A circulating renin activator in essential hypertension.

Sambhi, Mohinder P.; Eggena, Peter; Barrett, J. Carl; Tuck, Michael L.; Wiedeman, Charles E.; Thananopavarn, Chalemphol

doi:10.1161/01.res.36.6.28

Cited by 25 publications

(10 citation statements)

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“…This would appear inconsistent with the existence of a renin inhibitor in essential hypertension. It is, however, consistent with the data of Sambhi et al, 28 demonstrating an accelerated rate of A 1 production by renin in the presence of plasma from hypertensive subjects. They postulate the presence of a renin activator in the plasma of hypertensive subjects to account for this phenomenon.…”

Section: Discussionsupporting

confidence: 93%

Relation between plasma renin activity, angiotensin, and aldosterone and blood pressure in mild untreated hypertension.

Walker¹,

Horvath²,

Moore³

et al. 1976

Circulation Research

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SUMMARY Plasma renin activity, arterial and venous angiotensin II (A II), plasma aldosterone, and sodium excretion were measured in a group of 101 patients with mild essential hypertension. For the total hour; arterial A II was 5.2 ± 1.0 pg/ml; venous A II was 4.2 ± 0.6 pg/ml; and plasma aldosterone was 5.0 ± 0.45 ng/100 ml. All values were lower than corresponding values for normal subjects on a high salt intake despite the fact that salt intake in the normal subjects exceeded that for the hypertensive group more than 3-fold. Moreover, when the range of diastolic blood pressure up to 114 mm Hg was divided into three successive class intervals of increasing severity, there was a negative correlation between diastolic blood pressure and both PR A and plasma aldosterone. Arterial A II showed an anomalous increase in the class interval 105-114 mm Hg, despite the fact that this group exhibited the lowest level of PR A. At diastolic blood pressures above 114 mm Hg, the PR A appears to rise again. The anomalous increase in arterial A II in the presence of marked suppression of PR A is consistent with the presence of a renin activator or accelerator factor in hypertensive plasma as postulated by others. It also identifies a possible mechanism whereby even small increases in PR A could exert an adverse effect on the hypertensive state.HELMER'S early observation that plasma renin activity (PRA) is suppressed in some patients with essential hypertension' identified an interaction between the reninangiotensin system and the altered physiology of essential hypertension. Subsequent estimates of the incidence of suppressed PRA in groups of hypertensive patients have yielded frequencies ranging from 9% to 53%.2 * More recently, Brunner 5 ' 7 reported that patients with markedly suppressed PRA form a subset of hypertensives with a significantly lower incidence of cerebral vascular accidents and myocardial infarction. These findings have not been supported by the studies of Doyle 8 or Mroczek et al., 9 who failed to find any difference in the incidence of end organ disease between hypertensive patients with suppressed, normal, or elevated PRA. Sampling differences must be considered as a possible explanation for these discordant findings.These studies and others examining mineralocorticoid activity have sought to characterize low renin hypertension.4 -"• 7 Much of what has been written on this subject implies that low renin hypertension is a distinct nosological entity or a unique subset in the spectrum of essential hypertension. Evidence for this classification must be regarded as suggestive rather than conclusive at present.If low renin hypertension is a unique entity, i.e., a form of hypertension that always can be identified by the exhibition of abnormally low renin activity, then stratification of a sample of patients according to blood pressure levels should yield the same frequency of low renin values at different levels of blood pressure. Conversely, demonstration of a correlation between blood pressure and renin activit...

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Section: Discussionsupporting

confidence: 93%

Relation between plasma renin activity, angiotensin, and aldosterone and blood pressure in mild untreated hypertension.

Walker¹,

Horvath²,

Moore³

et al. 1976

Circulation Research

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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%

“…Received for publication 14 November 1977 and in revised form 27 March 1978. say underestimated the renin substrate concentration suggesting that other forms of renin substrate were present in these plasmas which could be cleaved by renin to generate angiotensin I, but did not crossreact with the antiserum produced against the renin substrate of normal plasma (2). The following study examines the various forms of plasma renin substrate in several clinical states associated with hypertension and in patients receiving agents known to stimulate renin substrate synthesis.…”

Section: Introductionmentioning

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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“…Indeed, there is increasing evidence in the literature for the existence of normally occurring renin inhibitors [ 14,[16][17][18][19][20]. Alternatively it has been suggested that in creased reactivity of exogenous renin in plasma of patients with essential hypertension may reflect the presence of a renin activator [21,22], If inhibitors or activators of renin are produced by the kidney, the results of the present study suggest that these factors are not produced, to a greater or lesser extent, by the ischemic kidney than by the nonconstricted contralateral kidney. Indeed, in patients with essential hypertension, we have found that PRR in renal venous and peripheral plasma does not differ [1], This does not necessarily refute the possibility that the kidney secretes a renin inhibitor.…”

Section: Discussionmentioning

confidence: 99%

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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A circulating renin activator in essential hypertension.

Cited by 25 publications

References 0 publications

Relation between plasma renin activity, angiotensin, and aldosterone and blood pressure in mild untreated hypertension.

Relation between plasma renin activity, angiotensin, and aldosterone and blood pressure in mild untreated hypertension.

Multiple forms of human plasma renin substrate.

Renal Venous Plasma Renin Reactivity in Clinical and Experimental Renovascular Hypertension

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