Wyse B, Waters M, Sernia C
Department of Physiology and Pharmacology, University of Queensland, Brisbane, Australia.
Am J Physiol. 1993 Aug;265(2 Pt 1):E332-9. doi: 10.1152/ajpendo.1993.265.2.E332.
A genetically growth hormone (GH)-deficient strain of Lewis rats was used to test the hypothesis that the actions of GH on electrolyte and fluid homeostasis are mediated by the renin-angiotensin-aldosterone system (RAAS). Dwarf rats injected with recombinant bGH (2 mg.kg-1 x day-1) for 7 days (group GH1+) and 28 days (group GH4+), respectively, were compared with saline-injected dwarf (group GH-) and normal (group N) Lewis rats. GH decreased Na+ excretion and increased renal glomerular filtration rate in dwarf rats. The dietary intake and plasma concentrations of Na+ and K+ remained unchanged. GH increased plasma insulin-like growth factor I (IGF-I) concentrations in dwarf rats (GH - = 109 +/- 9, GH1+ = 184 +/- 5, GH4+ = 189 +/- 28, N = 477 +/- 29 ng/ml plasma). Plasma angiotensinogen increased towards the levels found in normal Lewis rats (GH- = 859 +/- 38, GH1+ = 906 +/- 18, GH4+ = 1,027 +/- 19, N = 1497 +/- 80 ng angiotensin I/ml plasma); plasma renin activity increased above that of the normal Lewis (GH- = 10.2 +/- 0.6, GH1+ = 11.7 +/- 0.7, GH4+ = 16.7 +/- 2.4, N = 10.6 +/- 0.8 ng angiotensin I.ml plasma-1 x h-1). Plasma aldosterone, corticosterone, and triodothyronine concentrations were unchanged by GH treatment. Angiotensin II receptor densities in GH- rats (liver = 356 +/- 23, kidney = 228 +/- 28, adrenal = 478 +/- 58 fmol/mg protein) were upregulated by GH (GH4+ rats; liver = 573 +/- 27, kidney = 360 +/- 86, adrenal = 721 +/- 78 fmol/mg protein).(ABSTRACT TRUNCATED AT 250 WORDS)
利用基因工程培育的生长激素（GH）缺乏型Lewis大鼠来检验如下假设：GH对电解质及液体稳态的作用是由肾素-血管紧张素-醛固酮系统（RAAS）介导的。分别给侏儒大鼠注射重组牛GH（2毫克·千克⁻¹·天⁻¹），持续7天（GH1⁺组）和28天（GH4⁺组），并与注射生理盐水的侏儒大鼠（GH⁻组）及正常Lewis大鼠（N组）进行比较。GH降低了侏儒大鼠的Na⁺排泄，增加了肾小球滤过率。饮食摄入量以及血浆中Na⁺和K⁺的浓度保持不变。GH增加了侏儒大鼠血浆中胰岛素样生长因子I（IGF-I）的浓度（GH⁻组 = 109 ± 9，GH1⁺组 = 184 ± 5，GH4⁺组 = 189 ± 28，N组 = 477 ± 29纳克/毫升血浆）。血浆血管紧张素原向正常Lewis大鼠的水平升高（GH⁻组 = 859 ± 38，GH1⁺组 = 906 ± 18，GH4⁺组 = 1027 ± 19，N组 = 1497 ± 80纳克血管紧张素I/毫升血浆）；血浆肾素活性升高至高于正常Lewis大鼠的水平（GH⁻组 = 10.2 ± 0.6，GH1⁺组 = 11.7 ± 0.7，GH4⁺组 = 16.7 ± 2.4，N组 = 10.6 ± 0.8纳克血管紧张素I·毫升血浆⁻¹·小时⁻¹）。GH处理后，血浆醛固酮、皮质酮和三碘甲状腺原氨酸的浓度未发生变化。GH上调了GH⁻大鼠的血管紧张素II受体密度（肝脏 = 356 ± 23，肾脏 = 228 ± 28，肾上腺 = 478 ± 58飞摩尔/毫克蛋白质）（GH4⁺大鼠；肝脏 = 573 ± 27，肾脏 = 360 ± 86，肾上腺 = 721 ± 78飞摩尔/毫克蛋白质）。（摘要截取自250词）
