BRANCHING POINTS OF RENAL RESISTANCE ARTERIES ARE ENRICHED IN L-TYPE CALCIUM CHANNELS AND INITIATE VASOCONSTRICTION

The morphologic structures responsible for the drop in blood pressure along the preglomerular vasculature are not completely defined. Theoretical and videomicroscopic analyses of nonrenal vascular beds implicate bifurcations of resistance arteries as important sites of hemodynamic regulation. These structures contain pacemaker cells sensitive to calcium channel blockers and appear to initiate vasomotion. In the present study, we examined the possibility of functional diversity of smooth muscle cells along resistance arteries with regard to the density of voltage-gated L-type calcium channels. Staining of microdissected renal resistance arteries with Bodipy-labeled dihydropyridine and analysis by confocal microscopy showed enhanced binding at branching points compared with the distal sites in daughter vessels. Antibodies directed against the alpha(1)-subunit of the dihydropyridine-sensitive calcium channels confirmed the enhanced expression of L-type channels predominantly at the sites of bifurcations of renal resistance arteries. Fluorescence digital-image analysis of freshly microdissected branches of cortical radial (interlobular) and arcuate arteries intravitally labeled with a calcium indicator, flue 3, identified branching points as initiator sites of depolarization-induced intracellular Ca2+ concentration ([Ca2+](i)) transients, which propagated along the vascular wall at the rate of 2.0 +/- 0.7 mu m/s. Videomicroscopy of blood-perfused rat juxtamedullary resistance arteries showed that branching points exhibit more pronounced contractile responses to KCl-induced depolarization than distal sites along the daughter vessels. Collectively, these results demonstrate that branching points are enriched in L-type calcium channels, a finding that suggests these structures may serve as important regulators of renal hemodynamics.