The antihypertensive effect of calcium channel inhibitors (CCI) results mainly from their direct action on the vascular smooth muscle. However CCI may pass through the blood-brain barrier and may modulate central mechanisms involving calcium channels. Normotensive (WKY) and spontaneously hypertensive (SHR) (Okamoto) rats weighing 300 g were anaesthetized with pentobarbital (50 mg/kg i.p.) and ventilated. Mean arterial pressure (MAP) was measured from a catheter inserted into the femoral artery. Heart rate (HR) was electronically integrated. Vehicle (ethanol 95%), nifedipine and Bay k 8644 (Bay) were injected under a 1.5 microliter volume into the lateral ventricle of the brain (i.c.v.). Vehicle alone did not change significantly MAP or HR. The calcium-channel inhibitor nifedipine and the calcium-channel activator Bay had opposite effects, when i.c.v. injected: hypotension with bradycardia and hypertension without tachycardia, respectively. These effects are dose-dependent (5-50 micrograms/kg). They are of central origin since they are suppressed by ganglionic blockade by hexamethonium(100 mg/kg i.c.). Bilateral vagotomy suppressed the i.c.v.-nifedipine induced bradycardia. Previously i.c.v. administered nifedipine (5 micrograms/kg) suppressed the pressor response to Bay (5 micrograms/kg i.c.v.). Changes in MAP and HR are significantly more marked in SHR than in WKY. These results indicate that a calcium-channel inhibitor and a calcium-channel activator can modulate in opposite fashion central calcium-dependent mechanisms involved in blood pressure control.