Venodilator action of an organotransition-metal nitrosyl complex

Nitrovasodilators, such as nitroglycerin, cause endothelium-independent dilatation of arterial and capacitance vessels via the release of nitric oxide (NO). This study examined the venodilator effect of CpCr(NO)(2)Cl (organotransition-metal nitrosyl complex) relative to that of nitroglycerin in conscious, unrestrained rats. Organotransition-metal nitrosyl complexes have releasable NO directly attached to metal centres. The dose-response effects of CpCr(NO)(2)Cl and nitroglycerin on the mean arterial pressure and the mean circulatory filling pressure (index of the body venous tone) were obtained in rats continuously infused with either normal saline or noradrenaline. The results show that both CpCr(NO)(2)Cl and nitroglycerin reduced the mean arterial pressure in rats with normal or elevated vasomotor tone. However, maximum depressor response of CpCr(NO)(2)Cl was greater than that of nitroglycerin. In vehicle-treated rats, both compounds increased the mean circulatory filling pressure. In rats with elevated vasomotor tone through the infusion of noradrenaline, both agents reduced the mean circulatory filling pressure. These results show that CpCr(NO)(2)Cl is an efficacious depressor and venodilator agent.