Vascular contraction is modulated, in part, by the cytoplasmic Ca2+ concentration in smooth muscle cells (SMCs). Ca2+ influx through voltage gated Ca2+ channels (VGCC) is governed by membrane potential. In turn, membrane potential is determined by the relative conductance of the membrane to various ions. Increase in Cl- conductance depolarizes SMCs to activate VGCC. K+ channel activation or inhibition can favor hyperpolarization or depolarization, respectively, to modulate VGCC activity. The importance of the kidney in the determination of extracellular volume and blood pressure has motivated study of renal SMC channel architecture. VGCC mediated Ca2+ entry has been consistently found in the preglomerular microcirculation. In contrast, the route of Ca2+ entry in the postglomerular microcirculation varies with cortical location. Juxtamedullary efferent arterioles and descending vasa recta express VGCC while superficial efferent arterioles may not. The subtypes of K+ channel that govern membrane potential also varies along the renal microvascular circuit. Exploration of rodent models have tended to confirm an increase in VGCC activity in hypertension. Alterations in K+ channels and gap junction - connexin proteins also occur but are subtype specific. This review summarizes current knowledge of renal SMC channel architecture and its alteration in hypertension.