Ponec J, Lichardus B, Okolicány J
Institute of Experimental Endocrinology, Center of Physiological Sciences, Slovak Academy of Sciences, Bratislava.
Biomed Biochim Acta. 1987;46(12):959-63.
Acute hypophysectomy (a.h.) (i.e. pituitary ablation 120 min prior to the experiment) abolished the ability of anaesthetized rats to excrete sodium following isotonic saline load (4% body weight). The diuretic response remained even slightly increased as compared to control sham-operated animals (s.o.) (maximal UNaV a.h. rats +/- SE: 0.65 +/- 0.10 mumol/min vs maximal UNaV in s.o. rats: 4.54 +/- 0.50 mumol/min). Alpha h-atrial natriuretic factor 1-28 (ANF) in a doses of 3.3 micrograms/animal.40 min restored natriuresis in a.h. rats following isotonic saline load to the level observed in s.o. rats (4.25 +/- 0.64 mumol/min), the change being transient. A decrease of blood pressure to 78.6 +/- 3.21 mm Hg during ANF infusion was followed by a reduction in the natriuretic effect of ANF, while the diuretic effect remained unchanged. Based on own results and literary data it could be suggested that impairment of ANF release or its renal effect are involved in the abolishment of homeostatically effective natriuresis in a.h. animals.
急性垂体切除(a.h.)(即实验前120分钟进行垂体切除)消除了麻醉大鼠在给予等渗盐水负荷(4%体重)后排泄钠的能力。与假手术对照动物(s.o.)相比,利尿反应甚至略有增加(a.h.大鼠的最大尿钠排泄量(UNaV)±标准误:0.65±0.10 μmol/分钟,而s.o.大鼠的最大UNaV为:4.54±0.50 μmol/分钟)。剂量为3.3微克/只动物的α h-心房利钠因子1-28(ANF),在40分钟时使a.h.大鼠在给予等渗盐水负荷后的钠利尿恢复到s.o.大鼠所观察到的水平(4.25±0.64 μmol/分钟),但这种变化是短暂的。在输注ANF期间血压降至78.6±3.21毫米汞柱后,ANF的利钠作用降低,而利尿作用保持不变。根据自身结果和文献数据,可以认为ANF释放受损或其肾脏效应与a.h.动物中稳态有效钠利尿的消除有关。