Abstract
It has been considered that an altered vascular reactivity to various stimuli might play a role in the increased peripheral resistance in essential hypertension. This experiment was attempted to deter-mine the role of vascular reactivity in the mechanism of experimental renal hypertension. And it was designed to know the inter-relatronship of renal and neural factors in the maintenance mechanisms of chronic renal hypertension. Vascular responses to noradrenaline and angiotensin were compared by the isolated per-fusion of hindquarters preparations of rats in different groups ; acute and chronic experimental hypertensive rats, salt deficient or loaded rats and those given daily injections of angiotensin or noradrenaline. The results were as follows :-1) The response to noradrenaline and angiotensin were significantly increased in the chronic renal hypertensive group. (P<0.01) How-ever, the responses to noradrenaline and angiotensin were not increased in acute renal hypertension. 2) The responses to noradrenaline in DCA-salt hypertension and adrenal regeneration hypertension were in normal range. Responses to angiotensin were also unchanged in adrenal regeneration hypertension or adrenal insufficiency. 3) Noradrenaline responses were decreased in the salt deficient rats, while in the salt loaded group the responses were similar as the controls. 4) The responses to noradrenaline were slightly, though not significantly augmented in the angiotensin injected group. There were no increase in the responses to noradrenaline or angiotensin in the noradrenaline injected group. 5) No differences were found in mean initial pressures between the hypertensive and control rats. Since augmentation of responses to the vasopressor substances were found only in chronic renal hypertension and not in the other types of hypertension of the same duration, it was considered that this potentiation could not be explained merely by hypertrophy or other mechanical properties of the vascular walls produced by high blood pressure itself and peripheral vascular beds of chronic renal hypertension might have been sensitized by some mechanisms originating in renal factors. Furthermore, the responses to noradrenaline were also slightly augmented in rats having daily injections of angiotensin. Therefore, it is concluded that small doses of renin or angiotensin secreted from the ischemic kidney might be related to the hvperreactivity to the sympathetic neurohumoral substance, and thus participating in the maintenance of chronic renal hypertension.
