THE K-ATP CHANNEL OPENER NICORANDIL - EFFECT ON RENAL HEMODYNAMICS INSPONTANEOUSLY HYPERTENSIVE AND WISTAR-KYOTO RATS

Adenosine triphosphate-sensitive K channels (K-ATP) may subserve vasod ilation in the renal microvasculature. Using micropuncture techniques, we examined whether the renal vasomotor action of K-ATP differs in hy pertensive and normotensive animals. Nicorandil (NC), a K-ATP opener, was given i.v. (1 mg/hr/kg) to spontaneously hypertensive rats (SHR) o r Wistar Kyoto rats (WKY). Mean arterial blood pressure decreased in b oth groups. Renal blood flow was almost unchanged in SHR but increased significantly in WKY. This effect was completely abolished by pretrea tment with glibenclamide (GC, 3 mg/kg i.v.). To investigate the effect of NC on the regulatory mechanism of renal microcirculation, we measu red proximal tubular stop-flow pressure (SFP) and assessed tubuloglome rular feedback (TGF) by monitoring SFP during loop perfusion with arti ficial tubular fluid. NC significantly increased SFP in WKY, an effect abolished by pretreatment with GC. In SHR, however, treatment with NC elicited no significant change in SFP. TGF response was not affected by NC treatment in either group. The data suggest that K-ATP may modul ate preglomerular vascular resistance, especially in the larger vascul ar segments not subject to TGF regulation, and may be attenuated in SH R. This might, at least in part, be attributable to the increased vasc ular resistance in SHR.