Role of Brain Angiotensin II on Somatosensory-Induced Antinatriuresis in Hypertensive Rats

The aim of this investigation was to compare the contribution of brain angiotensin II in mediating the transmission of a somatosensory stimulus within the brain to generate a renal sympathetic nerve-dependent antidiuresis and antinatriuresis in normotensive Wistar rats and stroke-prone spontaneously hypertensive rats (SHRSP). In anesthetized Wistar rats, stimulation of somatosensory receptors by subcutaneous capsaicin increased blood pressure by 9%, had no effect on renal hemodynamics, but decreased urinary flow and sodium excretion by 30% to 40%. These antidiuretic and antinatriuretic, but not blood pressure, responses were absent after intracerebroventricular losartan administration to block angiotensin II type 1 receptors. By contrast, in the SHRSP, although subcutaneous capsaicin raised blood pressure and renal blood flow, neither glomerular filtration rate, urinary flow, nor sodium excretion changed, and this pattern of responses was unaffected after intracerebroventricular losartan. However, an intracerebroventricular infusion of angiotensin II increased basal blood pressure and fluid output, and the capsaicin challenge elicited vasopressor, antidiuretic, and antinatriuretic responses similar in magnitude to those observed in the Wistar rats. The capsaicin challenge in the SHRSP also caused a slowly developing, long-lasting fall in blood pressure and fluid excretion. These findings show that angiotensin II is a necessary component in the somatorenal reflex in normotensive rats but that endogenous angiotensin II is unable to exert this role in SHRSP.