de Gooyer T E, Farrugia W, Wlodek M E
Department of Physiology, The University of Melbourne, Parkville, Australia.
J Hypertens. 1999 Jun;17(6):777-84. doi: 10.1097/00004872-199917060-00009.
The present study aimed to determine whether there were alterations in intestinal calcium homeostasis in the spontaneously hypertensive rats (SHR) and to identify at which interface of the intestinal epithelial cell (brush border or basolateral) this occurs.
Controversy exists as to whether intestinal calcium transport is altered in association with hypertension. Studies using perfused duodenal segments of the SHR have shed little light on the problem; other studies have only measured calcium transport in brush border membrane vesicles. This study allows specific focus on calcium transport mechanisms at both the brush border and basolateral membrane using simultaneously prepared membrane vesicles.
Calcium transport was studied by measuring radiolabelled calcium (45Ca) uptake in isolated brush border and basolateral membrane vesicles, prepared from the small intestines of SHR and Wistar-Kyoto (WKY) rats. Calcium uptake was measured when vesicles were incubated in solutions containing different concentrations of ATP and calcium. Orientation and membrane marker assays were used to confirm the phenotypes of the two membrane vesicle preparations.
ATP-dependent calcium efflux was only observed in the basolateral membrane, which contains the Ca2+ -ATPase pump. SHR brush border membrane vesicles displayed no significant increase in calcium incorporation, whereas WKY brush border vesicles showed a 500% increase in uptake (ANOVA, P<0.05, n = 7).
This study indicates that deficiencies exist in SHR intestinal calcium transport at the brush border membrane of intestinal epithelial cells. While further studies are required to ascertain the exact mechanisms involved, postulated deficiencies in the actions of calcium regulating hormones at this membrane suggest the need for concurrent intake of a calcitrophic agent to assist calcium uptake at the brush border membrane.
本研究旨在确定自发性高血压大鼠（SHR）肠道钙稳态是否存在改变，并确定这种改变发生在肠上皮细胞的哪个界面（刷状缘或基底外侧）。
关于高血压是否伴有肠道钙转运改变存在争议。使用SHR灌注十二指肠段的研究对该问题的阐明很少；其他研究仅测量了刷状缘膜囊泡中的钙转运。本研究通过同时制备的膜囊泡，能够特别关注刷状缘和基底外侧膜的钙转运机制。
通过测量从SHR和Wistar-Kyoto（WKY）大鼠小肠分离的刷状缘和基底外侧膜囊泡中放射性标记钙（45Ca）的摄取来研究钙转运。当囊泡在含有不同浓度ATP和钙的溶液中孵育时，测量钙摄取。使用取向和膜标记测定法来确认两种膜囊泡制剂的表型。
仅在含有Ca2 + -ATP酶泵的基底外侧膜中观察到ATP依赖性钙外流。SHR刷状缘膜囊泡的钙掺入没有显著增加，而WKY刷状缘囊泡的摄取增加了500％（方差分析，P<0.05，n = 7）。
本研究表明，SHR肠上皮细胞刷状缘膜的肠道钙转运存在缺陷。虽然需要进一步研究以确定确切的机制，但推测该膜上钙调节激素作用的缺陷表明需要同时摄入促钙营养剂以协助刷状缘膜的钙摄取。
