Abstract
Isolated segments of the middle cerebral artery of the cat were used to determine whether noradrenaline (NA [norepinephrine]), neuropeptide Y (NPY), avian pancreatic polypeptide (APP), substance P (SP), vasoactive intestinal polypeptide (VIP) and gastrin releasing peptide (GRP) have effects that involve pre- and/or postsynaptic mechanisms. NA, clonidine, NPY and APP produced concentration-dependent contractions of cerebral artery segments, whereas SP and VIP induced relaxation of prostaglandin F2.alpha.-contracted arteries. GRP, in the concentrations tested, (up to 2 .times. 10-7 M) had no vasomotor activity. The .alpha.2-adrenoreceptor agonist clonidine (10-8 and 10-6 M) produced a reduction in the field stimulation-evoked release of 3H-NA previously incorporated into the noradrenergic transmitter pool of the arteries, whereas the .alpha.2-adrenoreceptor antagonist rauwolscine (10-8 and 10-6 M) resulted in increases in 3H-NA release. None of the peptides caused any significant change of the stimulation-evoked fractional release of 3H-NA. Apparently, NPY, APP, SP, and VIP have postjunctional effects in cat cerebral arteries and, in the concentrations tested, do not affect stimulation-evoked NA release.