Characteristics of the antivasoconstrictor effect of pinacidil on isolated radial artery
2010
Gojkovic-Bukarica, Lj., University of Belgrade, Belgrade (Serbia). Faculty of Medicine | Stojnic, N., University of Belgrade, Belgrade (Serbia). Faculty of Medicine | Peric, M., Institute for Cardiovascular Diseases Dedinje, Belgrade (Serbia) | Cvejic, J., University of Novi Sad, Novi Sad (Serbia). Faculty of Medicine | Bumbasirevic, M., Clinical Center of Serbia, Belgrade (Serbia). Institute of Orthopedics and Traumatology | Lesic, A., Clinical Center of Serbia, Belgrade (Serbia). Institute of Orthopedics and Traumatology | Cupic, V., University of Belgrade, Belgrade (Serbia). Faculty of Veterinary Medicine | Milosevic, I., Clinical Center of Serbia, Belgrade (Serbia). Institute of Orthopedics and Traumatology | Kanjuh, V., Serbian Academy of Sciences and Arts, Belgrade (Serbia)
Pinacidil, a previously studied potassium channel opener (PCO), is a potent antihypertensive agent in animals and humans. Its mechanism of action is not completly defined. The aim of our study was to investigate the antivasoconstricting effect of pinacidil on the isolated RA and to study whether this effect is endothelium-dependent. Contractions of isolated RA rings intact endothelium were provoked by electrical field stimulation (EFS, 20Hz) or exogenously applied noradrenaline (NA, 10 microM). Pinacidil (10 nM-0.1 mM) produced a concentration-dependent inhibition of both EFS- and NA-evoked contractions (P is greater than 0.05). NO synthesis inhibitor, L-NAME (10 microM) and the guanylate cyclase inhibitor, methylene blue (10 microM) did partly antagonize NA-evoked contractions and were without effect on EFS-induced contractions. Thus, the antivasoconstrictor effect of pinacidil on RA is partly endothelium-dependent and probably mediated via cGMP-dependent NO-pathway.
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