Renin, ACTH, and aldosterone during acute hypercapnia and hypoxia in conscious rats.
Renin, ACTH, and aldosterone during acute hypercapnia and hypoxia in conscious rats.
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DOI：
10.1152/ajpregu.1988.254.3.r431
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发表时间：
1988-03
期刊：
影响因子：
--
通讯作者：
H. Raff;T. Roarty
中科院分区：
文献类型：
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作者：
H. Raff;T. Roarty
在动脉血气的急性变化期间，醛固酮分泌的控制可能改变。我们研究了清醒、插管的Long-Evans大鼠对急性高碳酸血症（4和8%CO2）、急性低碳酸血症性缺氧（10%O2）、急性重度正常碳酸血症性缺氧（7%O2 - 4%CO2）和急性高碳酸血症性缺氧（7%O2 - 8%CO2）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。常氧导致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没有影响，但在8%CO2暴露期间确实导致ACTH（至298 +/- 69 pg/ml）和ALDO（至33 +/- 7 ng/dl）增加。正常碳酸性缺氧导致ACTH（至196 +/- 14 pg/ml）和ALDO（至30 +/- 3 ng/dl）显著增加。高碳酸血症缺氧导致PRA（至30 +/- 2 ng.ml-1. h-1）、ACTH（至397 +/- 114 pg/ml）和ALDO（至41 +/- 5 ng/dl）的最大增加。我们的结论是，在清醒大鼠中，1）高碳酸血症（低于80 Torr）对PRA没有显著影响，2）等碳酸血症，严重缺氧（Po 2约34 Torr）增加ACTH，3）高碳酸血症和缺氧的组合是对PRA，ACTH和ALDO的非常有效的刺激。在急性缺氧和/或高碳酸血症期间，清醒大鼠对内源性ACTH和血管紧张素II增加的ALDO反应似乎正常。
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.