The role of neural factors in experimental renal hypertension.

The role of neural factors in experimental renal hypertension was studied from the points of peripheral vascular reactivity, function of baroceptors and sympathetic activity in renal hypertensive dogs and the isolated smooth muscle strips of hypertensive rats. (1) The hypotensive responses to pentobarbital was more marked and continued longer in chronic renal hypertensive dogs than the controls. (2) The pressor responses to noradrenaline was remarkably augmented in renal hypertensive dogs, while the changes in those to angiotensin and Pitressin were not so marked. (3) The threshold for adrenaline or noradrenaline of isolated smooth muscle strips of intestine, rectum and uterus of rats was lower in hypertensive rats than in the operated normotensive and control groups. But the threshold for angiotensin and acetylcholine was rather higher in the hypertensive group. (4) The sensitivity of baroceptors examined by using the isolated perfusion method was unchanged and the baroceptors were resetted to the higher blood pressure level in chronic renal hypertension. (5) The influence of sympathetic innervation on carotid sinus activity was not different between the normotensive and renal hypertensive dogs. (6) The depressor responses to the sufficient amounts of ganglioplegics were not significantly changed in hypertensive dogs compared with the normotensives. (7) After the extensive sympathectomy the direct blood pressure fall was not significantly different between the normotensive and renal hypertensive dogs and the final blood pressure level was higher in renal hypertension than the control level. (8) The urinary excretion of adrenaline and noradrenaline was not significantly changed in chronic renal hypertensive dogs except the slight increase in the stage of blood pressure rising. Thus, increased sensitivity of peripheral blood vessels to noradrenaline was demonstrated in vivo and in vitro experiments in hypertensive animals. The baroceptors were resetted to the higher blood pressure level, and their sensitivity itself remained unchanged in renal hypertension. The sympathetic overactivity was not recognized in hypertension. Therefore, only the increased sensitivity of peripheral vessels to noradrenaline contributes to a part of the pressor mechanism in renal hypertension, while the baroceptors and sympathetic activities are passively adjusted to the higher blood pressure levels in hypertension.