Abstract
Blood pressure rose when carbachol was injected into the cerebral ventricles in conscious rats, but the heart rate fell. When rats were later anesthetized with urethane to allow recording of abdominal sympathetic nerve activity, carbachol injected similarly produced the following biphasic responses: initial vasodepression followed by a sustained pressor phase accompanied by corresponding changes in peripheral sympathetic nerve activity. The heart rate was transiently suppressed following the injection. Spinal section abolished the initial hypotensive phase and accompanying bradycardia and made the response purely pressor. By contrast, intravenous injections elicited purely vasodepressor responses. Thus, carbachol administered centrally caused vasopressor responses possibly via both activation of sympathetic vasomotor centers and a release of pituitary hormones. Since anesthesia attenuated the pressor responses and made them biphasic, these results indicate that central cholinergic mechanisms are inhibited during anesthesia and that a sympathoinhibitory mechanism of cholinergic receptors exists behind the pressor responses, as disclosed during anesthesia.
