AJP - Heart and Circulatory Physiology, Vol 257, Issue 2 483-H487, Copyright © 1989 by American Physiological Society
Somatostatin stimulates acetylcholine release in the canine heart
J. W. Wiley, L. Uccioli, C. Owyang and T. Yamada
Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor 48109.
Previous reports of somatostatin's atropine-sensitive negative inotropic
effect on cardiac function prompted the present studies to characterize the
molecular forms and actions of somatostatin in the canine heart.
Radioimmunoassay of cardiac extracts revealed concentrations of
somatostatin-like immunoreactivity ranging from 0.50 +/- 0.13 pmol/g tissue
(means +/- SE, n = 6) in the pulmonary artery to 0.78 +/- 0.23 pmol/g
tissue in the right ventricle. On gel filtration of the extracts, two major
molecular forms of somatostatin-like immunoreactivity were elicited, the
predominant one coeluting with somatostatin-14 and a minor peak
corresponding to somatostatin-28. Experiments performed with slices of
atrial septum indicated that somatostatin-14 (10(-10) to 10(-7) M)
stimulated the release of acetylcholine in a dose-dependent manner. This
action of somatostatin-14 was additive with K+-evoked acetylcholine
release, unaffected by hexamethonium, and blocked by tetrodotoxin,
suggesting mediation via a nonnicotinic postganglionic neural pathway. Our
studies lead us to conclude that somatostatin may function as a
neurotransmitter in the heart, which exerts its negative inotropic action
by promoting the release of acetylcholine.
