Prevention of renal hypertension and of the central pressor effect of angiotensin by ventromedial hypothalamic ablation.
Various lines of research have implicated the central nervous system in the development of renal hypertension. The ablation of a periventricular region surrounding the anteroventral third ventricle (AV3V) has been shown to block the development of renal hypertension. Because of hemodynamic effects produced by AV3V electrical stimulation can be abolished by a midline lesion of the ventromedial hypothalamic--median eminence region (VMH-ME), the effect of VMH-ME ablation on the development of renal hypertension was studied. Following recovery from surgery that destroyed the VMH-ME region the lesioned rats and controls were subjected to unilateral nephrectomy and figure-of-eight wrapping of the remaining kidney. Control animals developed renal hypertension but those with VMH-ME lesions did not. When the pressor response produced by intracerebroventricular injections of angiotensin II was studied, it was found that rats with VMH-ME lesions, as compared to neurologically intact animals, showed significantly attenuated responses. The data suggest that a neural system related to cardiovascular control descends through the VMH-ME region and that the integrity of this pathway is necessary for the development of renal hypertension.
D000804:Angiotensin II / Q000502:physiology*; D000818:Animals; D001794:Blood Pressure; D004326:Drinking; D006977:Hypertension, Renal / Q000503:physiopathology*; D007031:Hypothalamus / Q000503:physiopathology*; D007033:Hypothalamus, Middle / Q000503:physiopathology*; D007668:Kidney / Q000294:innervation*; D008297:Male; D008473:Median Eminence / Q000502:physiology; D009434:Neural Pathways / Q000502:physiology; D011301:Preoptic Area / Q000502:physiology; D051381:Rats
D000804:Angiotensin II