Vials, Amanda Jayne; (1994) Local control of coronary vascular resistance. Doctoral thesis (Ph.D), UCL (University College London).

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Abstract

This thesis presents a study of the responses to vasodilators in the guinea-pig and rat heart, carried out by perfusing the coronary circulation using the method of Langendorff. In the guinea-pig coronary vasculature it was found that the vasodilator response to substance P and low doses of 5-hydroxytryptamine acted almost exclusively via nitric oxide. The vasodilator responses to adenosine 5' -triphosphate and bradykinin appeared to involve other mechanisms in addition to nitric oxide. While a major part of the response to adenosine was mediated directly via A2 -receptors on the smooth muscle, activation of a subpopulation of A2 -receptors on the endothelial cells by adenosine and its analogues induced relaxation via production of nitric oxide. 2-MethylthioATP induced relaxation almost exclusively via a subpopulation of P2Y-purinoceptors on the endothelium, which when activated induced release of nitric oxide. In addition to adenosine 5' -triphosphate acting at this population of P2Y-purinoceptors adenosine 5' -triphosphate appears to induce relaxation via release of a prostanoid. Pyrimidines also induced relaxation via nitric oxide, possibly via a subclass of the P2y-purinoceptor superfamily. Prostanoids do not play any role in the relaxation induced by pyrimidines. During periods of increased flow, adenosine 5'-triphoshate release from the guinea-pig heart was rapidly and significantly increased. The pressure/flow ratio was reduced in high flow conditions suggesting that coronary vasodilatation had occurred. It is suggested that the release of adenosine 5' -triphosphate induced coronary vasodilatation. In the rat coronary vasculature the vasodilator response to 2-methylthioATP was inhibited by the P2"Purinoceptor antagonist suramin. However, the response to adenosine 5'-triphosphate was not inhibited by suramin or the P1-purinoceptor antagonist 8-(p-sulfophenyl) theophylline. It is suggested that adenosine 5' -triphosphate may be acting at another receptor site to elicit vasodilatation, which is neither a known P2y-or P1-purinoceptor.

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