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(Circulation. 1968;38:353.)
© 1968 American Heart Association, Inc.

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Renin Release in Patients with Benign Essential Hypertension

YOSHIHIRO KANEKO M.D.¹; TAKAO IKEDA M.D.¹; TADANAO TAKEDA M.D.¹; GOSUKE INOUE M.D.¹; HRROSHI TAGAWA M.D.¹; HIDEO UEDA M.D.¹

¹ From the Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Hongo, Tokyo, Japan.

In 16 of 28 patients with benign essential hypertension, reduction of mean arterial pressure to 75 to 120 mm Hg by infusion of sodium nitroprusside caused significant increase in renin release estimated by the renal-systemic difference of renin activity and renal plasma flow (RPF). The threshold at which renin release increased was shifted to a range that was intermediate between that previously reported for normotensive subjects and that for patients with renovascular hypertension, but the average magnitude of renin release was almost comparable to that in normotensive subjects. In the other 12 patients, no significant renin release occurred during reduction in pressure of comparable degree.

The difference in renin release was difficult to explain by the difference in severity of hypertensive disease or in sodium excretion, but increased renin release was usually associated with a decrease in RBF and a rise in renal vascular resistance, while insignificant release was usually associated with an insignificant change in RBF and a decrease in resistance. The average known duration of hypertension was significantly greater in the unresponsive patients. It is suggested that renal sympathetic nerve activity may be a factor in the variations in renin release in patients with essential hypertension.

Key Words: Pathogenesis of essential hypertension • Sympathetic nerve activity • Renovascular hypertension • Sodium excretion • Renal blood flow • Renal nerves • Sodium nitroprusside • Renal autoregulation • Primary aldosteronism

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