Renin Activation in the Venous Plasma from the Involved Kidney in the Patient with Renal Hypertension

Sambhi, Mohinder P.; Wiedeman, Charles E.

doi:10.1172/jci106792

Cited by 20 publications

(6 citation statements)

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“…In apparent contrast to our results, Sambhi and Wiedeman [8] have reported that the re activity of renin during a 20-min incubation is increased in venous plasma of the more in volved kidney compared to that from the contralateral kidney in patients with pre dominately unilateral renal hypertension. The difference between our results and those of Sambhi and Wiedeman may in part be related to patient selection.…”

Section: Discussioncontrasting

confidence: 99%

“…Correlations between the demonstration of greater renin activity from the ischemic kidney compared to the normal, contralateral kidney and cure or improvement of hypertension following revascularization are high [6,7]. Sambhi and Wiedeman [8] have recently reported that the in vitro rate of angiotensin generation is also greater in venous effluent from the more involved kidney than from the contralateral kidney in patients with renal hypertension. The purpose of the present report is to describe our measurements of renal venous PRR in both experimental and clinical renovascular hypertension.…”

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confidence: 99%

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Renal Venous Plasma Renin Reactivity in Clinical and Experimental Renovascular Hypertension

Welch¹,

Daugherty²,

Ernst³

1977

Nephron

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Plasma renin reactivity (PRR) is the in vitro rate of angiotensin generation after addition of exogenous renin to plasma. The purpose of the present study is to compare measurements of PRR in venous effluent from the involved and uninvolved kidneys in both experimental and clinical renovascular hypertension. A two-kidney model of experimental hypertension was created by placing an ameroid resin constrictor around one renal artery in each of seven dogs. Plasma renin activity (PRA) in venous plasma from the involved kidney increased (p < 0.001); comparing PRA in venous effluent from the stenotic and nonstenotic kidneys, the PRA ratio also increased (p < 0.005). Renal venous PRR did not change on either side after occlusion of the renal artery (p > 0.1), and the renal venous PRR ratio did not differ from the mean control ratio of 1.0 ± 0.1 SE (p > 0.1). Similarly, in 9 patients with renovascular hypertension, mean PRR in venous plasma from the two kidneys did not differ (p > 0.8). These results suggest that measurement of renal venous PRR is not helpful in confirming a diagnosis of renovascular hypertension.

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Section: Discussioncontrasting

confidence: 99%

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confidence: 99%

Renal Venous Plasma Renin Reactivity in Clinical and Experimental Renovascular Hypertension

Welch¹,

Daugherty²,

Ernst³

1977

Nephron

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“…Although the normal form of substrate is the major renin substrate form in all plasmas, the new forms of substrate may have a significant effect on the overall renin reaction in plasma because form III (Rf = 0.16) appears to lead to an accelerated rate of angiotensin production and form II (Rf = 0.35) decreases this rate. These new substrate forms may, therefore, possibly account for the altered kinetics of the renin reaction observed in some hypertensive states (13,14).…”

Section: Discussionmentioning

confidence: 99%

Multiple forms of human plasma renin substrate.

Eggena¹,

Hidaka²,

Barrett³

et al. 1978

J. Clin. Invest.

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A B S T R A C T The objective of this investigation was to determine whether heterogeneity of plasma renin substrate could be observed in states of steroid excess and various forms of hypertensive disease. In states of stimulated renin substrate production by estrogens or glucocorticoids, multiple forms of renin substrate were apparent when stimulation was excessive. Stimulation of substrate production caused by uremia associated with hypertension showed similar results. None, or only trace quantities of the additional forms of renin substrate were evident in subjects with normal or suppressed levels of plasma renin substrate. The additional forms of renin substrate could be distinguished from the normal form on the basis of crossreactivity with a specific antiserum to the normal form, electrophoretic mobility, and kinetic rate constants. Differences in rate constants of the various forms of plasma renin substrate may account for the altered rate of the renin reaction associated with several states of hypertension. In plasma of patients with renovascular hypertension, significant quantities of a protein which cross-reacted with the antiserum but could not generate angiotensin I were observed. INTRODUCTION We have previously described the purification of renin substrate from normal human plasma (1) and the development of a direct radioimmunoassay for this protein (2). The direct assay for renin substrate in normal human plasma was validated by demonstrating a 1:1 correlation to substrate measured by the generation of angiotensin I by prolonged incubation with exogenous homologous renin (indirect method). Results of preliminary experiments indicated, however, that in plasma samples in which renin substrate concentration was elevated at least 2 SD above normal as measured by angiotensin I generation, the direct as-

