Kawata T, Mimuro T, Onuki T, Tsuchiya K, Nihei H, Koike T
Department of Internal Medicine II, School of Medicine, Hokkaido University, Sapporo, Japan.
Kidney Int Suppl. 1998 Sep;67:S231-3. doi: 10.1046/j.1523-1755.1998.06758.x.
Adenosine triphosphate-sensitive K channels (K(ATP)) may subserve vasodilation in the renal microvasculature. Using micropuncture techniques, we examined whether the renal vasomotor action of K(ATP) differs in hypertensive and normotensive animals. Nicorandil (NC), a K(ATP) opener, was given i.v. (1 mg/hr/kg) to spontaneously hypertensive rats (SHR) or Wistar Kyoto rats (WKY). Mean arterial blood pressure decreased in both groups. Renal blood flow was almost unchanged in SHR but increased significantly in WKY. This effect was completely abolished by pretreatment with glibenclamide (GC; 3 mg/kg i.v.). To investigate the effect of NC on the regulatory mechanism of renal microcirculation, we measured proximal tubular stop-flow pressure (SFP) and assessed tubuloglomerular feedback (TGF) by monitoring SFP during loop perfusion with artificial 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 modulate preglomerular vascular resistance, especially in the larger vascular segments not subject to TGF regulation, and may be attenuated in SHR. This might, at least in part, be attributable to the increased vascular resistance in SHR.
三磷酸腺苷敏感性钾通道（K(ATP)）可能参与肾微循环的血管舒张。我们采用微穿刺技术，研究了K(ATP)在高血压动物和正常血压动物中的肾血管运动作用是否存在差异。给自发性高血压大鼠（SHR）或Wistar Kyoto大鼠（WKY）静脉注射（1毫克/小时/千克）K(ATP)开放剂尼可地尔（NC）。两组的平均动脉血压均下降。SHR的肾血流量几乎未变，但WKY的肾血流量显著增加。用格列本脲（GC；3毫克/千克静脉注射）预处理可完全消除这种作用。为了研究NC对肾微循环调节机制的影响，我们测量了近端肾小管停流压力（SFP），并通过在人工肾小管液的髓袢灌注过程中监测SFP来评估管球反馈（TGF）。NC使WKY的SFP显著增加，GC预处理可消除这种作用。然而，在SHR中，NC处理未引起SFP的显著变化。两组的TGF反应均不受NC处理的影响。数据表明，K(ATP)可能调节肾小球前血管阻力，尤其是在不受TGF调节的较大血管段，并且在SHR中可能减弱。这可能至少部分归因于SHR中血管阻力的增加。
