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January 1, 1970Annals of Internal Medicine194 citations

Suppressed Plasma Renin Activity in Essential Hypertension

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AJA. JoseJCJ. Richard CroutNKNorman M. Kaplan

Structured PICO

What are the physiological mechanisms underlying suppressed plasma renin activity in patients with essential hypertension?

P
Population
12 patients with essential hypertension (7 with normally responsive plasma renin activity [PRA] and 5 with suppressed PRA)
I
Intervention
Maneuvers to affect the renin-angiotensin system, including shrinkage of plasma volume (low-sodium diet plus upright posture), moderate fall in blood pressure (induced by guanethidine), and norepinephrine infusion
C
Comparator
Patients with normally responsive PRA compared to patients with suppressed PRA undergoing the same maneuvers
O
Outcome
Plasma renin activity (PRA) response, aldosterone excretion, sodium conservation, and catecholamine excretionsurrogate

In essential hypertension, suppressed plasma renin activity is linked to expanded extracellular fluid volume and impaired sodium conservation rather than sympathetic nervous system defects.

Abstract

Possible mechanisms causing suppressed plasma renin activity (PRA) in about 25% of patients with essential hypertension are examined. Seven patients with normally responsive PRA were compared to five patients with suppressed PRA. Measurements were made during and after manuevers known to affect the renin-angiotensin system, including shrinkage of plasma volume induced by a low-sodium diet plus upright posture and a moderate fall in blood pressure induced by guanethidine. Sympathetic nervous system involvement was examined by catecholamine excretion and responses to norepinephrine infusion. A relative inhibition of the renin-release mechanism that fails to respond normally to various stimuli is indicated. Suppression of PRA was accompanied by subnormal rise in aldosterone excretion and inability to conserve sodium. This inhibition is associated with expanded extracellular fluid volume but does not appear to be caused by an excess of mineralocorticoid or an intrinsic defect in the sympathetic nervous system.

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Cite This Study

Jose et al. (1970) studied this question.

synapsesocial.com/papers/6a12d1b345487b7639a737achttps://doi.org/10.7326/0003-4819-72-1-9
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