Bertuzzi M L, Bensi N, Mayer N, Niebylski A, Armario A, Gauna H F
Departamento de Biología Celular, Orientación Fisiología Animal, Universidad Nacional de Río Cuarto, Córdoba, Argentina.
Arch Physiol Biochem. 2003 Jul;111(3):259-64. doi: 10.1076/apab.111.3.259.23453.
The present study was conducted to investigate if changes in sodium and water excretion in stressed animals were due to modifications in the glomerular filtration rate (GFR) and to determine the participation of angiotensin II (Ang II) and alpha and beta-adrenoceptors on sodium and water renal excretion in rats subjected to immobilization stress (IMO). Male Wistar rats (250-300 g) were randomly separated into five different groups and vehicle (0.9% NaCl) via intraperitoneal (i.p.) or propanolol (3 mg/kg i.p.) or captopril (6 mg/kg i.p.) or yohimbine (3 mg/kg i.p.) or prazosin (1 mg/kg i.p.) were injected respectively. During experimental measurements, the animals were kept in metabolic cages for 6 h and sodium, potassium and water renal excretion and saline (1.5% NaCl) and water intake were determined at day 1 (drug effect) and day 7 (drug + IMO effects). GFR was measured by creatinine clearance in control and IMO rats. A stress-induced antinatriuresis and antidiuresis was reversed by alpha 1 and alpha 2-adrenoceptor antagonists, while captopril inhibited only the antidiuresis and propranolol had no effect on either parameter. No differences were observed in creatinine clearance in the studied groups. Since yohimbine blocks alpha 2-adrenoceptors and prazosin blocks alpha 1-adrenoceptors and alpha 2B-adrenoceptors, the stress-induced renal sodium reabsorption mainly could be attributed to alpha 2B-adrenoceptors. The present results indicate that beta-adrenoceptors do not participate in this response and, Ang II only reverses the antidiuresis and shows a slight participation in antinatriuresis. The increment in sodium and water reabsorption caused by IMO occurred without changes in the glomerular filtration rate.
本研究旨在调查应激动物钠和水排泄的变化是否归因于肾小球滤过率（GFR）的改变，并确定血管紧张素II（Ang II）以及α和β肾上腺素受体在遭受固定应激（IMO）的大鼠肾钠和水排泄中的作用。将雄性Wistar大鼠（250 - 300 g）随机分为五个不同组，分别经腹腔注射（i.p.）溶媒（0.9% NaCl）或普萘洛尔（3 mg/kg i.p.）或卡托普利（6 mg/kg i.p.）或育亨宾（3 mg/kg i.p.）或哌唑嗪（1 mg/kg i.p.）。在实验测量期间，将动物置于代谢笼中6小时，并在第1天（药物作用）和第7天（药物 + IMO作用）测定肾钠、钾和水排泄以及盐水（1.5% NaCl）和水摄入量。通过肌酐清除率测量对照组和IMO大鼠的GFR。α1和α2肾上腺素受体拮抗剂可逆转应激诱导的钠利尿和抗利尿作用，而卡托普利仅抑制抗利尿作用，普萘洛尔对这两个参数均无影响。在所研究的组中，肌酐清除率未观察到差异。由于育亨宾阻断α2肾上腺素受体，哌唑嗪阻断α1肾上腺素受体和α2B肾上腺素受体，应激诱导的肾钠重吸收主要可归因于α2B肾上腺素受体。目前的结果表明，β肾上腺素受体不参与此反应，并且Ang II仅逆转抗利尿作用，并在钠利尿中有轻微作用。IMO引起的钠和水重吸收增加发生时，肾小球滤过率未发生变化。
