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细胞外钙在钒酸盐诱导的肾血管收缩中的关键作用。

Critical role of extracellular calcium in vanadate-induced renal vasoconstriction.

作者信息

Benabe J E, Cruz-Soto M A, Martínez-Maldonado M

出版信息

Am J Physiol. 1984 Mar;246(3 Pt 2):F317-22. doi: 10.1152/ajprenal.1984.246.3.F317.

DOI:10.1152/ajprenal.1984.246.3.F317
PMID:6422775
Abstract

Intra-arterial infusion of vanadate (VO4) in dogs produces a reduction in renal blood flow (RBF), glomerular filtration rate (GFR), urine flow (V), and the fractional excretion of sodium (FENa+). To evaluate the role of Ca2+ in these changes VO4 was infused into the renal artery in the presence of the calcium antagonists trifluoperazine (TFP), verapamil, or EGTA. TFP inhibited the effect of VO4 on RBF (TFP + VO4:64.1, VO4:38.5 ml/min; P less than 0.05), GFR (TFP + VO4:22.9, VO4:9.3, ml/min; P less than 0.05) and V (TFP + VO4: 0.80, VO4: 0.38 ml/min; P less than 0.05) without changing FENa+ (TFP + VO4: 3.8, VO4: 3.2%). Similar changes were obtained with verapamil as well as with EGTA. Furthermore thyroparathyroidectomy (TPTX) decreased serum calcium (control: 8.78, TPTX: 4.98 mg/100 ml; P less than 0.05) and blunted the effects of VO4 on renal hemodynamics. Reestablishing normal serum Ca2+ by an intra-arterial infusion of CaCl2 elicited the VO4 effects of vasoconstriction and decreased GFR; V was not affected and FENa+ rose. The data support the idea that influx of extracellular calcium into smooth muscle cells mediates the hemodynamic effects of VO4 in the dog.

摘要

给犬肾动脉内输注钒酸盐(VO4)会导致肾血流量(RBF)、肾小球滤过率(GFR)、尿流量(V)和钠分数排泄率(FENa+)降低。为评估Ca2+在这些变化中的作用,在存在钙拮抗剂三氟拉嗪(TFP)、维拉帕米或乙二醇双(2-氨基乙基)醚四乙酸(EGTA)的情况下,将VO4注入肾动脉。TFP抑制VO4对RBF(TFP + VO4:64.1,VO4:38.5 ml/分钟;P<0.05)、GFR(TFP + VO4:22.9,VO4:9.3 ml/分钟;P<0.05)和V(TFP + VO4:0.80,VO4:0.38 ml/分钟;P<0.05)的影响,而不改变FENa+(TFP + VO4:3.8,VO4:3.2%)。维拉帕米和EGTA也得到了类似的变化。此外,甲状旁腺切除术(TPTX)降低了血清钙(对照:8.78,TPTX:4.98 mg/100 ml;P<0.05),并减弱了VO4对肾血流动力学的影响。通过动脉内输注氯化钙使血清Ca2+恢复正常,引发了VO4的血管收缩作用和GFR降低;V未受影响,FENa+升高。这些数据支持这样的观点,即细胞外钙流入平滑肌细胞介导了VO4对犬的血流动力学效应。

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