T. Kawata et al., THE K-ATP CHANNEL OPENER NICORANDIL - EFFECT ON RENAL HEMODYNAMICS INSPONTANEOUSLY HYPERTENSIVE AND WISTAR-KYOTO RATS, Kidney international, 54, 1998, pp. 231-233
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.