Central cardiovascular effects of intracerebroventricular propranolol

Abstract

Injection of propranolol (1–4 mg) into the lateral cerebral ventricle of α-chloralose-anaesthetized dogs elicited a biphasic cardiovascular response - an initial, short-lived pressor phase with tachycardia followed by a prolonged depressor phase and bradycardia. These effects were analysed by surgical and pharmacological interruption of neural pathways concerned with the response. Spinal transection at C 2 prevented the cardiovascular response. The initial pressor response and tachycardia were due to endogenous release of catecholamines (CA) from the adrenals since there was a significant increase in the CA content of adrenal vein blood and these responses could not be elicited in adrenalectomized dogs. Activation of central β-adrenoceptive sites, possibly in the hypothalamus, is held responsible for centrally-mediated release of adrenal CA because the response could be prevented by prior central β-blockade or by depletion of brain CA stores. The prolonged depressor response and bradycardia are attributed to a central inhibition of symphathetic tone Prior stellate ganglionectomy and adrenalectomy significantly abolished the bradycardia but had no effect on the depressor phase. Injection of propranolol into the fourth ventricle elicited the electrically evoked medullary topical application of propranolol on the floor of the fourth ventricle inhibited the electrically evoked medullary vasopressor responses.