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Intermedin (IMD/AM2) dilates the pig coronary vascular bed through release of nitric oxide
Author(s) -
Doganci Suat,
Yildirim Vedat,
Bolcal Cengiz,
Demirkilic Ufuk,
Tatar Harun,
Gumusel Bulent,
Lippton Howard
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1380
Subject(s) - medicine , vasodilation , vascular resistance , cardiology , calcitonin gene related peptide , hemodynamics , nitric oxide , coronary flow reserve , calcitonin , coronary circulation , anesthesia , blood flow , receptor , neuropeptide
The present study was designed to investigate the effects of IMD/AM2 (IMD), an endogenous agonist for calcitonin‐like calcitonin receptors (CLCR), on coronary and systemic hemodynamics. Ultrasonic transit time flow probes were placed around the left anterior descending artery in the anesthetized, open‐chest pig. Intracoronary arterial bolus injections (IAB) of IMD, hADM 13–52 and CGRP increased coronary blood flow in a dose‐dependent manner. IMD at the doses studied was more potent than CGRP and hADM 13–52 and did not alter systemic arterial pressure, cardiac output and cardiac index. IAB of L‐NAME significantly decreased the coronary vasodilatory response (CVR) to IMD. The present data suggest that IMD possesses marked vasodilator activity in the pig coronary vascular bed. The present data further suggest the CVR to IMD in the pig is mediated by release of nitric oxide from endothelial CLCR. The degree of the CVR to IMD may serve as functional marker for the integrity of endothelial cells in resistance segments of the coronary circulation. This study was supported by Gulhane Military School of Medicine (# AR‐2006‐20).