Abstract
After many years of use of ephedrine, there is still confusion as to its exact mode of action: direct agonism (Liles et al., 2007) or actions as an indirect sympathomimetic, or both. We have previously shown that cardiovascular actions of the stimulant cathinone are largely indirect by release of noradrenaline (Alsufyani & Docherty, 2015). We have now investigated, using the same techniques, the cardiac and pressor responses to (±)‐ and (−)‐ephedrine in pentobarbitone anaesthetised male wistar rats. The tachycardiac responses to (±)‐ and (−)‐ephedrine were similar, but pressor responses to (−)‐ephedrine (10 mg/kg) were significantly greater than those to (±)‐ephedrine, and for both, the pressor response was followed by a small depressor response. Sympathectomy did not affect the pressor response, but significantly increased the later depressor response to both compounds. Sympathectomy did not significantly affect cardiac or depressor responses to the direct beta‐adrenoceptor agonist isoprenaline. Sympathectomy significantly reduced the tachycardia to (±)‐ephedrine. It is concluded, firstly, that (−)‐ephedrine is more potent than the racemate mixture at producing pressor responses. Secondly, since the depressor response to the direct agonist isprenaline was unaffected, sympathectomy presumably reduced a later pressor component to the response to (±)‐ and (−)‐ephedrine. Hence, the early pressor response to both (±)‐ and (−)‐ephedrine is direct, but the later pressor response is largely indirect. Ephedrine has both direct and indirect actions on blood pressure.
Support or Funding Information
Supported by King Abdelaziz University
This is from the Experimental Biology 2018 Meeting. There is no full text article associated with this published in The FASEB Journal.