Yutaka Takabatake

Effect of ganglion-blocking agents on renin release in hypertensive patients.

In 18 patients with benign essential hypertension, renin release during reduction of arterial pressure due to sodium nitroprusside infusion was measured before and after administration of ganglion-blocking agents (pentolinium or trimethaphan). In 12 patients, renin release induced by reduction in pressure was significantly reduced but not abolished by ganglion blockade. Simultaneously, ganglion blockade significantly reduced renal vascular resistance (RVR) and almost abolished a decrease in renal blood flow (RBF) due to hypotension. In 6 other patients in whom no significant renin release resulted from hypotension, ganglion blockade caused little changes in renin release, RVR or RBF. The results support the hypothesis that renal sympathetic nerve activity is a factor in variations in renin release in patients with essential hypertension. Following ganglion blockade in the responsive patients, the significant reciprocal correlation between renal venous renin activity and sodium excretion rate shifted but still persisted, suggesting that the renin-releasing mechanism related to sodium excretion may be independent of innervation. On the other hand, the correlation between renin activity and the degree of reduction in pressure was insignificant after ganglion blockade. It is concluded that two intrarenal mechanisms, nerve-dependent and nerve-independent, are involved in renin release due to reduction in pressure. Ganglion blockade also exerted an inhibitory effect on renin release due to hypotension in 4 normotensive subjects and 5 patients with renovascular hypertension.

The Size of Kidney with Renovascular Hypertension in Patients with Aortitis Syndrome

Renal atrophy due to the renal artery stenosis associated with aortitis syn drome was studied in seven patients. Severe hypertension, high plasma renin activity and normal overall renal functions were present in all. The luminal diameter of the stenosed renal artery seen on the angiogram was less than 1.5 mm at the maximum area of stenosis in all patients. The size of the kidney with renal artery stenosis was diminished, ranging from 8.0 to 14.0 cm in longitudi nal diameter on the nephrogram. Histological findings of the small kidney re vealed ischemic atrophy. Although the rate of progression of the arterial stenosis was uncertain, the collateral circulation was found to be rich. Renal atrophy was not frequent and not marked even in the presence of high grade renal stenosis or obstruction in case of renovascular hypertension secondary to the arteritis.