Cardiovascular responses of sinoaortic-denervated rats to intracerebroventricular injection of alpha 1- and alpha 2-adrenoceptor agonists.
The aim of the present work was to analyse the cardiovascular responses induced by i.c.v. administration of the alpha 1- and alpha 2-adrenoceptor agonists, phenylephrine and clonidine, respectively, in conscious normal and sinoaortic-denervated rats. Sinoaortic denervation involves changes in central and peripheral catecholaminergic pathways. Clonidine (1-10 micrograms) produced a dose-dependent rise in blood pressure and a bradycardiac response in sham-operated animals, whereas in sinoaortic-denervated rats it provoked a brief rise in blood pressure followed by a marked fall as well as bradycardia. The responses involved mostly activation of central alpha 2-adrenoceptors, but the blood pressure responses induced by clonidine in sinoaortic-denervated rats may also have involved alpha 1-adrenoceptors. The bradycardia induced by the alpha 2-agonist in both groups of rats involved preferentially central alpha 2-adrenoceptors but also partially stimulated alpha 1-adrenoceptors. Phenylephrine, at a dose of 10-60 micrograms, induced a rise in blood pressure and a bradycardiac response while 90 micrograms produced a biphasic pressure response (early transient rise followed by a fall) as well as bradycardia in both sham-operated and sinoaortic-denervated animals. Phenylephrine activated alpha 1-adrenoceptors in every case, but the fall in blood pressure and the bradycardia also involved alpha 2-adrenoceptors. The responses were significantly higher in the sinoaortic-denervated rats than in the sham-operated. Our findings suggest that arterial baroreceptor reflexes can modify the effects of alpha-agonists initiated in the central nervous system. Sinoaortic denervation preparations enable one to unmask the depressor response to clonidine and also demonstrate the true magnitude of the phenylephrine response.
Cátedra de Farmacología, Facultad de Farmacia y Bioquímica, UBA, CONICET, Buenos Aires, Argentina.
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D000316:Adrenergic alpha-Agonists / Q000008:administration & dosage / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D003000:Clonidine / Q000494:pharmacology; D003714:Denervation; D004146:Dioxanes / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects*; D019329:Idazoxan; D007276:Injections, Intraventricular; D010656:Phenylephrine / Q000494:pharmacology; D011224:Prazosin / Q000494:pharmacology; D011311:Pressoreceptors / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains
D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D004146:Dioxanes; D010656:Phenylephrine; D003000:Clonidine; D011224:Prazosin; D019329:Idazoxan