Purinoceptor-mediated regulation of the renal microvasculature

1. Recent evidence supports the contention that numerous paracrine factors are released into the intrarenal interstitial environment where they can influence renal microvascular and tubular function. Studies have shown that P1 and P2 purinoceptor activation by adenosine and ATP, respectively, can selectively evoke alterations in renal microvascular diameter. 2. Vasoconstrictor responses to extracellular ATP, which are almost exclusively preglomerular, are biphasic, develop rapidly and are rapidly reversible. ATP-mediated afferent arteriolar vasoconstriction is largely dependent on the influx of extracellular calcium and the sustained vasoconstriction is maintained by calcium influx through voltage-dependent L-type calcium channels. 3. Microvascular responses to adenosine include vasoconstriction at low concentrations and vasodilation at higher concentrations. Adenosine elicits a vasoconstrictor response which develops more slowly than responses to ATP and the vasoconstriction is elicited from both the preglomerular and postglomerular arterioles. 4. Studies were performed to evaluate the possible involvement of P2 purinoceptor activation in the renal vascular autoregulatory response. Inactivation of P2 receptor-dependent preglomerular microvascular responses by purinoceptor desensitization or purinoceptor saturation completely abolished autoregulatory adjustments in afferent arteriolar calibre. 5. These studies demonstrate that the renal microvasculature is responsive to purinoceptor activation. Furthermore, the data support an important role for the involvement of intrarenal P2 receptors in the regulation of renal haemodynamics.