Brain Angiotensin II and Baroreceptor Reflex Function in Spontaneously Hypertensive Rats

We examined whether the increase in baroreceptor reflex function previously reported in lifetime-captopril-treated spontaneously hypertensive rats (SHR) was due to an inhibition of brain angiotensin II mechanisms. Pregnant and lactating SHR were given oral captopril (100 mg/kg/day). After weaning, pups were maintained on captopril (50 mg/kg/day) until the study (19-21 weeks). Control rats received tap water. One week before study captopril-treated and control SHR were given an intracerebroventricular infusion of angiotensin II (7.5 ng/hr, osmotic pump) or vehicle (artificial cerebrospinal fluid). Baroreceptor reflex control of heart rate was assessed by the slope of the relation between the change in mean arterial pressure (mm Hg) versus the change in pulse interval (msec beat"'). Arterial pressure was raised or lowered by intravenous bolus injections of phenylephrine or nitroprusside, respectively. Central infusion of angiotensin II had no significant effect on mean arterial pressure in captopril or control SHR (captopril-angiotensin II 125±4 vs. captopril-vehicle 121±2; control-angiotensin II 169±5 vs. control-vehicle 173±7 mm Hg), but it produced a significant rise in basal heart rate (captopril-angiotensin H 371 ±10 vs. captopril-vehicle 323 ±8, p< 0.0002; control-angiotensin II 338 ±7 vs. control-vehicle 312 ±8 beats/min,p< 0.0183) and in daily water intak