The effects of angiotensin II, adrenaline, and valsartan on isolated bovine coronary artery

Abstract

Introduction: Coronary artery disease is the main cause of mortality and morbidity in many countries. Angina pectoris is one of its clinical presentations. The basic pathologic change of angina is myocardial ischaemia. Neuroendocrine hormones play important role in the development of the disease. Angiotensin II and adrenaline are two important neuroendocrine factors in coronary or ischaemic heart disease. Their interaction at the tissue level was the main focus of this study. Materials and Methods: This is an in vitro study that looked at the effects of angiotensin II, adrenaline, and angiotensin II receptor blocker on the isolated bovine coronary artery. The experiment consisted of two parts. The first part was the determination of effective potassium chloride concentration that causes 70 % contraction (KCl-EC10) of the bovine artery. The second part of the study was that of the arterial response to various drugs, alone or in combination after precontraction at KCl-EC10. Drugs used (adrenaline, angiotensin II, and Valsartan [ angiotensin II receptor blocker]) were at five times the normal plasma human value, in order to mimic the plasma neurohormonal levels during myocardial ischaemia in human. The Wilcoxon-signed rank test was used to analyse the data obtained. Results: The KCl-EC10 was 0.3g/ml. There was a significant reduction in the contraction of the bovine coronary artery in the presence of adrenaline alone and in the presence of both Valsartan and angiotensin II. Angiotensin II on its own did not cause a significant relaxation or contraction of the artery. No other drug or drug combination caused any significant change. Discussion: The presence of increased level of adrenaline induced relaxation of the isolated bovine coronary artery. This relaxation most likely occurred via activation of the beta-adrenoceptor. Angiotensin II probably facilitated and helped maintain the contraction induced by potassium chloride. This effect was abolished by Valsartan. It was unlikely for Valsartan to act through any other mechanisms as it has a predilection towards the AT1 receptor. Conclusion: Adrenaline and Valsartan at five times the normal plasma human concentration cause bovine coronary artery relaxation. Valsartan may have a promising role in the treatment of myocardial ischaemia due to its indirect vasodilatory effect.