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It is still not well documented what the basic roles for the regulation of renin secretion from the kidney take place. Since the early study on the renal ischemia for the production of hypertension was introduced, the renin-angiotensin system has been regarded as the possible pathogenetic mechanism for the renovascular hypertension. The renin-angiotensin system, however, could be activated by various stimuli, such as, the changes of intrarenal perfusion pressure, the load or concentriation of sodium at the sites of macular densa, the changes of the sympathetic nervous activity and the changes of potassium balance. To investigate the renin-angiotensin system and the influence of sympathetic nervous system on the regulation of renin secretion, the renovascular hypertension was induced in the dogs by constriction of unilateral renal artery, and the plasma renin activity was measured. The sodium load at the sites of macula densa was attained by furosemide, and then the activity of sympathetic nervous system was depressed by reserpine. The plasma renin activity was assayed by the method of Helmer and Cohn. By this bio-assay method, the plasma renin activity equivalent to 1 nanogram angiotensin-II can be measurable and the prepared plasma was found to have still vasopressor activity. The results observed in this experimental work are summarized as follows. 1. The blood pressure reached maximum on the 3rd postoperative day, and declined gradually to the level of preoperative day on the day of from the 6th to 12th day following constriction of renal artery. 3. The plasma renin activity was found to be well correlated with the increase of blood pressure, and then declined to its preoperative level with the reduction of blood pressure. It appears, therefore, that the renin-angiotensin system plays an important role in the pathogenesis of renovascular hypertension. 4. The urine flow rate in normal and reserpinized dogs was the same before administration of furosemide, but its rate was significantly increased in both groups after furosemide. The urine flow rate of reserpinized dogs, however, was significantly lower than that of the normal dogs during the first 5 minutes. 5. The urinary sodium excretion in normal and reserpinized dogs was significantly increased in both groups after administration of furosemide and there were no difference between the two groups. 6. The plasma renin activity of renal venous blood was significantly higher than that of femoral arterial blood in both groups before and after administration of furosemide. 7. The plasma renin activity of reserpinized dogs was significantly lower than that of normal dogs before administration of furosemide. After furosemide, however, the plasma renin activity was significantly increased in 30 minutes in both groups. This increase of plasma renin activity was less prominent in resepinized dogs than in normal. This results would suggest that the intrarenal mechanism regulating renin secretion also requires an intact sympathetic nervous system.
Animals ; Blood Pressure ; Constriction ; Dogs ; Furosemide ; Hypertension ; Hypertension, Renovascular ; Ischemia ; Kidney ; Perfusion ; Plasma ; Potassium ; Renal Artery ; Renin* ; Renin-Angiotensin System ; Reserpine ; Sodium ; Sympathetic Nervous System

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