Endogenous Opioid Involvement in the Cardiovascular Effects of Clonidine in Rats: Role of the Parasympathetic Nervous System
George Kunos, Rogelio Mosqueda‐Garcia
Abstract
George Kunos, Rogelio Mosqueda‐Garcia
Abstract
The interaction between intravenously administered clonidine and naloxone on blood pressure and heart rate was studied in urethane-anesthetized, normotensive Sprague-Dawley rats. In rats pretreated with propranolol, 1 mg/kg i.v., to eliminate sympathetic tone in the heart clonidine, 5 micrograms/kg i.v. produced hypotension and bradycardia which were inhibited by naloxone, 2 mg/kg i.v. These effects were similar to effects observed in earlier studies in the absence of propranolol. In contrast, in rats pretreated with atropine, 5 mg/kg i.v., to eliminate the effects of changes in vagal tone, the hypotensive and bradycardic effects of clonidine were not influenced by naloxone. These findings are interpreted to indicate that an endogenous opioid is involved in the clonidine-induced increase in parasympathetic outflow to the myocardium.
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The interaction between intravenously administered clonidine and naloxone on blood pressure and heart rate was studied in urethane-anesthetized, normotensive Sprague-Dawley rats. In rats pretreated with propranolol, 1 mg/kg i.v., to eliminate sympathetic tone in the heart clonidine, 5 micrograms/kg i.v. produced hypotension and bradycardia which were inhibited by naloxone, 2 mg/kg i.v. These effects were similar to effects observed in earlier studies in the absence of propranolol. In contrast, in rats pretreated with atropine, 5 mg/kg i.v., to eliminate the effects of changes in vagal tone, the hypotensive and bradycardic effects of clonidine were not influenced by naloxone. These findings are interpreted to indicate that an endogenous opioid is involved in the clonidine-induced increase in parasympathetic outflow to the myocardium.
Key concepts: Clonidine, (+)-Naloxone, Propranolol, Atropine, Bradycardia, Endogenous opioid, Medicine, Internal medicine