Why the study?
Does inhibition of NO synthesis with L-NMMA alter resting renin secretion and renin secretory responses in healthy subjects?
Does inhibition of NO synthesis with L-NMMA alter resting renin secretion and renin secretory responses in healthy subjects?
Nitric oxide participates in the regulation of resting renin secretion in humans but does not significantly contribute to renin responses to macula densa activation or sympathetic mechanisms.
Answers are grounded in this paper and cite their sources.
Supports nitric oxide in basal renin secretion; leaves open its role in stimulated responses.
Nitric oxide (NO) has been implicated in the control of renin secretion in experimental animals but little information is available concerning its role in humans. The aim of the present study was to investigate the effects of inhibition of NO synthesis on resting renin secretion and on the renin secretory responses to activation of the macula densa and sympathetic neural mechanisms controlling renin secretion. In eight healthy subjects, injection of furosemide increased plasma renin activity (PRA) with little or no change in blood pressure or heart rate. Injection of the NO synthase inhibitor L-NMMA increased blood pressure and decreased heart rate and PRA, but failed to alter the PRA response to furosemide. In another ten subjects, standing increased PRA. L-NMMA again decreased PRA but failed to alter the PRA response to standing. These results suggest that NO participates in the regulation of resting renin secretion in humans, and provide preliminary evidence that NO does not contribute significantly to the renin responses to activation of the macula densa or sympathetic mechanisms controlling renin secretion.
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Chiu et al. (1999) studied this question.
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