Ozawa Yuri, Hayashi Koichi, Nagahama Takahiko, Fujiwara Keiji, Kanda Takeshi, Homma Koichiro, Saruta Takao
Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Nephron. 2002 Dec;92(4):905-13. doi: 10.1159/000065460.
Both nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF) are established as important factors determining the vascular tone. The relative contribution of these factors to the renal microvascular tone, however, has not been delineated.
Isolated perfused hydronephrotic rat kidneys were used to characterize the relative role of NO and EDHF in mediating the tone of interlobular arteries (ILA) and afferent arterioles (AFF).
During the norepinephrine constriction, acetylcholine (ACH, 1 micromol/l) induced a sustained vasodilation of ILA (90 +/- 9% reversal) and AFF (117 +/- 13% reversal). In the presence of nitro-L-arginine methylester (LNAME), the ACH-induced vasodilation of ILA and AFF was converted to transient dilation, with only 53 +/- 7 and 32 +/- 7% reversal observed 10 min after 1 micromol/l ACH (i.e sustained phase). In contrast, LNAME had no effect on the initial phase of ACH-induced dilation. In the presence of apamin + charybdotoxin, the initial vasodilator response to ACH (1 micromol/l) was diminished (ILA, from 108 +/- 8 to 46 +/- 9%; AFF, from 108 +/- 14 to 58 +/- 8%), whereas no impairment was observed in sustained phases. Furthermore, the magnitude of the vasoconstriction caused by LNAME was greater at smaller vessel segments. Finally, the LNAME-induced inhibition of the sustained phase of ACH-induced vasodilation was greater as the vessel diameter decreased.
That the relative contribution of NO and EDHF differs, with a greater role of NO in the basal tone and ACH-induced vasodilation at smaller vascular segments of ILA and AFF.
一氧化氮(NO)和内皮衍生超极化因子(EDHF)均被确认为决定血管张力的重要因素。然而,这些因素对肾微血管张力的相对贡献尚未明确。
采用离体灌注的肾积水大鼠肾脏,以表征NO和EDHF在介导小叶间动脉(ILA)和入球小动脉(AFF)张力方面的相对作用。
在去甲肾上腺素收缩期间,乙酰胆碱(ACH,1微摩尔/升)可诱导ILA(90±9%逆转)和AFF(117±13%逆转)持续血管舒张。在存在硝基-L-精氨酸甲酯(LNAME)的情况下,ACH诱导的ILA和AFF血管舒张转变为短暂舒张,在1微摩尔/升ACH作用10分钟后(即持续阶段),仅观察到53±7%和32±7%的逆转。相比之下,LNAME对ACH诱导舒张的初始阶段无影响。在存在蜂毒明肽+蝎毒素的情况下,对ACH(1微摩尔/升)的初始血管舒张反应减弱(ILA,从108±8%降至46±9%;AFF,从108±14%降至58±8%),而在持续阶段未观察到损害。此外,LNAME引起的血管收缩幅度在较小血管段更大。最后,随着血管直径减小,LNAME对ACH诱导血管舒张持续阶段的抑制作用更大。
NO和EDHF的相对贡献不同,在ILA和AFF较小血管段的基础张力和ACH诱导的血管舒张中,NO发挥更大作用。