Effect of sensory neuropeptides on canine bronchial and pulmonary vessels in vitro

Abstract

Sensory neuropeptides may be important in the noncholinergic component of parasympathetic vasodilation in the tracheobronchial circulation. We studied the effects of substance P (SP), neurokinin A (NKA), neurokinin B (NKB) and calcitonin gene-related peptide (CGRP) on the isolated canine bronchial artery and used pulmonary artery and vein of similar size for comparison. CGRP (10pM-300nM) was a potent relaxant of the bronchial and pulmonary arteries, and the pulmonary vein with equal potency in all vessels. SP in low concentrations (10pM-100nM) caused vasodilation of the precontracted bronchial artery and in high concentration (10–100μM) contracted the vessel from resting tone. SP also relaxed the pulmonary artery and vein. NKA and NKB caused relaxation in all three vessels. All of the vascular effects of the sensory neuropeptides were concentration-dependent. The order of potency of the neuropeptides in the bronchial and pulmonary artery was SP>NKA>CGRP>NKB. In the pulmonary vein NKB caused a much larger relaxation than SP and NKA but it was less potent than either NKA or CGRP. Capsaicin (1 μM) caused a large contraction of the bronchial artery, similar in magnitude to the contraction caused by high dose of SP. Neuropeptide Y was also studied and found to cause no consistent constriction of any of the vessels studied. In conclusion, CGRP is a universal dilator of the bronchial and pulmonary blood vessels. SP and NKA exert their main effect on arterial vasomotor tone, whereas NKB is the only tachykinin producing marked dilation of the pulmonary vein.