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Open AccessJournal ArticleDOI

The Role of Renin in the Exaggerated Natriuresis of Hypertension

TLDR
The enhanced capacity of the renin-unresponsive hypertensive subjects to excrete a salt load suggests either a functionally significant degree of extracellular fluid volume expansion or a direct role for renin in the natriuresis accompanying volume expansion.
Abstract
Hypertensive patients were classified according to their plasma renin response when challenged by the potent diuretics, ethacrynic acid (50 mg IV), or furosemide (40 mg IV), into renin-unresponsive and renin-responsive groups In the latter plasma renin activity rose by at least 05 ng of angiotensin/ml/hr after the diuretic The response to volume expansion with 2 L of isotonic saline infused over 60 min was then studied Peak rate of sodium excretion after saline loading was 994±186 µEq/min in the renin-unresponsive group and peak urine flow was 119 ± 21 ml/min In the renin-responsive hypertensives peak sodium excretion was 448 ± 149 µEq/min and peak urine flow was 54 ± 15 ml/min Both the sodium excretion and urine flow responses were significantly higher (P < 005) in the renin-unresponsive group The degree of saline-induced diuresis and natriuresis was not related to the preexisting level of aldosterone production Plasma renin changed little in either group during saline infusion but tended to

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Journal ArticleDOI

Oral-Contraceptive-Induced Hypertension After Adrenalectomy and Hypophysectomy

TL;DR: In this adrenalectomized patient, the estrogenic component of the pill acting synergistically with a fixed ("nonsuppressible") replacement dose of mineralocorticoid seems to have caused a volume-related hypertension.
Book ChapterDOI

Low-Renin Essential Hypertension: Diminution of Aldosterone Suppression?

TL;DR: This paper will attempt to summarize what is known about LREH, particularly with respect to adrenal function, and propose a hypothesis of the pathophysiology involved.
Journal ArticleDOI

Modifications Induced By -10° Trendelenburg's Posture in Sodium Tubular Handling in Patients with Essential Hypertension

TL;DR: In essential hypertensive patients “exaggerated natriuresis” is a response to acute volume expansion, but the underlying mechanisms for this remain to be determined.
Journal ArticleDOI

An exaggerated natriuretic response to hypertonic saline infusion in the stage II (who stage classification) essential hypertensive patients.

TL;DR: The results suggest that development of essential hypertension induces a functional state that resembles expansion of extracellular fluid volume.
Journal ArticleDOI

Effects of Diet on Exaggerated Natriuresis in Hypertension

TL;DR: Diet did not affect the saline-induced natriuresis in hypertensive patients, there was no apparent association between plasma renin activity and exaggerated natriURESis in hypertension, and other factors such as the capacitance system and vasopressin may play an important role in volume expansion natriureis.
References
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Journal ArticleDOI

Role of the Sympathetic Nervous System in Regulating Renin and Aldosterone Production in Man

TL;DR: It is suggested that both upright posture and sodium depletion lead to decreases in effective plasma volume and increases in sympathetic nervous system activity, which is responsible for an increase in renal afferent arteriolar constriction, leading to a increase in renin secretion and, ultimately, an increaseIn aldosterone secretion.
Journal ArticleDOI

Suppression of Plasma Renin Activity in Primary Aldosteronism: Distinguishing Primary From Secondary Aldosteronism in Hypertensive Disease

TL;DR: It is now clear that, when hypersecretion of aldosterone occurs in human renal hypertension (secondary aldosteronism), it is the result of increased activity of the renin-angiotensin system.
Journal ArticleDOI

Micropuncture studies on the filtration rate of single superficial and juxtamedullary glomeruli in the rat kidney.

TL;DR: A mechanism by which the kidney adjusts sodium excretion by altering the contribution of each nephron type to total kidney GFR is suggested by suggesting the highest TF/P inulin values and lowest intratubular flow rates were found in the descending limb.
Journal ArticleDOI

Effect of an Adrenal Inhibitor in Hypertensive Patients With Suppressed Renin

TL;DR: From the results of this study one might infer either that some unidentified mineralocorticoid is present in excessive quantities in the patients with suppressed plasma renin activity or that even normal levels of aldosterone are normal in patients with essential hypertension.
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