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There has been an intense interest in multiple interacting paracrine systems that influence renal hemodynamics. The contractile responses at different sites along the renal vascular network exhibit distinct characteristics, depending on their receptor populations or activation mechanisms. These differences in effector mechanisms have also coupled with variations in paracrine signals from adjoining endothelial and epithelial cells. In this review, we have focused on the roles of nitric oxide (NO) and adenosine in the regulation of renal microvasculature and how they interact with other vasoactive factors. Vasopressin (VP) V2 receptors as well as V1 receptors exist in renal vasculature, especially in afferent arterioles, and V2-receptor stimulation induced vasodilation. V2-receptor-mediated vasodilation was attenuated by L-NNA. In addition, Ang II did not affect the diameter of isolated rabbit afferent arterioles, but after the treatment of L-NNA, Ang II exerted a dose-dependent vasoconstriction. Thus, NO modulated the renal vascular actions of VP and Ang II. Adenosine causes vasoconstriction via the A1 receptors, which are restricted primarily to the afferent arterioles. This selective action of adenosine suggests that adenosine exerts selective control of the renal vasculature. Adenosine augmented renal vasoconstriction by NE and Ang II via the adenosine A1 receptor, and the A1 receptor antagonist significantly reduced NE- or Ang II-induced renal vasoconstriction. The plurality of these interactions indicates that while it is very important to understand the specific direct cellular actions of each individual factor, it is equally important to understand how the various interactions are orchestrated under in vivo conditions.

Paracrine regulation of renal hemodynamics