Abstract: CGRP is present in nerve fibres in central and peripheral arteries, where it is a potent vasodilator. The purpose of our research is to examine the effect of CGRP on human cerebral arteries and cerebral blood flow (CBF). Our results show that 1) CGRP can significnatly blunt the vasoconstriction caused by ebdothelin, neuropeptide Y (NPY), serotonin, noradrenaline, and CCK; 2) 50μg CGRP injected iv for 10 minutes into three patients who had cerebral embolisms increased CBF 32%～80% as measured by single photon emission computed tomography (SPECT), the levels of NPY, renin and angiotensin II in the patients' blood did not change after administration of CGRP; 3) an increase in CBF was seen in rabbits following injections of CGRP (4μg) into the internal carotid artery; 4) the intracerebroventricular (i. c. v. ) administration of endothelin (5ng) caused a decrease in CBF in rats, but it was reversed by CGRP (5ng, i. c. v. ); and 5) endothelin (5ng, i. c. v.) also induced an elevation of plasma alsosterone, but it was not antagonized by CGRP (5ng, i. c. v.). We conclude that CGRP can counteract the constriction of human arteries by various agents and increase CBF significantly. We deduce that the effect of CGRP is mediated by the increased calcium influx through dihydropyridine-sensitive calcium channels.

Key words: caleitonin gene related peptide, cerebral blood flow