Over the past decade, second messenger communication has emerged as one of the intriguing topics in the field of vasomotor control. Of particular interest has been the idea of second messenger flux from smooth muscle to endothelium initiating a feedback response that attenuates constriction. Mechanistic details of the precise signaling cascade have until recently remained elusive. In this perspective, we introduce readers to how myoendothelial gap junctions could enable sufficient inositol trisphosphate flux to initiate endothelial Ca(2+) events that activate Ca(2+) sensitive K(+) channels. The resulting hyperpolarizing current would in turn spread back through the same myoendothelial gap junctions to moderate smooth muscle depolarization and constriction. In discussing this defined feedback mechanism, this brief manuscript will stress the importance of microdomains and of discrete cellular signaling.
Keywords: calcium wavelets; constriction; gap junctions; inositol trisphosphate; potassium channels.