Regular ArticleRelative Contributions of NO and Gap Junctional Communication to Endothelium-Dependent Relaxations of Rabbit Resistance Arteries Vary with Vessel Size
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Inhibitors of connexin and pannexin channels as potential therapeutics
2017, Pharmacology and TherapeuticsGap26, a connexin mimetic peptide, inhibits currents carried by connexin43 hemichannels and gap junction channels
2012, Pharmacological ResearchCitation Excerpt :The generality of the early effect on Ihc and the delayed effect on Ij by the mimetic peptide warrants discussion. Extensive studies have demonstrated high level inhibition of functions underwritten by GJs after exposure to Cx-mimetic peptides Gap26 and Gap27, usually for 30–60 min, but sometimes longer [7,8]. The longer exposure times explain the inhibition of gap junctional coupling but the presence of smaller GJ plaques in cultured cells compared to the situation found in tissues and organs [2] may also influence the efficacy and speed of inhibition.
Endothelium-derived hyperpolarizing factor in vascular physiology and cardiovascular disease
2009, AtherosclerosisCitation Excerpt :Gap27 and Gap26 have been shown to attenuate endothelium-dependent hyperpolarization and relaxation without influence on NO- and prostanoids-mediated responses both in vitro and in vivo[101–104]. Paired or triple CMPs combinations are used to target more than one Cx subtype to attenuate EDHF-mediated relaxation [105–108], suggesting that, in general, more than one Cx subtype is involved in construction of MEGJs. A triple combination of CMPs has been recommended as the most effective and reliable way to block vascular gap junctions [100].
Perturbing plasma membrane hemichannels attenuates calcium signalling in cardiac cells and HeLa cells expressing connexins
2009, European Journal of Cell BiologyThe vascular effects of rotigaptide in vivo in man
2008, Biochemical PharmacologyCitation Excerpt :EDHF activity has been demonstrated in the microcirculation of a variety of human vascular beds including the peripheral [2], mesenteric [3] and subcutaneous [4,5] circulations in addition to the coronary [6,7] and renal [8] vasculature. Consistently, its contribution is most prominent in the small resistance arteries [3,9] that regulate systemic blood pressure and local tissue perfusion. Furthermore, the release of t-PA from the endothelium is independent of both nitric oxide and prostacyclin production [10,11], and it has been suggested that EDHF may mediate its release [11,12].
The Pulmonary Microcirculation
2008, Microcirculation
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