BMS-191011 (BMS-A) is an opener of the large-conductance, Ca2+-activated potassium (maxi-K) channel, effective in stroke models. It has also shown neuroprotective properties in two distinct animal models of stroke- MCAO in the SHR rat and a normotensive model of focal stroke.
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HazMat fee for 500 gram (Estimated)
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Potassium (K+) channels participate in many physiological processes, cardiac function, cell proliferation, neuronal signaling, muscle contractility, immune function, hormone secretion, osmotic pressure, changes in gene expression, and are involved in critical biological functions, and in a variety of diseases[1]. BMS-191011 (BMS-A) is an opener of the large-conductance, Ca2+-activated potassium (maxi-K) channel, effective in stroke models[2]. BMS-191011 (10-100 µg/kg, i.v.) and NS 1619 (0.1-1.0 µg/kg, i.v.) increased the diameter of retinal arterioles without altering systemic blood pressure and heart rate significantly. The vasodilator responses to BMS-191011 were significantly diminished by intravitreal injection of iberiotoxin (an inhibitor of BK(Ca) channels, 20 pmol/eye)[3]. A 29-day treatment with L-citrulline, significantly ameliorated the impaired acetylcholine- and BMS-191011-induced retinal vasodilation in diabetic rats without affecting their plasma glucose levels[4]. BMS 191011 caused fetal coronary artery relaxation and BKCa current activation that was unaffected by maternal nutrient restriction[5].
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