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This Article Full Text Full Text (PDF) All Versions of this Article: 291/1/H385    most recent 01047.2005v2 01047.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (12) Citing Articles via Google Scholar Google Scholar Articles by Sokoya, E. M. Articles by Tare, M. Search for Related Content PubMed PubMed Citation Articles by Sokoya, E. M. Articles by Tare, M.

Evidence for the involvement of myoendothelial gap junctions in EDHF-mediated relaxation in the rat middle cerebral artery

Departments of ¹Anesthesiology and ²Medicine, Baylor College of Medicine, Houston, Texas; and ³Department of Physiology, Monash University, Clayton, Victoria, Australia

Submitted 4 October 2005 ; accepted in final form 20 January 2006

The mechanisms underlying endothelium-dependent hyperpolarizing factor (EDHF) in the middle cerebral artery (MCA) remain largely unresolved. In particular, very little is known regarding the way in which the signal is transmitted from endothelium to smooth muscle. The present study tested the hypothesis that direct communication via myoendothelial gap junctions contributes to the EDHF response in the male rat MCA. EDHF-mediated dilations were elicited in rat MCAs by luminal application of ATP or UTP in the presence of N-nitro-L-arginine methyl ester and indomethacin. Maximum dilation to luminal ATP (10^–4 M) was reduced significantly after incubation with a gap peptide cocktail (9 ± 4%, n = 6) compared with a scrambled gap peptide cocktail (99 ± 1%, n = 6, P < 0.05). A gap peptide cocktail had no effect on amplitude of endothelial cell hyperpolarization in response to 3 x 10^–5 M UTP (22 ± 3 vs. 22 ± 1 mV, n = 4), whereas smooth muscle cell hyperpolarization was significantly attenuated (17 ± 1 vs. 6 ± 1 mV, n = 4, P = 0.004). Connexin (Cx) 37 was localized to smooth muscle and Cx43 to endothelium, whereas Cx40 was found in endothelium and smooth muscle. Electron microscopy revealed the existence of frequent myoendothelial junctions. The total number of myoendothelial junctions per 5 µm of MCA sectioned was 2.5 ± 0.5. Our results suggest that myoendothelial communication contributes to smooth muscle cell hyperpolarization and EDHF dilation in male rat MCA.

connexins; endothelium-derived hyperpolarizing factor; vascular smooth muscle

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