Helou C M, Marchetti J
Laboratoire de Physiologie Cellulaire, Centre National de la Recherche Scientifique, Collège de France, Paris, France.
Am J Physiol. 1997 Jul;273(1 Pt 2):F84-96. doi: 10.1152/ajprenal.1997.273.1.F84.
The present study compares cytosolic calcium concentration ([Ca2+]i) responses to angiotensin II (ANG II) of afferent (AA) and efferent arterioles (EA) by taking account of the localization and morphological differences of EA. In outer cortex, 1 nM ANG II induced smaller [Ca2+]i increases in thin EA than in AA[48 +/- 10 (n = 12) vs. 94 +/- 7 nM (n = 11); P < 0.001]. In inner cortex, two types of EA were considered, i.e., thin and muscular ones. The response to 1 nM ANG II was 35% lower in thin than in muscular EA (P < 0.05) but did not differ from that obtained with corresponding AA. In EA of the outer cortex, 1 microM nifedipine, a dihydropyridine blocker of voltage-operated channels (VOCC), did not affect calcium influx, which was suppressed by 1 mM NiCl2, a nonselective calcium entry blocker. In other arterioles, nifedipine inhibited by approximately 40% calcium entry, and remaining influx was blocked by NiCl2. These results indicate a relationship between the magnitude of [Ca2+]i responses, activation of dihydropyridine-sensitive VOCC by ANG II, and the muscular morphology in renal glomerular arterioles. They suggest that ANG II regulates differently local renal microcirculation. They do not, however, support the hypothesis of a greater sensitivity to ANG II of EA compared with the AA of a given nephron.
本研究通过考虑出球小动脉(EA)的定位和形态差异,比较了传入小动脉(AA)和出球小动脉对血管紧张素II(ANG II)的胞质钙浓度([Ca2+]i)反应。在外皮质,1 nM ANG II引起的细EA中[Ca2+]i升高幅度小于AA[48±10(n = 12)对94±7 nM(n = 11);P < 0.001]。在内皮质,考虑了两种类型的EA,即细的和肌性的。细EA对1 nM ANG II的反应比肌性EA低35%(P < 0.05),但与相应AA的反应无差异。在外皮质的EA中,1 μM硝苯地平(一种电压门控通道(VOCC)的二氢吡啶阻滞剂)不影响钙内流,而1 mM NiCl2(一种非选择性钙内流阻滞剂)可抑制钙内流。在其他小动脉中,硝苯地平抑制约40%的钙内流,其余内流被NiCl2阻断。这些结果表明[Ca2+]i反应的幅度、ANG II对二氢吡啶敏感VOCC的激活与肾小体小动脉的肌性形态之间存在关系。它们提示ANG II对局部肾微循环的调节方式不同。然而,它们并不支持与给定肾单位的AA相比,EA对ANG II更敏感的假说。