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  • Title: Mechanism of adrenomedullin-induced relaxation in isolated canine retinal arteries.
    Author: Okamura T, Ayajiki K, Kangawa K, Toda N.
    Journal: Invest Ophthalmol Vis Sci; 1997 Jan; 38(1):56-61. PubMed ID: 9008630.
    Abstract:
    PURPOSE: To analyze the mechanism of action of adrenomedullin (AM), a peptide recently isolated from human pheochromocytoma, in isolated canine central retinal arteries and to compare the action of calcitonin gene-related peptide (CCRP). METHODS: Changes in isometric tension were recorded in helical strips of the arteries with and without the endothelium. RESULTS: Both AM and CGRP produced relaxation: EC50s were 2.62 and 0.71 x 10(-9) mol/l, respectively, and maximal relaxations were 85.1% and 84.3%, respectively. The AM-induced relaxation was endothelium-independent and unaffected by indomethacin, Ng-nitro-L-arginine, methylene blue, and glibencaalmide. Treatment with [8-37] CGRP markedly inhibited the relaxations caused by AM and CGRP. Treatment with a high concentration of sodium nitroprusside abolished the relaxation caused by nitroglycerin and atrial natriuretic peptide and reduced the relaxation caused by AM and CGRP. A high concentration of beraprost, a stable analog of prostaglandin I2, suppressed the response to AM and CGRP but not to nitroglycerin. CONCLUSIONS: Endothelium-independent relaxations to AM of canine retinal arteries may be mediated primarily by intracellular cyclic adenosine monophosphate by stimulation of CGRP1 receptors and partially by cyclic guanosine monophosphate; cyclic guanosine monophosphate is unlikely ot be produced by methylene blue-sensitive soluble guanylate cyclase. Prostanoids, nitric oxide, and adenosine triphosphate-dependent K+ channel opening do not appear to be involved in the AM-induced relaxation.
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