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α2受体介导美洲鳗鲡空肠中儿茶酚胺刺激的酸分泌。

Alpha 2-receptors mediate catecholamine-stimulated acid secretion in Amphiuma jejunum.

作者信息

Hinton C F, White J F

机构信息

Department of Physiology, Emory University, Atlanta, Georgia 30322.

出版信息

Am J Physiol. 1988 Nov;255(5 Pt 1):G640-6. doi: 10.1152/ajpgi.1988.255.5.G640.

Abstract

The receptors mediating adrenergic stimulation of acid secretion by Amphiuma jejunum were characterized in this study using alpha- and beta-adrenergic agonists and antagonists. Isolated segments of jejunum were mounted in Ussing chambers and bathed in Cl- -free (SO4(2-] medium. Shortcircuit current (Isc) and acid secretion (JH) were recorded, the latter by measuring the rate of alkalinization of the serosal medium. The beta-adrenergic receptor antagonist, propranolol (10(-4) M), had no effect on the Isc and JH stimulated by norepinephrine (NE). The alpha 2-adrenergic agonists, clonidine and UK-14,304, mimicked the effect of NE, with effective concentrations providing 50% maximal delta Isc of 2.0 X 10(-7) and 9.0 X 10(-8) M, respectively. NE added subsequently produced no greater stimulation. In contrast, the alpha 1-adrenergic agonists, phenylephrine and methoxamine, produced little stimulation of JH and Isc; NE added subsequently stimulated the Isc. The alpha 1-adrenergic antagonist prazosin had no effect on the NE-induced Isc or JH, whereas the alpha 2-adrenergic antagonist yohimbine inhibited the NE-stimulated Isc with a half-maximal effective concentration of 3.5 X 10(-7) M. Yohimbine (10(-4) M) reduced the NE-stimulated Isc by 88%, whereas the spontaneous Isc was reduced by only 12%. These results demonstrate that alpha 2-adrenergic receptors on the basolateral membrane of Amphiuma enterocytes mediate NE-enhanced, but not spontaneous, intestinal acid secretion.

摘要

本研究使用α-和β-肾上腺素能激动剂及拮抗剂,对美西螈空肠肾上腺素能刺激酸分泌的受体进行了表征。将分离的空肠段安装在尤斯灌流小室中,置于无氯(SO4(2-))培养基中。记录短路电流(Isc)和酸分泌(JH),后者通过测量浆膜培养基的碱化速率来测定。β-肾上腺素能受体拮抗剂普萘洛尔(10(-4) M)对去甲肾上腺素(NE)刺激的Isc和JH无影响。α2-肾上腺素能激动剂可乐定和UK-14,304模拟了NE的作用,有效浓度分别为2.0×10(-7) M和9.0×10(-8) M时可提供50%的最大δIsc。随后添加的NE未产生更大的刺激作用。相比之下,α1-肾上腺素能激动剂去氧肾上腺素和甲氧明对JH和Isc的刺激作用较小;随后添加的NE刺激了Isc。α1-肾上腺素能拮抗剂哌唑嗪对NE诱导的Isc或JH无影响,而α2-肾上腺素能拮抗剂育亨宾抑制NE刺激的Isc,半数有效浓度为3.5×10(-7) M。育亨宾(10(-4) M)使NE刺激的Isc降低了88%,而自发Isc仅降低了12%。这些结果表明,美西螈肠上皮细胞基底外侧膜上的α2-肾上腺素能受体介导NE增强的而非自发的肠酸分泌。

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