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 toread more
Citations
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Low-Renin Essential Hypertension: Diminution of Aldosterone Suppression?
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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.
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An exaggerated natriuretic response to hypertonic saline infusion in the stage II (who stage classification) essential hypertensive patients.
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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.
Michael Horster,Klaus Thurau +1 more
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 Article
Renin-angiotensin system, aldosterone, and sodium balance.
Gross F,Brunner H,Ziegler M +2 more
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.