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β-肾上腺素能受体介导清醒绵羊体内活性肾素和非活性肾素的分泌。

Beta-adrenoceptor mediated secretion of active and inactive renin in conscious sheep.

作者信息

al Kattan A H, Parker J C, Noble A R

机构信息

Department of Physiology and Pharmacology, University of Southampton, UK.

出版信息

Clin Exp Pharmacol Physiol. 1990 Jun;17(6):427-37. doi: 10.1111/j.1440-1681.1990.tb01341.x.

Abstract
  1. Beta-adrenoceptor linked regulation of plasma active and inactive renin was investigated in sheep with indwelling artery, vein and bladder catheters. Concurrent changes in renal function were also monitored. 2. The beta-adrenoceptor agonist isoprenaline (bolus intravenous (i.v.) dose 0.5 mg/kg, 0.05 microgram/kg per min) increased plasma active renin concentration within 15 min and reached a plateau increase of 306%. Initially plasma inactive renin remained unchanged but after 105 min it decreased. 3. The non-selective beta-adrenoceptor antagonist propranolol (bolus i.v. dose 4 mg/kg, 40 micrograms/kg per min) did not significantly alter basal plasma active renin but selectively reduced inactive renin. The absence of any change in active renin may reflect the relatively low level of stress-induced sympathetic activation in these conscious animals compared to equivalent studies carried out on human subjects. 4. Using the same dose schedules, propranolol completely blocked the isoprenaline-induced increases in plasma active renin secretion even though it had no effect on the basal active renin levels. 5. The selective beta 1-adrenoceptor antagonist atenolol (bolus i.v. dose 5 mg/kg) decreased basal plasma active renin by 24% (+ 135 min) but reduced plasma inactive renin by 75% compared to control. 6. Therefore, both a beta-adrenoceptor agonist (isoprenaline) and two beta-adrenoceptor antagonists (propranolol and atenolol) decreased plasma inactive renin concentration in conscious sheep. 7. These results are discussed in relation to the accompanying changes in arterial blood pressure and aspects of renal function.
摘要
  1. 利用留置动脉、静脉及膀胱导管的绵羊,研究了β-肾上腺素能受体对血浆活性肾素和非活性肾素的调节作用。同时监测了肾功能的相应变化。2. β-肾上腺素能受体激动剂异丙肾上腺素(静脉推注剂量0.5mg/kg,每分钟0.05μg/kg)在15分钟内使血浆活性肾素浓度升高,并达到306%的平台期升高。最初血浆非活性肾素保持不变,但105分钟后下降。3. 非选择性β-肾上腺素能受体拮抗剂普萘洛尔(静脉推注剂量4mg/kg,每分钟40μg/kg)未显著改变基础血浆活性肾素,但选择性降低了非活性肾素。活性肾素无任何变化可能反映了与在人类受试者上进行的等效研究相比,这些清醒动物中应激诱导的交感神经激活水平相对较低。4. 使用相同的给药方案,普萘洛尔完全阻断了异丙肾上腺素诱导的血浆活性肾素分泌增加,尽管它对基础活性肾素水平没有影响。5. 选择性β1-肾上腺素能受体拮抗剂阿替洛尔(静脉推注剂量5mg/kg)使基础血浆活性肾素在135分钟时降低了24%,但与对照组相比,血浆非活性肾素降低了75%。6. 因此,β-肾上腺素能受体激动剂(异丙肾上腺素)和两种β-肾上腺素能受体拮抗剂(普萘洛尔和阿替洛尔)均降低了清醒绵羊的血浆非活性肾素浓度。7. 结合动脉血压的相应变化和肾功能方面对这些结果进行了讨论。

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