抄録
Using a total number of 30 anesthetized dogs, embolism was produced by injecting air into the right vertebral artery. The efferent impulses from left renal nerve were recorded simultaneously with the arterial pressure. The renin activity in the renal venous blood and aortic blood was measured by the Helmer's method.
A slight initial step up in blood pressure and transient increase in renal sympathetic discharge were observed immediately after the embolism. Then the blood pressure rose up markedly and the nerve activity was depressed, which was considered that the phase of reduced sympathetic nerve activity was produced by excitation of the buffer nerves caused by the second rise in pressure. Thereafter, with the falling of the pressure to the control level, bursts of sympathetic discharge started again.
Renin release following vertebral embolism was estimated by a percent change of circulating renin activity of the left renal vein from each animal's control level, by multiplying the activity of renal venous blood with the left renal plasma flow. The circulating renin activity thus ob-tained in the control phase was 363±238ng angiotensin/min. It starts to increase during 6-10min after embolism, then within 20-30min it attained its peak of 217±104% in average compared with control values.The latter increase was highly significant (p<0.01). It is most likely that the first increase in renal sympathetic nerve activity caused the increase in renin release and the second rise in blood pressure was caused not by the increase in renin activity but by the increase in catecholamines.
