Why the study?
Are plasma renin reactivity and prostaglandin A levels altered in patients with low renin essential hypertension compared to normal renin hypertension and controls?
Are plasma renin reactivity and prostaglandin A levels altered in patients with low renin essential hypertension compared to normal renin hypertension and controls?
Patients with low renin essential hypertension exhibit suppressed plasma renin reactivity and lower prostaglandin A levels, suggesting altered renin reaction kinetics contribute to apparent renin suppression.
Suppressed PRR and PGA in low-renin hypertension may reflect altered kinetics; hypothesis-generating and requires prospective validation before clinical consideration.
Plasma renin reactivity (PRR) is the rate of angiotensin generation in vitro after addition of exogenous renin to plasma. To evaluate the hypothesis that suppressed plasma renin activity (PRA) in patients with low renin essential hypertension may be related to an alteration of the kinetics of the in vitro renin reaction, PRR was compared in plasma of patients with low renin and normal renin essential hypertension. Prostaglandin A (PGA) inhibits renin, and PGA was also measured to determine if suppressed PRA may be related to increased PGA. Low renin and normal renin hypertension were defined by comparing PRA responses of 30 hypertensive patients and 16 matched control subjects to upright posture and furosemide (80 mg p.o.). Nine of 30 patients had low PRA. Compared to that in plasma of patients with normal renin hypertension, PRR was suppressed (P < 0.005) during 30, 60, and 180 min incubations in the low renin patients. Overall, in the hypertensive patients, there was a significant positive correlation (r = +0.58; P < 0.01) between PRR and the PRA response to furosemide. PGA in patients with low renin hypertension (0.86 ng/ml ± 0.06 SE) was less (P < 0.05) than that in patients with normal renin hypertension (1.10 ng/ml ± 0.07 SE) and control subjects (1.18 ng/ml ± 0.10 SE); PGA of normal renin patients and control subjects did not differ (P > 0.1). These results suggest that an alteration of the kinetics of the renin reaction may contribute to the apparent renin suppression in patients with low renin hypertension. Hypertensive patients with suppressed PRA also have low PGA.
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Brooks et al. (1977) studied this question.
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