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α1b - 肾上腺素能受体介导大鼠肾小管钠和水的重吸收。

Alpha 1b-adrenoceptors mediate renal tubular sodium and water reabsorption in the rat.

作者信息

Elhawary A M, Pang C C

机构信息

Department of Pharmacology & Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, Canada.

出版信息

Br J Pharmacol. 1994 Mar;111(3):819-24. doi: 10.1111/j.1476-5381.1994.tb14811.x.

Abstract
  1. It is known that activation of alpha 1-adrenoceptors causes renal vasoconstriction and increased tubular Na+ and water reabsorption, with the alpha 1a-subtype mediating the constrictor effect. 2. This study examines which subtype of alpha 1-adrenoceptors mediates tubular Na+ and water reabsorption in pentobarbitone-anaesthetized rats. In order to avoid systemic effects, phenylephrine (0.3 to 30 micrograms kg-1), methoxamine (0.1-10 micrograms kg-1) and vehicle were infused into the right renal artery (via the suprarenal artery) of three groups of rats. Two other groups of rats were continuously infused with the irreversible selective alpha 1b-adrenoceptor antagonist, chloroethylclonidine (3 mg kg-1 h-1) for 1 h, prior to the construction of dose-response curves to phenylephrine or methoxamine. Another group was continuously infused with the irreversible selective alpha 1a-adrenoceptor antagonist, SZL-49 (10 micrograms kg-1 h-1) for 1 h, prior to the construction of dose-response curves to phenylephrine. Mean arterial pressure (MAP), heart rate (HR), urine flow, Na+ and K+ excretion, and urine osmolality were monitored. 3. Phenylephrine and methoxamine did not affect MAP or HR but dose-dependently and significantly decreased urine flow, urine osmolality as well as Na+ excretion and, slightly increased K+ excretion, although this was significant only for phenylephrine. 4. The antidiuretic, antinatriuretic and kaliuretic effects of phenylephrine were abolished by pretreatment with chloroethylclonidine, but were not inhibited by SZL-49. The inhibitory effects of methoxamine on urine flow and Na+ excretion were also almost totally abolished by chloroethylclonidine. 5. Our results show that alpha 1b-adrenoceptors mediate renal tubular Na+ and water reabsorption.
摘要
  1. 已知α1 -肾上腺素能受体的激活会导致肾血管收缩以及肾小管钠和水重吸收增加,其中α1a亚型介导收缩效应。2. 本研究考察在戊巴比妥麻醉的大鼠中,哪种α1 -肾上腺素能受体亚型介导肾小管钠和水重吸收。为避免全身效应,将去氧肾上腺素(0.3至30微克/千克)、甲氧明(0.1 - 10微克/千克)及赋形剂注入三组大鼠的右肾动脉(经肾上腺动脉)。另外两组大鼠在构建去氧肾上腺素或甲氧明的剂量反应曲线前1小时,持续输注不可逆的选择性α1b -肾上腺素能受体拮抗剂氯乙可乐定(3毫克/千克·小时)。另一组在构建去氧肾上腺素剂量反应曲线前1小时,持续输注不可逆的选择性α1a -肾上腺素能受体拮抗剂SZL - 49(10微克/千克·小时)。监测平均动脉压(MAP)、心率(HR)、尿流量、钠和钾排泄以及尿渗透压。3. 去氧肾上腺素和甲氧明不影响MAP或HR,但剂量依赖性且显著降低尿流量、尿渗透压以及钠排泄,并轻微增加钾排泄,不过仅去氧肾上腺素的这种作用具有显著性。4. 氯乙可乐定预处理可消除去氧肾上腺素的抗利尿、利钠和利尿钾作用,但SZL - 49未抑制这些作用。氯乙可乐定也几乎完全消除了甲氧明对尿流量和钠排泄的抑制作用。5. 我们的结果表明,α1b -肾上腺素能受体介导肾小管钠和水重吸收。

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