Different pathways for Ca2+ mobilization by angiotensin II and carbachol in the circular muscle of the guinea-pig ileum

• Published in: European journal of pharmacology Vol. 367; no. 1; pp. 59 - 66
• Main Authors: SHIMUTA, S. I, BORGES, A. C. R, PRIOSTE, R. N, PAIVA, T. B
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier 12-02-1999
• Subjects: Angiotensin II - antagonists & inhibitors; Angiotensin II - pharmacology; Angiotensin Receptor Antagonists; Animals; Biological and medical sciences; Calcium - metabolism; Calcium - pharmacology; Calcium Channel Blockers - pharmacology; Carbachol - pharmacology; Electric Stimulation; Female; Fundamental and applied biological sciences. Psychology; Guinea Pigs; Ileum - drug effects; Ileum - physiology; Imidazoles - pharmacology; In Vitro Techniques; Intestine. Mesentery; Isradipine - pharmacology; Losartan - pharmacology; Male; Membrane Potentials - drug effects; Muscarinic Agonists - pharmacology; Muscle Contraction - drug effects; Muscle, Smooth - drug effects; Muscle, Smooth - physiology; Nickel - pharmacology; Nifedipine - pharmacology; Potassium Chloride - pharmacology; Pyridines - pharmacology; Receptor, Angiotensin, Type 1; Receptor, Angiotensin, Type 2; Tetrodotoxin - pharmacology; Vasoconstrictor Agents - pharmacology; Verapamil - pharmacology; Vertebrates: digestive system; Peptides; Digestive system; Gut; Rodentia; Smooth muscle; Muscle contraction; Ileum; In vitro; Vertebrata; Mammalia; Calcium ion; Guinea pig; Animal; Angiotensin II; Biological receptor
• ISSN: 0014-2999; 1879-0712
• DOI: 10.1016/S0014-2999(98)00919-4

Ca2+ pathways activated by angiotensin II and carbachol were evaluated in the circular muscle of the guinea-pig ileum by recording mechanical and electrical activities. Transient contractions induced by angiotensin II were greatly reduced by Ca2+ removal from the medium whereas carbachol-induced responses were not significantly altered. Nifedipine had no effect on the responses to both agonists. A high concentration of tetrodotoxin (0.1 microM) inhibited angiotensin II-induced contractile responses without affecting the depolarization, whereas 1 mM Ni2+ inhibited the mechanical and electrical effects. Neither tetrodotoxin nor Ni2+ affected carbachol-induced effects. These results indicate that angiotensin II-induced phasic contractions depend on extracellular Ca2+ but not on voltage-dependent L-type Ca2+ channels. It is suggested that angiotensin II activates Ni2+-sensitive Na+ and non-specific cationic channels, whereas the responses to carbachol are dependent on receptor-activated Ca2+ release. Furthermore the different response of the longitudinal and circular muscles to the inhibitory effects of tetrodotoxin and Ni2+ on the angiotensin II- and carbachol-induced contractions indicates that these agonists exert their own myogenic effects on each layer and are able to trigger different Ca2+ mobilization pathways.