Ergotamine-induced constriction of cranial arteriovenous anastomoses in dogs pretreated with phentolamine and pizotifen.

Previous investigations from our laboratory have shown that ergotamine causes a selective vasoconstriction in the carotid vascular bed of the dog and that the drug constricts arteriovenous anastomoses (AVAs) in cats and pigs. Since ergotamine can act via alpha-adrenergic or D-serotonergic receptors in certain vascular and non-vascular tissues, we have attempted to ascertain here if these receptors mediate the constriction of AVAs. Using radioactive microspheres of 15 microns diameter we found in the dog that about 40% of the carotid arterial blood is shunted to the venous side via AVAs. Ergotamine (2-20 micrograms X kg-1, i.v.) reduced total carotid blood flow to a larger extent in the AVA part than in the extracerebral part (muscles, ears, skin and fat). The cerebral component of carotid blood did not change. These results, confirming that ergotamine decreases arteriovenous shunting, show that the drug has a more selective action on the AVAs than on the arterioles. Pretreatment with phentolamine (0.5 mg X kg-1), pizotifen (0.5 mg X kg-1) or their combination did not effectively modify the responses to ergotamine. It is concluded that the vasoconstriction of cranial AVAs (and arterioles) by ergotamine does not appear to be primarily mediated by either alpha-adrenergic or D-serotonergic receptors. However, the role of atypical serotonin receptors has yet to be determined.