[Central modulation of the baroreflex response to phenylephrine in rats. Lack of interaction between calcium channel modulators and the renin-angiotensin system].

We have previously shown that a calcium channel activator (BAY K 8644) can decrease the baroreflex control of heart rate in SHR when intracerebroventricularly (i.c.v.) administered. In pentobarbital anesthetized SHR, the inhibitory effect of BAY (3 micrograms/kg i.c.v.) on baroreflex sensitivity (BRS; ramp method: phenylephrine 2 micrograms i.v.; BAY: 0.14 +/- 0.05 vs control: 0.39 +/- 0.08 msec/mmHg; p less than 0.01) was fully suppressed after pretreatment with the muscarinic antagonist atropine methylnitrate (80 micrograms/kg i.c.v.) suggesting the involvement of cholinergic pathways in the inhibitory effect. Since A II was reported to centrally increase arterial pressure through an enhanced release of acetylcholine and to depress BRS, we tested whether the effect of BAY on BRS could involve central A II systems. The A II antagonist [Sar 1Ile8] A II (30 micrograms/kg/min i.c.v.) suppressed the inhibitory effect of A II on BRS (control: 0.32 +/- 0.09; A II: 0.10 +/- 0.02; Sar1 Ile8 + A II: 0.39 +/- 0.08 msec/mmHg) but not the inhibitory effect of BAY (3 mu g/kg i.c.v.) on BRS. These results suggest that the central inhibition of BRS by BAY unlikely involves central A II systems.