Participation of alpha 1- and beta 1-adrenoceptors in norepinephrine-induced contraction and relaxation of isolated equine coronary artery in vitro.

This study uses experiments in isolated horse coronary arterial rings to show that the contractile response to norepinephrine is mediated by stimulation of alpha 1-adrenoceptors, while the stimulation of beta 1-adrenoceptors modifies the contraction by inducing relaxation.

Research Objective and Methodology

• The researchers aimed to understand the roles of alpha 1- and beta 1- adrenoceptors in the contraction and relaxation of the coronary artery in the context of norepinephrine (NE).(10(-7) – 10(-5) M) administration.
• NE-induced contractions in isolated coronary rings from horse hearts were measured, and the impacts of various antagonists were assessed. These antagonists included prazosin, yohimbine, propranolol, phentolamine, atenolol, and butoxamine.

Key Findings

• It was found that NE-induced contractions were unaffected by the removal of the endothelium – the thin layer of cells that lines the interior of blood vessels.
• Use of the alpha 1-antagonist prazosin inhibited the contraction created by NE, while the alpha 2-antagonist yohimbine did not interfere with the contraction. This implies a major role for alpha 1-adrenoceptors in mediating these contractions.
• The beta-antagonist propranolol intensified the contraction, suggesting that beta-adrenoceptors might be involved in modulating the contraction.
• Pretreatment with phentolamine, an alpha-antagonist, changed the NE-induced contraction into relaxation in coronary rings that were precontracted with ONO11113 (a thromboxane A2 derivative).
• This relaxation was not influenced by the removal of endothelium, and was halted by propranolol and atenolol (a beta 1-antagonist), but was unaffected by butoxamine (a beta 2-antagonist), affirming the specific role of beta 1-adrenoceptors in modifying contractions via relaxation.

Conclusion

• The researchers concluded that the contractile effects of NE in equine coronary arteries are mediated by the action on alpha 1-adrenoceptors located on the artery’s smooth muscle. Significantly, the action of beta 1-adrenoceptors modifies the contraction by inducing relaxation, providing important insight into the pathways through which the vascular system modulates contraction and relaxation in response to certain stimuli.