Ca fluxes across duodenum and colon of spontaneously hypertensive rats: effect of 1,25(OH)2D3.
Ca fluxes across duodenum and colon of spontaneously hypertensive rats: effect of 1,25(OH)2D3.
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Ca 流过自发性高血压大鼠的十二指肠和结肠：1,25(OH)2D3 的影响。
DOI：
10.1152/ajprenal.1986.251.2.f278
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Lau,K
中科院分区：
文献类型：
--
作者：
Gafter,U;Kathpalia,S;Zikos,D;Lau,K
据报道，自发性高血压大鼠 (SHR) 的钙吸收与血压正常的 Wistar-Kyoto (WKY) 对照组不同。此外，还假设对 1,25-二羟基维生素 D3 [1,25(OH)2D3] 的肠道作用的反应减弱。为了评估这一假设，通过使用 Ussing 技术测量十二指肠和降结肠的钙通量，无论是否经过 1,25(OH)2D3 治疗。十二指肠粘膜-浆膜钙通量 (Jm----s)（44.9 vs. 52.4 nmol X cm-2 X h-1）、浆膜-粘膜钙通量 (Js----m)（25.6 vs. 28.4 nmol X cm-2 X h-1）和净通量 (Jnet) 相当。 1,25(OH)2D3 增加了 SHR 和 WKY 组的十二指肠 Jm----s（95.2 和 86.8 nmol X cm-2 X h-1）。 SHR 中的 Js----m 较低（26.1 对比 35.6 nmole X cm-2 X h-1，P 小于 0.01），尽管 SHR 中 Jnet 较高的趋势（68.6 对比 51.2 nmole X cm-2 X h-1）在统计上不显着。在 1,25(OH)2D3 之前和之后，SHR 结肠中的短路电流均较高，表明钠转运增加。两组的基底结肠 Jnet 实际上为零，但由于仅对 Jm----s 进行刺激，因此 1,25(OH)2D3 相对增加。与高血压 SHR 相比，从第 4 周开始使用肼屈嗪预防高血压并没有改变研究结果，这表明钙转运率不受高血压的影响。这些数据表明 SHR 的体外、十二指肠和结肠活性钙转运与 WKY 相似。他们对 1,25(OH)2D3 的正常反应并不支持肠道抵抗的假设。
Calcium absorption by spontaneously hypertensive rats (SHR) was variably reported to be different from normotensive Wistar-Kyoto (WKY) controls. Furthermore, blunted responsiveness to the intestinal effects of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] has also been postulated. To evaluate this hypothesis, calcium fluxes were measured by the Ussing technique across duodenum and descending colon with or without prior 1,25(OH)2D3 treatment. Duodenal mucosal-to-serosal calcium flux (Jm----s) (44.9 vs. 52.4 nmol X cm-2 X h-1), serosal-to-mucosal flux (Js----m) (25.6 vs. 28.4 nmol X cm-2 X h-1), and net flux (Jnet) were comparable. 1,25(OH)2D3 increased duodenal Jm----s in both SHR and WKY groups (95.2 and 86.8 nmol X cm-2 X h-1). Js----m was lower in SHR (26.1 vs. 35.6 nmol X cm-2 X h-1, P less than 0.01), although the tendency for a higher Jnet in SHR (68.6 vs. 51.2 nmoles X cm-2 X h-1) was statistically insignificant. Short-circuit current was higher in the colon of SHR, both before and after 1,25(OH)2D3, suggesting increased sodium transport. Basal colonic Jnet was virtually zero in both groups but comparably increased by 1,25(OH)2D3 because of stimulation in only Jm----s. Prevention of hypertension by hydralazine since the 4th wk of age did not alter the findings compared with the hypertensive SHR, suggesting calcium transport rates were unaffected by hypertension. These data indicate that in vitro, duodenal, and colonic active calcium transport by the SHR is similar to WKY. Their normal responses to 1,25(OH)2D3 do not support the hypothesis of intestinal resistance.