Brain alpha 1-adrenoceptor in the cardiovascular responses to BHT-920 and phenylephrine

1. It is well known that alpha 1A-adrenoceptors have binding sites for imidazolic and for phenylethylaminic drugs. A study was made relating alpha 1A-adrenoceptor involvement in cardiovascular responses to intracerebroventricular (ICV) injection of BHT-920, an imidazoliclike drug, and phenylephrine, a phenylethylaminic drug, in conscious sham-operated and sinoaortically-denervated rats. 2. In sham-operated rats, cardiovascular responses to BHT-920 (30 micrograms, ICV) were increase of blood pressure and bradycardia but in sinoaortically denervated rats, after the pressor response, a decrease of blood pressure was also seen. The pressor and bradycardic responses to agonist were greater in sinoaortically denervated rats than in sham-operated rats. Phenylephrine (90 micrograms, ICV) showed a biphasic effect on blood pressure: an increase followed by a decrease, and bradycardia. The cardiovascular responses to phenylephrine in sinoaortic-denervated rats were greater than in sham-operated rats. 3. In sinoaortically denervated and sham-operated rats subchronically treated with the alpha 1-adrenoceptor antagonist prazosin (0.5 mg kg-1, intraperitoneally twice daily, for 6 days), an increase of cardiovascular responses to ICV administration of BHT-920 and phenylephrine was seen. 4. Baroreceptor deafferentation by sinoaortic denervation enhances the cardiovascular responses to BHT-920 and phenylephrine. The effects of BHT-920 could be mediated by brain alpha 1A adrenoceptors because this agonist has an imidazoliclike structure; phenylephrine could also be activating central alpha 1A-adrenoceptors. The enhanced cardiovascular responses after prazosin treatment could also be due to a supersensitivity of brain alpha 1A-adrenoceptors.