Is the inhibitory effect of somatostatin on the heart due to K+ channel activation?

• Published in: General pharmacology Vol. 22; no. 6; p. 1043
• Main Authors: Freeman, S E, Lau, W M, Szilagyi, M
• Format: Journal Article
• Language: English
• Published: England 1991
• Subjects: Action Potentials - drug effects; Animals; Apamin - pharmacology; Binding, Competitive - drug effects; Carbachol - pharmacology; Electrophysiology; Ethylmaleimide - pharmacology; GTP-Binding Proteins - metabolism; Guinea Pigs; Heart - drug effects; In Vitro Techniques; Myocardial Contraction - drug effects; Pertussis Toxin; Potassium Channels - drug effects; Quinuclidinyl Benzilate - pharmacology; Receptors, Muscarinic - drug effects; Receptors, Purinergic - drug effects; Somatostatin - pharmacology; Tacrine - pharmacology; Virulence Factors, Bordetella - pharmacology
• ISSN: 0306-3623
• DOI: 10.1016/0306-3623(91)90575-Q

1. Somatostatin (SS) was found to shorten the action potential of both left and right atrium, and to reduce the force of contraction of the atrium. Action potential shortening was antagonized by the potassium channel blocking drugs tacrine and apamin. They were less effective in reducing the negative inotropic effect of SS. 2. Alkylation of the intact atrium with N-ethylmaleimide abolished both the AP shortening and the negative inotropic effect of SS. 3. Pretreatment of guinea pigs with pertussis toxin abolished the negative inotropic effect of SS and reduced the AP shortening. 4. Binding studies showed there was virtually no interaction between SS and muscarinic and adenosine receptors. 5. It is suggested that the cardiac SS receptor is linked with G protein-K+ channel-adenylyl cyclase system which is analogous to but not identical with the muscarinic and adenosine receptor systems.