EPITHELIAL ABNORMALITIES IN INTESTINE AND KIDNEY OF THE SPONTANEOUSLY HYPERTENSIVE RAT

被引：4

作者：

DRUEKE, TB

HENNESSEN, U

LUCAS, PA

NABARRA, B

BENNASR, L

THOMASSET, M

LACOUR, B

COUDRIER, E

MCCARRON, DA

机构：

[1] INSERM Unite 90, Department de Néphrologie, Portland

[2] Unite 25, Portland

[3] Hôpital Necker, Unite de Biologie des Membranes, Department de Biologie Moléculaire, In-stitut Pasteur, Paris

[4] INSERM Unite 120, Le Vésinet

[5] The Division of Nephrology and Hypertension, Oregon Health Sciences University, Portland

来源：

AMERICAN JOURNAL OF HYPERTENSION | 1990年 / 3卷 / 08期

关键词：

Calcitriol; Calcium metab olism; Epithelium; Intestine; Kidney; Spontaneously hypertensive rat;

D O I：

10.1093/ajh/3.8.195

中图分类号：

R6 [外科学];

学科分类号：

1002 ; 100210 ;

摘要：

A variety of perturbations of calcium metabolism are reported to occur in the spontaneously hypertensive rat (SHR) compared to its genetic control the Wistar-Kyoto rat (WKY), including significant dysfunction of calcium handling by the proximal renal tubule of the SHR, resulting in impaired active calcium transport in the gut and an apparent renal calcium leak. We explored the intestinal and renal epithelia of 12- to 14-week-old SHR and WKY using electron microscopy. Biochemical comparisons of these transport epithelia included measurements of three vitamin D dependent cellular proteins and one structural protein: alkaline phosphatase, intestinal CaBP9K, renal CaBP28K, and villin expression. Electron microscopy demonstrated a patchy loss in microvilli in the SHR, accounting for approximately 10 to 15% of the total microvillar surface. In the kidney, morphological abnormalities were observed only in the proximal renal tubule. Again, there was patchy loss of microvilli from the brush border membrane. In SHR duodenal alkaline phosphatase activity was significantly reduced compared to the WKY (0.145 ± 0.002 v 0.186 ± 0.002 integrated extinction/min/μm3× 103brush border (P <. 001). Duodenal CaBP9Kand renal CaBP28Kwere significantly reduced in SHR compared to WKY. There were no differences in villin expression. These data are consistent with the previously characterized disturbances of active calcium transport in the intestine and inappropriate renal calcium leak in the SHR. While a possible link between these disturbances and hypertension remains to be determined, this study provides supportive evidence for a primary disturbance in cell calcium handling and transporting epithelia in this form of genetic hypertension. © 1990 by the American Journal of Hypertension, Ltd.

引用

页码：S195 / S201

页数：7

共 32 条

[1]

Postnov Y.V., Orlov S.N., Ion transport across plasma membrane in primary hypertension, Physiol Rev, 7, pp. 904-907, (1985)

[2]

Young E., Bukoski R.D., McCarron D.A., Calcium metabolism in experimental hypertension, Proc Soc Exp Biol Med, 187, pp. 123-141, (1988)

[3]

Lau K., Langman C.B., Gafter U., Dudeja P.K., Brasitus T.A., Increased calcium absorption in prehypertensive spontaneously hypertensive rat: Role of serum 1, 25-dihydroxyvitamin D3 levels and intestinal brush border membrane fluidity, J Clin Invest, 78, pp. 1083-1090, (1986)

[4]

McCarron D.A., Lucas P.A., Shneidman R.J., Lacour B., Drueke T., Blood pressure development of the spontaneously hypertensive rat following concurrent manipulations of dietary Ca2 + and Na+: Relation to intestinal Ca2 + fluxes, J Clin Invest, 76, pp. 1147-1154, (1986)

[5]

Schedl H.P., Miller D.L., Horst R.D., Wilson H.D., Natarajan K., Conway T., Intestinal calcium transport in the spontaneously hypertensive rat: Response to calcium depletion, Am J Physiol, 250, pp. G412-G419, (1985)

[6]

Schedl H.P., Miller D.L., Pape J.M., Horst R.L., Wilson J.D., Calcium and sodium transport and vitamin D metabolism in the spontaneously hypertensive rat, J Clin Invest, 73, pp. 980-986, (1984)

[7]

Lucas P.A., Brown R.C., Drueke T., Lacour B., Metz J.A., McCarron D.A., Abnormal vitamin D metabolism, intestinal calcium absorption, and bone calcium status in the spontaneously hypertensive rat compared with its genetic control, J Clin Invest, 78, pp. 221-227, (1986)

[8]

Kurtz T.W., Portale A.A., Morris R.C., Evidence for a difference in vitamin D metabolism between spontaneously hypertensive and Wistar-Kyoto rats, Hypertension, 8, pp. 1015-1020, (1986)

[9]

McCarron D.A., Yung N.N., Ugoretz B.A., Krutzik S., Disturbances of calcium metabolism in the spontaneously hypertensive rat, Hypertension, 3, pp. I162-I167, (1987)

[10]

Merke J., Slotkowski A., Mann H., Lucas P.A., Drueke E., Ritz E., Abnormal l, 25(OH)2D3 receptors status in genetically hypertensive rats (abstract), Kidney Int, 31, (1987)

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