1988•Clinical and Experimental HypertensionRequires access

Endogenous Opioid Involvement in the Cardiovascular Effects of Clonidine in Rats: Role of the Parasympathetic Nervous System

George Kunos, Rogelio Mosqueda‐Garcia

Open publisher page 2 citations

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.

About this research paper

What this paper is about

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.

Why it matters

OpenAlex reports 2 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available 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.

Key concepts: Clonidine, (+)-Naloxone, Propranolol, Atropine, Bradycardia, Endogenous opioid, Medicine, Internal medicine

Related papers

Back to paper searchBrowse research topicsOriginal source
Endogenous Opioid Involvement in the Cardiovascular Effects of Clonidine in Rats: Role of the Parasympathetic Nervous System — Research Paper | ScholarLens