Abstract
The putative roles of α-1 and α-2 adrenoceptors in renal tubular sodium transport led us to compare the effects of intrarenal infusions in adult dogs of phentolamine (Ph), an α-1, α-2 adrenergic antagonist (n=6), prazosin (Pr) an α-1 antagonist (n=6), and yohimbine (Y), an α-2 antagonist (n=6) on renal hemodynamics and sodium excretion. Mean arterial blood pressure, renal blood flow and glomerular filtration rate did not change during the infusions. Sodium excretions (UNaV-uEq/min/g kidney) were M±SEM:The changes in fractional sodium excretion paralleled UNaV. Lineweaver-Burk plots indicated that maximum percent responses (Emax) were 242% Ph, 279% Pr and 128% Y respectively. The M concentrations producing an effect equal to Emax/2 were 1.4×10-8 for Ph, 1.8×10-8 for Pr, and 1.4×10-7 for Y. The y-intercept(1/Emax) for Pr was different from Y indicating actions on different adrenoceptors. This is supported by the fact that the addition of Pr (2×10-7M) to Y (5×10-6M) significantly increased UNaV from 0.87 ±0.11 to 1.35±0.23 mEq/min/g kidney(n=3). Thus both α-1 and α-2 adrenoceptors mediate renal tubular sodium transport in the dog.
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