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C‐Type Natriuretic peptide (CNP) release does not contribute to endothelium‐derived hyperpolarizing factor (EDHF) mediated relaxation in porcine coronary artery
Author(s) -
Ng Kwok Fu Jacobus,
Leung Susan Wai Sum,
Man Ricky Ying Keung,
Vanhoutte Paul M
Publication year - 2008
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.22.1_supplement.914.3
Subject(s) - phosphoramidon , bradykinin , endothelium derived hyperpolarizing factor , medicine , endocrinology , artery , atrial natriuretic peptide , chemistry , mesenteric arteries , vasoconstriction , cardiology , nitric oxide , endothelin receptor , receptor , charybdotoxin
Objective: The release of CNP accounts for EDHF‐mediated relaxations in the rat mesenteric artery1 and is Gi protein dependent2. EDHF‐mediated relaxations in the porcine coronary artery are not Gi dependent3. This study investigates whether or not CNP release accounts for EDHF‐responses in this artery. Methods: (1) CNP concentration was measured by enzyme immunoassay in bathing solution containing porcine coronary arterial rings where EDHF response was initiated by bradykinin (100 nM). (2) EDHF‐mediated relaxations induced by SFLLRN were compared with those to exogenous CNP in the presence of phosphoramidon (10 μM; known to potentiate CNP induced relaxations). Results: There was no significant difference in the CNP concentrations between chambers containing rings that did or did not exhibit a EDHF‐mediated response. Relaxations induced by CNP alone were potentiated by phosphoramidon (maximal relaxation 60.7 ± 7.7 % vs 84.1 ± 7.5 %, control vs phosphoramidon, P <0.05) but the EDHF‐mediated responses to SFLLRN were not (maximal relaxation 69.9 ± 9.1 % vs 72.8 ± 9.9 %, control vs phosphoramidon) Conclusions: Unlike in the mesenteric artery and the heart of the rat, CNP release does not contribute to EDHF‐mediated relaxations in the porcine coronary artery.