Surgical Correction of Renovascular Hypertension: Effect on Plasma Renin and Blood Pressure

1980 ◽  
Vol 58 (2) ◽  
pp. 27P-27P
Author(s):  
M. R. Maskill ◽  
R. F. Bing ◽  
H. Thurston ◽  
P. R. F. Bell ◽  
J. D. Swales
Keyword(s):  
Blood Pressure ◽  
Renovascular Hypertension ◽  
Plasma Renin ◽  
Surgical Correction

Hemodynamic changes induced by reversal of early and late renovascular hypertension

1983 ◽  
Vol 245 (5) ◽  
pp. H734-H740
Author(s):  
G. I. Russell ◽  
R. F. Bing ◽  
J. D. Swales ◽  
H. Thurston
Keyword(s):  
Blood Pressure ◽  
Renovascular Hypertension ◽  
Early Phase ◽  
Peripheral Resistance ◽  
Chronic Phase ◽  
Plasma Renin ◽  
Chronic Hypertension ◽  
Radioactive Microspheres ◽  
Hemodynamic Changes ◽  
Rapid Reduction

The hemodynamic changes associated with reversal of Goldblatt two-kidney, one-clip hypertension in conscious rats were studied using radioactive microspheres. In both the early phase (less than 6 wk from clipping) when plasma renin was elevated and the chronic phase (greater than 4 mo) when plasma renin was normal, hypertension was maintained by elevated peripheral resistance. Unclipping or removal of the ischemic kidney normalized blood pressure within 24 h by reduction in peripheral resistance. In early-phase hypertension blood pressure remained normal at 60 days after nephrectomy or unclipping, but in chronic-phase hypertension blood pressure was significantly elevated at 60 days after nephrectomy despite a similar fall in peripheral resistance. Plasma renin fell to normal or subnormal values after reversal in both early and chronic hypertension. Thus reversal of hypertension is associated with a rapid reduction in peripheral resistance even in longstanding hypertension. Since removal of the ischemic kidney and unclipping were equally effective, reversal must depend on either inhibition of a pressor system derived from the ischemic kidney or activation of a peripheral vasodepressor system not dependent on a revascularized kidney.

scholarly journals Renovascular hypertension using a modified two-kidney, one-clip approach in mice is not dependent on the α1 or α2 Na-K-ATPase ouabain-binding site

2011 ◽  
Vol 301 (3) ◽  
pp. F615-F621 ◽  
Author(s):  
John N. Lorenz ◽  
Valerie M. Lasko ◽  
Michelle L. Nieman ◽  
Thomas Damhoff ◽  
Vikram Prasad ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Binding Site ◽  
Renovascular Hypertension ◽  
Plasma Renin ◽  
Mutant Mice ◽  
Ouabain Binding ◽  
Α Subunit ◽  
Pressure Changes ◽  
2K1c Hypertension

Endogenous cardiotonic steroids, through their interaction with the ouabain-binding site of the Na-K-ATPase α-subunit, have been implicated in a variety of cardiovascular disease states including hypertension. We have previously shown that ACTH-induced hypertension is abolished in mutant mice expressing ouabain-resistant α1- and α2-subunits. To further evaluate hypertension resistance in these mutant mice, we examined blood pressure changes in a modified model of 2-kidney, 1-clip (2K1C) renovascular hypertension. To reliably generate 2K1C hypertension, we used polyvinyl tubing (inner diameter: ∼0.27 mm) to accurately gauge the degree of renal artery stenosis. Using this method, virtually all of the clipped mice became hypertensive and there was no incidence of apparent renal ischemia. By telemetry, in response to renal artery clipping, blood pressure in wild-type mice (α1 ouabain-resistant, α2 ouabain-sensitive) increased from 97 ± 3 to 136 ± 7 mmHg. In α1-resistant, α2-resistant mice, pressure increased from 93 ± 2 to 123 ± 4 mmHg, and in α1-sensitive, α2-resistant mice, blood pressure increased from 95 ± 2 to 139 ± 5 mmHg. Blood pressure changes were equivalent in all three groups. In sham mice, blood pressure did not change (96 ± 1 to 95 ± 2 mmHg). Renin mRNA expression was dramatically elevated in the left vs. the right kidney, and plasma renin concentration was elevated similarly in all genotypes. These data indicate that sensitivity of the α1- or α2-Na-K-ATPase binding site to cardiotonic steroids is not a prerequisite for the development of 2K1C renovascular hypertension. In addition, use of a polyurethane cuff to constrict the renal artery provides a reliable method for producing 2K1C hypertension in mice.

scholarly journals Natriuretic peptides buffer renin-dependent hypertension

2014 ◽  
Vol 306 (12) ◽  
pp. F1489-F1498 ◽  
Author(s):  
Theo Demerath ◽  
Janina Staffel ◽  
Andrea Schreiber ◽  
Daniela Valletta ◽  
Frank Schweda
Keyword(s):  
Blood Pressure ◽  
Renovascular Hypertension ◽  
Natriuretic Peptide ◽  
Natriuretic Peptides ◽  
Plasma Renin ◽  
Control Mechanisms ◽  
Wild Type ◽  
Renal Vasoconstriction ◽  
Arterial Blood ◽  
Independent Effects

