Aminophylline inhibits renal vasoconstriction produced by intrarenal hypertonic saline

Abstract

An intrarenal infusion of hypertonic saline to sodium-depleted dogs causes an acute reduction in renal blood flow (RBF) which has been postulated to be due to tubuloglomerular feedback (TGF). Adenosine has been suggested as a mediator of TGF, as adenosine receptor blockade with methylxanthines inhibits TGF. In order to test further the hypothesis that the renal response to hypertonic saline is mediated by TGF, the RBF response to intrarenal hypertonic saline infusions have been investigated in sodium-depleted dogs before and after either an infusion of vehicle or an intrarenal infusion of aminophylline. Aminophylline (2.5 mg/min), at a dose which did not change basal RBF or responses to bolus doses of angiotensin II, inhibited the responses to intrarenal bolus doses of adenosine. In control dogs (n = 5), a 10-min intrarenal infusion of hypertonic saline significantly (P less than .05) reduced RBF both before (-27 +/- 4%) and during (-16 +/- 9%) an infusion with aminophylline vehicle. In a second group of animals (n = 5), an intrarenal hypertonic saline infusion reduced RBF before (-33 +/- 8%; P less than .05), but not during an intrarenal aminophylline infusion (2.5 mg/min). We conclude that aminophylline inhibits the renal vascular response to hypertonic saline and that the renal response to hypertonic saline might be mediated by intrarenal adenosine release.