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Relaxation of human placental arteries and veins by ATP‐sensitive potassium channel openers
Author(s) -
Jewsbury S.,
Baker P. N.,
Wareing M.
Publication year - 2007
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.2007.01749.x
Subject(s) - cromakalim , pinacidil , potassium channel opener , nitric oxide , chemistry , potassium channel , adenosine triphosphate , vasodilation , adenosine , relaxation (psychology) , anatomy , biophysics , medicine , agonist , endocrinology , glibenclamide , biochemistry , biology , receptor , diabetes mellitus
Background Adenosine triphosphate (ATP)‐sensitive potassium channels (K ATP ) are important modulators of vascular tone. Preliminary data from our laboratory suggests that K ATP channels are expressed in the fetoplacental vasculature where addition of pinacidil, a specific K ATP opener, promotes relaxation. We aimed to assess the effects of KRN2391 and KRN4884 on the fetoplacental vasculature, which are putative K ATP channel openers. Materials and methods Functional activity of K ATP channels was assessed in chorionic plate arteries and veins using wire myography. Cromakalim‐, KRN2391‐ and KRN4884‐induced relaxations were assessed in the presence and absence of agonist‐induced pretone. Cromakalim, an established K ATP channel opener, acted as control. Results KRN2391 evoked significantly greater relaxation of chorionic plate arteries and veins than either KRN4884 or cromakalim. KRN2391‐induced relaxation of precontracted arteries and veins was reduced in the presence of inhibitiors of the nitric oxide pathway (L‐NNA or LY83583). With KRN4884, there was no contribution of nitric oxide to the induced relaxation. Conclusions We conclude that K ATP channels play an important role in controlling placental vascular tone. KRN2391 induces relaxation of human placental blood vessels by activation of K ATP channels and via activation of nitric oxide‐dependent pathways.