The renin-angiotensin-aldosterone system and cardiac natriuretic peptides [atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP)] are opposing control mechanisms for arterial blood pressure. Accordingly, an inverse relationship between plasma renin concentration (PRC) and ANP exists in most circumstances. However, PRC and ANP levels are both elevated in renovascular hypertension. Because ANP can directly suppress renin release, we used ANP knockout (ANP−/−) mice to investigate whether high ANP levels attenuate the increase in PRC in response to renal hypoperfusion, thus buffering renovascular hypertension. ANP−/− mice were hypertensive and had reduced PRC compared with that in wild-type ANP+/+ mice under control conditions. Unilateral renal artery stenosis (2-kidney, 1-clip) for 1 wk induced similar increases in blood pressure and PRC in both genotypes. Unexpectedly, plasma BNP concentrations in ANP−/− mice significantly increased in response to two-kidney, one-clip treatment, potentially compensating for the lack of ANP. In fact, in mice lacking guanylyl cyclase A (GC-A−/− mice), which is the common receptor for both ANP and BNP, renovascular hypertension was markedly augmented compared with that in wild-type GC-A+/+ mice. However, the higher blood pressure in GC-A−/− mice was not caused by disinhibition of the renin system because PRC and renal renin synthesis were significantly lower in GC-A−/− mice than in GC-A+/+ mice. Thus, natriuretic peptides buffer renal vascular hypertension via renin-independent effects, such as vasorelaxation. The latter possibility is supported by experiments in isolated perfused mouse kidneys, in which physiological concentrations of ANP and BNP elicited renal vasodilatation and attenuated renal vasoconstriction in response to angiotensin II.

Effect of celecoxib on the antihypertensive effect of losartan in a rat model of renovascular hypertension

2011 ◽  
Vol 89 (2) ◽  
pp. 103-107 ◽  
Author(s):  
Vivian Boshra ◽  
Gehan Abdel Hamid El Wakeel ◽  
Manar A Nader
Keyword(s):  
Blood Pressure ◽  
Renovascular Hypertension ◽  
Aortic Coarctation ◽  
Oral Treatment ◽  
Antihypertensive Agents ◽  
Plasma Renin ◽  
Prostaglandin E ◽  
Sprague Dawley ◽  
Hypertensive Patients ◽  
Arterial Blood

Certain nonsteroidal anti-inflammatory drugs have been reported to elevate blood pressure in some hypertensive patients, who are either untreated or treated with antihypertensive agents. This study was undertaken to determine the effect of a selective cyclooxygenase-2 (COX-2) inhibitor, celecoxib, on the antihypertensive effects of the angiotensin II type 1 receptor (AT1) antagonist, losartan potassium. We studied the effect of oral treatment with losartan (30 mg/kg), celecoxib (3 mg/kg), and their combination on the mean arterial blood pressure (MAP), plasma renin activity (PRA), and plasma prostaglandin E2(PGE2) in male Sprague–Dawley rats with renovascular hypertension (RVH) induced by partial subdiaphragmatic aortic constriction. Treatment was continued for 7 days after aortic coarctation. Aortic coarctation led to significant increases in the MAP, PRA, and plasma PGE2. In RVH rats, losartan treatment caused a significant decrease of MAP with a significant increase in both plasma PGE2and PRA. Celecoxib caused a nonsignificant change in MAP with a significant decrease in the raised levels of plasma PGE2and PRA. Concomitant administration of celecoxib and losartan did not significantly affect the lowering effect of losartan on MAP with a subsequent significant decrease in the plasma PGE2and PRA in RVH rats. Therefore, celecoxib could be used in renin-dependent hypertensive patients who receive losartan, without fear of a rise in their blood pressure.

scholarly journals Postoperative Course of Blood Pressure and Plasma Renin Activity in Patients with Renovascular Hypertension

1976 ◽  
Vol 118 (1) ◽  
pp. 35-43 ◽  
Author(s):  
YOICHI OTSUKA ◽  
KEISHI ABE ◽  
TETSUO SAITO ◽  
NOBUO IROKAWA ◽  
SEIJI MIYAZAKI ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Renovascular Hypertension ◽  
Plasma Renin ◽  
Renin Activity ◽  
Postoperative Course

Inhibition of angiotensin conversion and prevention of renal hypertension

1975 ◽  
Vol 228 (2) ◽  
pp. 448-453 ◽  
Author(s):  
Miller ED ◽  
AI Samuels ◽  
E Haber ◽  
AC Barger
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Renovascular Hypertension ◽  
Renal Hypertension ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Activity ◽  
Angiotensin System ◽  
The One ◽  
Renal Artery Constriction

Renal artery constriction in the unilaterally nephrectomized, trained dog, with maintained renal arterial hypotension, produces a prompt increase in systemic renin activity and blood pressure. The hypertension normally induced by renal artery stenosis is prevented by prior treatment with the nonapeptide Pyr-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro (SQ 20, 881), which blocks conversion of angiotensin I to angiotensin II. Constant intravenous infusion of the inhibitor over several days of renal artery constriction prevents the development of chronic renovascular hypertension. Furthermore, a single injection of the nonapeptide restores blood pressure to normal in the early phase of renovascular hypertension, but becomes progressively less effective as salt and water retention occurs in the chronic stage when plasma renin activity returns to control levels. These data provide strong evidence that the renin-angiotensin system is responsible for the initiation of renovascular hypertension in the one-kidney Goldblatt dog, but that other factors become increasingly important in chronic renovascular hypertension.

