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甲状腺功能减退影响大鼠结肠中对阿米洛利敏感的电生性钠转运的表达。

Hypothyroidism affects the expression of electrogenic amiloride-sensitive sodium transport in rat colon.

作者信息

Pácha J, Pohlová I, Zemanová Z

机构信息

Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.

出版信息

Gastroenterology. 1996 Dec;111(6):1551-7. doi: 10.1016/s0016-5085(96)70017-3.

Abstract

BACKGROUND & AIMS: Both hyperthyroidism and hypothyroidism as well as hyperaldosteronism have been associated with changes of epithelial transport. The aim of this study was to evaluate the role of thyroid hormones in the regulation of electrogenic amiloride-sensitive sodium transport by aldosterone in the distal colon of immature and adult rats.

METHODS

The changes in amiloride-sensitive short-circuit current (Isc) and Na+, K(+)-adenosine triphosphatase (ATPase) activity were measured in suckling, weanling, and adult euthyroid and methimazole-induced hypothyroid rats.

RESULTS

The developmental increase of thyroid hormones in control pups was associated with an increase in plasma aldosterone concentration and amiloride-sensitive Isc. The inhibition of the developmental increase of thyroxine and triiodothyronine in hypothyroid pups was followed by suppression of amiloride-sensitive Isc while aldosterone concentrations remained elevated. Moreover, the induction of amiloride-sensitive Isc by secondary hyperaldosteronism was inhibited in hypothyroid adult rats, and the effect of thyroid hormones on amiloride-sensitive Isc could not be explained by changes in the plasma aldosterone concentration. Hypothyroidism also led to a decrease of colonic Na+, K(+)-ATPase activity. Replacement therapy of hypothyroid pups with triiodothyronine restored amiloride-sensitive Isc and increased Na+, K(+)-ATPase activity.

CONCLUSIONS

Thyroid hormones have a permissive role in the regulation of electrogenic amiloride-sensitive Na+ transport by aldosterone.

摘要

背景与目的

甲状腺功能亢进和减退以及醛固酮增多症均与上皮转运变化有关。本研究旨在评估甲状腺激素在未成熟和成年大鼠远端结肠中对醛固酮介导的电生性氨氯地平敏感钠转运调节中的作用。

方法

测量了哺乳、断奶和成年正常甲状腺及甲巯咪唑诱导的甲状腺功能减退大鼠中氨氯地平敏感短路电流(Isc)和钠钾ATP酶(ATPase)活性的变化。

结果

对照组幼崽甲状腺激素的发育性增加与血浆醛固酮浓度和氨氯地平敏感Isc的增加相关。甲状腺功能减退幼崽中甲状腺素和三碘甲状腺原氨酸发育性增加的抑制,随后是氨氯地平敏感Isc的抑制,而醛固酮浓度仍保持升高。此外,甲状腺功能减退的成年大鼠中继发性醛固酮增多症诱导的氨氯地平敏感Isc受到抑制,且甲状腺激素对氨氯地平敏感Isc的影响不能用血浆醛固酮浓度的变化来解释。甲状腺功能减退还导致结肠钠钾ATP酶活性降低。用三碘甲状腺原氨酸替代治疗甲状腺功能减退幼崽可恢复氨氯地平敏感Isc并增加钠钾ATP酶活性。

结论

甲状腺激素在醛固酮对电生性氨氯地平敏感钠转运的调节中起允许作用。

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