Regional differences in the response to nicotine in isolated canine arteries

Helically cut strips of canine cerebral, coronary, femoral, mesenteric and renal arteries were contracted with prostaglandin F2alpha. In response to 10(-4)M nicotine, cerebral arterial strips showed a transient relaxation, which was abolished by hexamethonium, cocaine and propranolol but was not significantly influenced by sotalol and tetrodotoxin. In coronary arteries, biphasic response, relaxation followed by contraction, to 8 X 10(-4)M nicotine and contractile response to 10(-4)M nicotine were not influenced by hexamethonium, cocaine and propranolol. Initial contraction and relaxation of femoral arteries induced by nicotine were abolished by hexamethonium and cocaine. Phentolamine (2 X 10(-7)M) attenuated the contraction but not the relaxation, while sotalol (10(-5)M) reduced the relaxation without alterations in the contractile response. In mesenteric and renal arteries, the contractile response to nicotine was abolished by hexamethonium, cocaine, bretylium and phentolamine, but was attenuated only partially by tetrodotoxin. It may be concluded that nicotine exerts a relaxation in cerebral arteries by a mechanism different from the adrenergic one, and a non-specific relaxation and contraction in coronary arteries. It appears that initial contractions of femoral, mesenteric and renal arteries and also relaxation of femoral arteries in response to nicotine are associated with the release of noradrenaline; however, the mechanism of the amine release is different from that with transmural stimulation, in which the nerve action potential is involved.