Raff H, Roarty T P
Endocrine Research Laboratory, St. Luke's Hospital, Milwaukee, Wisconsin 53215.
Am J Physiol. 1988 Mar;254(3 Pt 2):R431-5. doi: 10.1152/ajpregu.1988.254.3.R431.
The control of aldosterone secretion may be altered during acute changes in arterial blood gases. We studied the blood gas, plasma electrolyte, renin (PRA), adrenocorticotropic hormone (ACTH), and aldosterone (ALDO) responses to acute hypercapnia (4 and 8% CO2), acute hypocapnic hypoxia (10% O2), acute severe normocapnic hypoxia (7% O2-4% CO2), and acute hypercapnic hypoxia (7% O2-8% CO2) in conscious, cannulated Long-Evans rats. Normoxia resulted in normal levels of PRA (6.9 +/- 2.0 ng.ml-1.h-1), ACTH (96 +/- 32 pg/ml), and ALDO (10 +/- 3 ng/dl). Hypercapnia had no effect on PRA but did lead to an increase in ACTH (to 298 +/- 69 pg/ml) and ALDO (to 33 +/- 7 ng/dl) during 8% CO2 exposure. Normocapnic hypoxia resulted in a significant increase in ACTH (to 196 +/- 14 pg/ml) and ALDO (to 30 +/- 3 ng/dl). Hypercapnic hypoxia resulted in the greatest increases in PRA (to 30 +/- 2 ng.ml-1.h-1), ACTH (to 397 +/- 114 pg/ml), and ALDO (to 41 +/- 5 ng/dl). We conclude that in conscious rats 1) hypercapnia (less than 80 Torr) had no significant effect on PRA, 2) isocapnic, severe hypoxia (Po2 approximately 34 Torr) increased ACTH, and 3) the combination of hypercapnia and hypoxia was a very potent stimulus to PRA, ACTH, and ALDO. The ALDO responses to increases in endogenous ACTH and angiotensin II appear to be normal in conscious rats during acute hypoxia and/or hypercapnia.
在动脉血气发生急性变化时,醛固酮分泌的控制可能会改变。我们研究了清醒的、已插管的Long-Evans大鼠对急性高碳酸血症(4%和8%二氧化碳)、急性低碳酸血症性缺氧(10%氧气)、急性重度等碳酸血症性缺氧(7%氧气 - 4%二氧化碳)以及急性高碳酸血症性缺氧(7%氧气 - 8%二氧化碳)的血气、血浆电解质、肾素(PRA)、促肾上腺皮质激素(ACTH)和醛固酮(ALDO)反应。常氧状态下PRA(6.9±2.0 ng·ml⁻¹·h⁻¹)、ACTH(96±32 pg/ml)和ALDO(10±3 ng/dl)水平正常。高碳酸血症对PRA无影响,但在暴露于8%二氧化碳期间确实导致ACTH增加(至298±69 pg/ml)和ALDO增加(至33±7 ng/dl)。等碳酸血症性缺氧导致ACTH显著增加(至196±14 pg/ml)和ALDO显著增加(至30±3 ng/dl)。高碳酸血症性缺氧导致PRA(至30±2 ng·ml⁻¹·h⁻¹)、ACTH(至397±114 pg/ml)和ALDO(至41±5 ng/dl)增加幅度最大。我们得出结论,在清醒大鼠中:1)高碳酸血症(低于80 Torr)对PRA无显著影响;2)等碳酸血症、重度缺氧(Po2约为34 Torr)会增加ACTH;3)高碳酸血症和缺氧的组合是对PRA、ACTH和ALDO的非常强效的刺激因素。在急性缺氧和/或高碳酸血症期间,清醒大鼠中醛固酮对内源性ACTH和血管紧张素II增加的反应似乎正常。