Thomas J. Heppner

TL;DR: Results support the concept that Ca2+ influx through single TRPV4 channels is leveraged by the amplifier effect of cooperative channel gating and the high Ca2- sensitivity of IK and SK channels to cause vasodilation.

TL;DR: It is concluded that TRPV4 forms a novel Ca2+ signaling complex with ryanodine receptors and BKCa channels that elicits smooth muscle hyperpolarization and arterial dilation via Ca2-induced Ca1+ release in response to an endothelial-derived factor.

TL;DR: Using functional evidence from cardiac myocytes, and histological evidence from smooth muscle, it is explored whether Ca2+ channels, RyR channels, and KCa channels function as a coupled unit, through Ca2- and voltage, to regulate arterial smooth muscle membrane potential and vascular tone.

TL;DR: Changes in intracellular Ca(2+) are central to the function of smooth muscle, which lines the walls of all hollow organs, and these changes take a variety of forms, from sustained, cell-wide increases to temporally varying, localized changes.

TL;DR: A new mechanism for cyclic nucleotide-mediated dilations through an increase in Ca2+ spark frequency is suggested, caused by effects on SRCa2+ load and possibly on the RyR channel, which leads to increased STOC frequency, membrane potential hyperpolarization, closure of voltage-dependent Ca2-dependent channels, decrease in arterial wall Ca2+, and, ultimately, vasodilation.