽  
Vol 59 (1) ◽  
pp. 55-62 ◽  
Author(s):  
M. Epstein ◽  
M. D. Lifschitz ◽  
R. Re ◽  
E. Haber
Keyword(s):  
Plasma Renin Activity ◽  
Volume Expansion ◽  
Water Immersion ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Prostaglandin E ◽  
Plasma Aldosterone Concentration ◽  
Normal Man

1. The relationship of the renin-angiotensin-aldosterone axis with renal prostaglandin E is complex. Although studies have suggested that these two hormonal systems respond to experimental manipulations in a parallel manner, their interdependence has not been assessed fully during volume expansion. Since studies have demonstrated that in normal man the central hypervolaemia induced by water immersion to the neck produces a prompt and profound suppression of plasma renin activity and plasma aldosterone concentration without concomitant alteration of plasma composition, immersion afforded a unique opportunity to assess simultaneously the effects of central hypervolaemia on plasma renin activity, plasma aldosterone concentration and prostaglandin E excretion. 2. Seven normal subjects were studied twice while in balance on a diet containing 10 mmol of sodium/day, 100 mmol of potassium/day: with indomethacin administration (50 mg given every 6 h for five doses) and without indomethacin. Urinary prostaglandin E excretion was measured hourly and plasma renin activity and plasma aldosterone concentration at 30 min intervals. 3. Immersion was associated with a marked suppression of plasma renin activity (59 ± 7%) and plasma aldosterone concentration (55 ± 3%) with a return to pre-study values during the recovery hour. Concomitantly, urinary prostaglandin E excretion increased from 4.7 to a peak of 10.9 ng/min. Although administration of indomethacin lowered the basal rate of urinary prostaglandin E excretion and plasma renin activity, it did not prevent the subsequent augmentation of urinary prostaglandin E or the suppression of plasma renin activity and plasma aldosterone during the subsequent 4 h of immersion. 4. These results demonstrate a dissociation of renin-aldosterone and prostaglandin E during hypervolaemia and suggest that whereas prostaglandin E may constitute one of the major determinants of renin release clinically and experimentally, these two hormonal systems can be dissociated from each other in response to central volume expansion in man.

Effect of Chronic Low-Dose Arginine Vasopressin Infusion on Body Fluid Homoeostasis during Adaptation from a High-to a Low-Sodium Diet in Normal Man

1993 ◽  
Vol 85 (4) ◽  
pp. 465-470 ◽  
Author(s):  
M. Sutters ◽  
D. J. S. Carmichael ◽  
S. L. Lightman ◽  
W. S. Peart
Keyword(s):  
Plasma Renin Activity ◽  
Arginine Vasopressin ◽  
Plasma Renin ◽  
Sodium Concentration ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Angiotensin I ◽  
Salt Restriction ◽  
Plasma Sodium Concentration ◽  
Plasma Arginine

1. A diuresis occurs within the first 36 h of salt restriction. A decline in plasma arginine vasopressin concentration may contribute to both the diuresis and antinatriuresis. 2. We have studied six normal human subjects during 36 h of dietary sodium restriction. In one study subjects received an intravenous infusion of D-glucose, and in the other an infusion of arginine vasopressin (6 fmol min−1 kg−1). 3. In the D-glucose phase plasma arginine vasopressin concentration fell (1.77 +034 to 1.02 +0.13 pg/ml), urine flow increased (67.9 +113 to 89.8 + 17.1 ml/h), haemoconcentration occurred (packed cell volume 40.8 +0.3 to 42.8 +03%, protein concentration 71.6 +03 to 74.5 + 0.6 g/l), plasma sodium concentration fell (140 +0.2 to 138 +0.2 mmol/l) and plasma renin activity increased (1600+153 to 3700 + 356 pg of angiotensin I h−1 ml−1). 4. In the arginine vasopressin phase plasma arginine vasopressin concentration remained constant (13 + 0.13 to 134 +0.11 pg/ml), the diuresis was reversed (65.7 +9.9 to 52.1 +8.9 ml/h), plasma sodium concentration fell further (139.8 +0.4 to 136.1 +0.4 mmol/l), the rise in plasma renin activity was reduced (arginine vasopressin 2552 + 292; D-glucose, 3700 + 356 pg of angiotensin I h−1 ml−1) and creatinine clearance was lower in the last 12 h of salt restriction (arginine vasopressin, 96.1 +6.9; D-glucose 116.5 + 6.8 ml/min). Renal sodium excretion was unaffected by arginine vasopressin infusion. 5. We conclude that the fall in plasma arginine vasopressin concentration during dietary salt restriction, whilst not affecting renal sodium excretion, may be important in the regulation of plasma sodium concentration, plasma renin activity and glomerular filtration.

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
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