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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

Role of atrial natriuretic polypeptides for exaggerated natriuresis in essential hypertension

TL;DR: The present findings suggest that the enhanced secretion of ANP is an important determinant for exaggerated natriuresis observed in patients with renin-unresponsive hypertension.
Journal ArticleDOI

Relationship of Sodium Balance to Arterial Pressure in Black Hypertensive Patients

TL;DR: Spearman correlations showed no relationship between sodium balance and mean arterial pressure, suggesting that salt-sensitive hypertension results not from the magnitude of sodium retention, but from the pressor mechanisms evoked.
Journal ArticleDOI

The effects of rapid saline infusion on sodium excretion, renal function, and blood pressure at different sodium intakes in man.

TL;DR: The data suggest that although natriuresis following rapid saline infusion is dependent upon prior sodium intake, under given circumstances it may be independent of glomerular filtration rate, renal blood flow, or blood pressure.
Journal ArticleDOI

Perspectives on the renin-angiotensin-aldosterone system in hypertension.

TL;DR: It is suggested that the same factors, clearly abnormal in hypertensive states of more defined etiology, are also at play in causing essential hypertension, perhaps through some as yet undefined abnormal interrelationship.
Journal ArticleDOI

Spectrum of deranged sodium homeostasis in essential hypertension.

TL;DR: The heterogeneity in Na excretion indicates that an exaggerated natriuresis is not a uniform concomitant of essential hypertension, and the significant inverse correlation between basal plasma aldosterone level and peak urinary as well as cumulativeNa excretion suggests that plasma a Aldosterone constitutes a determinant of the differing natriuretic responses.
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.
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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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