The Value of Plasma Renin Concentration Per Se, and in Relation to Plasma and Extracellular Fluid Volume in Diagnosis and Prognosis of Human Renovascular Hypertension

1970 ◽  
Vol 39 (5) ◽  
pp. 559-576 ◽  
Author(s):  
G. Bianchi ◽  
L. Campolo ◽  
A. Vegeto ◽  
V. Pietra ◽  
U. Piazza
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Renal Disease ◽  
Renovascular Hypertension ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Plasma Renin Concentration ◽  
Diagnosis And Prognosis

1. Plasma renin concentration (PRC) has been measured in 212 hypertensive patients. In fourteen patients with essential hypertension and in seventeen patients with renovascular hypertension, plasma volume (PV) and extracellular fluid volume (ECFV) were measured. 2. The results obtained have been discussed in three ways: (a) PRC in relation to the aetiology of hypertension; (b) PRC in relation to the effect on blood pressure of surgery for unilateral renal diseases; (c) PRC, PV and ECFV in ‘essential’ and renovascular hypertension. 3. Excluding patients with ophthalmoscopic signs of malignant hypertension, PRC is significantly higher in renovascular hypertension than in normal subjects and patients suffering from ‘essential’ hypertension and hypertension associated with bilateral renal disease; but the overlapping of the single values of the patients with these diseases is marked. Thus a normal PRC has no diagnostic value, while a high PRC without sodium deficiency or retinopathy might favour a diagnosis of renovascular disease. 4. In twenty-seven out of thirty-three patients submitted to surgery for unilateral renal disease and followed up for 12 months or longer, blood pressure has been significantly reduced. This group includes twelve patients with a normal preoperative PRC and fifteen patients with a high PRC. These results clearly demonstrate that unilateral renal disease may maintain a high blood pressure without increasing PRC and that PRC has no prognostic value. 5. Concurrent estimations of PRC, PV and ECFV in patients with renovascular or essential hypertension revealed the following differences. In cases of renovascular hypertension with normal PRC, PV and ECFV were significantly increased while in those with raised PRC, PV did not differ and ECFV was barely raised with respect to values obtained in patients with essential hypertension. PV of renovascular patients with normal renin was significantly higher than that of renovascular patients with high renin. The analysis of these results with quadratic discriminant functions demonstrated that an integrated evaluation of blood pressure, PV, ECFV and PRC allows a separation between the two types of hypertension. In other words these factors, taken together, in some way seem to reflect a difference between the two diseases. These results may indicate a new type of approach to the diagnosis and prognosis of renovascular hypertension.

Maximal Discrimination of Renovascular from Essential Hypertension by the Saralasin Test

1978 ◽  
Vol 55 (s4) ◽  
pp. 297s-299s ◽  
Author(s):  
M. H. Maxwell ◽  
P. Varady ◽  
E. T. Zawada ◽  
J.-F. Burkhalter ◽  
U. Waks ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Renovascular Hypertension ◽  
Feedback Loop ◽  
Plasma Renin ◽  
Pressure Control ◽  
Control Blood Pressure ◽  
Volume Depletion ◽  
Linear Discriminant ◽  
Blood Pressures

1. Thirty-four patients with essential hypertension and 37 with proven renovascular hypertension were tested with saralasin after frusemide-induced diuresis. 2. Variables used for analysis were: pre-saralasin plasma renin activity (PRA), post-saralasin PRA, and ratios of systolic and diastolic blood pressures (saralasin blood pressure/control blood pressure). 3. Stepwise linear discriminant analysis demonstrated that the most significant variables were diastolic ratio, systolic ratio, and post-saralasin PRA. 4. Minimal misclassification (14·1%) was achieved by combining diastolic ratio, baseline supine PRA and post-saralasin PRA; but using post-saralasin PRA alone resulted in misclassification of only 15·5% (7 essential hypertension and 4 renovascular hypertension). 5. Thus, PRA increased disproportionately after saralasin in renin-dependent renovascular hypertension because of the fall in blood pressure and/or interruption of the short, negative angiotensin II feedback loop. 6. It is concluded that the rise in PRA after the combined stimuli of volume depletion and saralasin is more sensitive than the fall in blood pressure in discriminating between essential hypertension and renovascular hypertension, although minimal misclassification is achieved by analysing baseline PRA, diastolic ratio and post-saralasin PRA simultaneously.

Sign in / Sign up

Export Citation Format

Share Document