| Autor: |
Talukder MA; Department of Cardiovascular Medicine, Kyushu University, Graduate School of Medical Sciences, Fukuoka 812-8582, Japan., Fujiki T, Morikawa K, Motoishi M, Kubota H, Morishita T, Tsutsui M, Takeshita A, Shimokawa H |
| Jazyk: |
angličtina |
| Zdroj: |
Journal of cardiovascular pharmacology [J Cardiovasc Pharmacol] 2004 Oct; Vol. 44 (4), pp. 437-45. |
| DOI: |
10.1097/01.fjc.0000139450.64337.cd |
| Abstrakt: |
It has been reported that endothelium-dependent relaxations are preserved in isolated coronary arteries of endothelial nitric oxide synthase-deficient (eNOS-/-) mice with a possible involvement of nNOS. However, it remains to be examined whether nNOS compensates coronary flow response in a beating heart of eNOS-/- mice and if so, whether and where nNOS is up-regulated. Coronary flow response to bradykinin was examined in Langendorff-perfused hearts from WT and eNOS-/- mice. Bradykinin-induced coronary flow was greater in eNOS-/- mice than in WT mice, and indomethacin had no inhibitory effect on it. Bradykinin receptor antagonist HOE-140 abolished the bradykinin response in both strains. Non-selective NOSs inhibitor L-NNA inhibited the bradykinin-induced coronary flow in both strains, whereas specific inhibitors of nNOS, SMTC, and 7-NI, significantly attenuated the coronary flow response only in eNOS-/- mice. A guanylate cyclase inhibitor ODQ also attenuated the bradykinin response in eNOS-/- mice. Immunohistochemistry revealed the presence of nNOS mainly in coronary vascular smooth muscle cells (VSMCs) in both strains and Western blot analysis demonstrated a marked increase in cardiac nNOS expression in eNOS-/- mice. These results indicate that nNOS compensates coronary flow response to bradykinin in eNOS-/- mice, for which up-regulation of nNOS in VSMCs may be involved. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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