Abstract

Afferent arterioles (AA) are highly responsive to purinoceptor stimulation. ATP contributes importantly to renal autoregulation by activating P2 receptors. Pressure‐mediated, and ATP and β,γ‐methylene ATP (P2X1 receptor agonist)‐induced AA vasoconstriction is impaired in DOCA‐salt hypertensive rats (DOCA rats) while the function of other purinoceptors is unclear. We postulated that P2Y and A1 receptor reactivity is intact in AA from DOCA rats. AA responses to UTP (a P2Y2 receptor agonist) and adenosine were studied in juxtamedullary nephrons. Systolic blood pressure averaged 125±5 and 180±7 mmHg in uninephrectomized (UNx) and DOCA rats, respectively. UTP (10−8 to 10−4 mol/L, n=5) evoked concentration‐dependent vasoconstriction of AA in UNx rats. Diameter declined by 2±1, 6±2, 12±2, 23±5 and 49±9%, respectively. UTP‐induced vasoconstriction was unchanged in DOCA rats (n=5, p>0.05) leading to declines of 3±2, 10±2, 14±3, 29±5 and 43±9%, respectively. The AA response to adenosine was also indistinguishable between two groups (n=6 each, p>0.05). Preglomerular microvascular P2X1 receptor protein expression was unaltered in DOCA rats. These data demonstrate that AA P2Y2 and A1 receptor signaling is preserved in DOCA rats. This study suggests that impairment of AA autoregulatory behavior in DOCA‐salt hypertension cannot be attributed to impaired P2Y2 and A1 receptor signaling.

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