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“…These components include renin substrate concentration and "renin reactivity," a measure of inhibitors or accelerators of the renin reaction. Accelerating factors (or the lack of inhibitors) producing an increase in renin reactivity have been observed in a variety of primary and secondary hypertensive states (12)(13)(14)(15)(16) and thus far appear to be common to all forms of hypertension studied. Our second objective was to examine these components of the renin reaction in coarctation hypertension, to assess their contribution to the conventional plasma renin activity, and to seek further insight into the pathophysiological significance of the in vitro renin reactivity measurement in hypertensive states.…”

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confidence: 99%

“…Increases have, however, been reported in a variety of other hypertensive states in man, including essential hypertension of both normal-and low-plasma renin activity categories (13,14), renovascular hypertension (12,15), and primary aldosteronism (16). The addition of coarctation hypertension to this group provides further evidence that increased renin reactivity is a common feature of most, if not all, hypertensive states.…”

mentioning

confidence: 99%

Abnormalities of renal perfusion and the renal pressor system in dogs with chronic aortic coarctation.

Bagby¹,

McDonald²,

Strong³

et al. 1975

Circulation Research

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To clarify the role of the renin-angiotensin system in coarctation hypertension, 2-year-old inbred dogs with chronic neonatally induced thoracic aortic coarctation were subjected to 6 days of rigorous salt restriction. The following parameters were then measured: glomerular filtration rate, renal plasma flow, plasma renin activity, plasma renin concentration, renin reactivity, and renin substrate concentration. Glomerular filtration rate and renal plasma flow were significantly lower in salt-restricted coarcted dogs: 3.0 ± 0.2 and 9.0 ± 1.5 ml/min kg" 1 , respectively, compared with values of 4.0 ± 0.2 (P < 0.005) and 13.2 ± 0.9 (P < 0.025) ml/min kg" 1 in salt-restricted controls. Plasma renin activity was abnormally high in experimental dogs: 13.5 ± 2.5 vs. 4.5 ± 1.5 ng angiotensin I/ml hour" 1 in controls (P < 0.005). In addition, a significant elevation of renin reactivity (indicating a relative increase in circulating accelerators or a relative decrease in inhibitors of the renin reaction) was apparent in the plasma of coarcted dogs. Plasma renin concentration was elevated but to an insignificant degree in coarcted dogs, and renin substrate concentration was comparable with that of controls. The impaired renal perfusion and abnormal elevation of plasma renin activity during salt restriction is analogous to clinical and experimental observations in hypertensive states associated with total renal underperfusion and supports a major role for the renal pressor system in the pathogenesis of coarctation hypertension. The insignificant elevation of plasma renin concentration is not incompatible with this view. The demonstration of increased renin reactivity in coarctation hypertension provides additional evidence that acceleration of the renin reaction is common to all hypertensive states.

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Renin Activation in the Venous Plasma from the Involved Kidney in the Patient with Renal Hypertension

Cited by 20 publications

References 14 publications

Renal Venous Plasma Renin Reactivity in Clinical and Experimental Renovascular Hypertension

Renal Venous Plasma Renin Reactivity in Clinical and Experimental Renovascular Hypertension

Multiple forms of human plasma renin substrate.

Abnormalities of renal perfusion and the renal pressor system in dogs with chronic aortic coarctation.

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