DOPAMINERGIC SUPPRESSION OF ANGIOTENSIN-II-INDUCED ALDOSTERONE SECRETION IN MAN - DIFFERENTIAL RESPONSES DURING SODIUM LOADING AND DEPLETION
被引:41
作者:
DRAKE, CR
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UNIV VIRGINIA, MED CTR,SCH MED,DEPT INTERNAL MED, DIV ENDOCRINOL & METAB, CHARLOTTESVILLE, VA 22901 USAUNIV VIRGINIA, MED CTR,SCH MED,DEPT INTERNAL MED, DIV ENDOCRINOL & METAB, CHARLOTTESVILLE, VA 22901 USA
DRAKE, CR
[1
]
RAGSDALE, NV
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UNIV VIRGINIA, MED CTR,SCH MED,DEPT INTERNAL MED, DIV ENDOCRINOL & METAB, CHARLOTTESVILLE, VA 22901 USAUNIV VIRGINIA, MED CTR,SCH MED,DEPT INTERNAL MED, DIV ENDOCRINOL & METAB, CHARLOTTESVILLE, VA 22901 USA
RAGSDALE, NV
[1
]
KAISER, DL
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UNIV VIRGINIA, MED CTR,SCH MED,DEPT INTERNAL MED, DIV ENDOCRINOL & METAB, CHARLOTTESVILLE, VA 22901 USAUNIV VIRGINIA, MED CTR,SCH MED,DEPT INTERNAL MED, DIV ENDOCRINOL & METAB, CHARLOTTESVILLE, VA 22901 USA
KAISER, DL
[1
]
CAREY, RM
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UNIV VIRGINIA, MED CTR,SCH MED,DEPT INTERNAL MED, DIV ENDOCRINOL & METAB, CHARLOTTESVILLE, VA 22901 USAUNIV VIRGINIA, MED CTR,SCH MED,DEPT INTERNAL MED, DIV ENDOCRINOL & METAB, CHARLOTTESVILLE, VA 22901 USA
CAREY, RM
[1
]
机构:
[1] UNIV VIRGINIA, MED CTR,SCH MED,DEPT INTERNAL MED, DIV ENDOCRINOL & METAB, CHARLOTTESVILLE, VA 22901 USA
来源:
METABOLISM-CLINICAL AND EXPERIMENTAL
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1984年
/
33卷
/
08期
关键词:
D O I:
10.1016/0026-0495(84)90207-5
中图分类号:
R5 [内科学];
学科分类号:
1002 ;
100201 ;
摘要:
Aldosterone secretion may be inhibited by dopaminergic mechanisms in man. Dopamine does not inhibit aldosterone responses to angiotensin II in Na replete normal subjects. Since Na deficiency is associated with a reduction in renal dopamine formation, the effect of dopamine on angiotensin II-induced aldosterone secretion in the Na-depleted state. Six normal subjects in balance at 10 meq-Na intake (UNaV 17 .+-. 2 meq/24 h) received dopamine 4 .mu.g/kg per min or vehicle for 210 min on 2 consecutive days. After 60 min of the dopamine or vehicle infusion, the subjects received successive 30 min infusions of angiotensin II in increasing doses of 0.5, 1, 2, 4 and 6 picomol/kg per min. Control plasma aldosterone concentrations before vehicle or dopamine were 15 .+-. 3 (mean 1 .+-. SE) and 25 .+-. 3 ng/dl, respectively. Aldosterone responses to angiotensin II were greater with vehicle than dopamine at angiotensin II doses of 4 and 6 picomol/kg per min (P < 0.025). The slope of angiotensin-aldosterone dose-response curve was steeper with vehicle (0.33) than with dopamine (0.16), P < 0.01. Serum prolactin concentrations were lower with dopamine (1.6 .+-. 0.8 ng/ml) than with vehicle (6.4 .+-. 1.2 ng/ml, P < 0.05) by 120 min of infusion and remained suppressed with dopamine for the remainder of the dopamine infusion. Diastolic blood pressure was higher (P < 0.05) with vehicle than with dopamine at angiotensin II doses of 2,4 and 6 picomol/kg per min. Dopamine administration was associated with an increase in plasma cortisol concentration from 90 to 150 min of infusion (P < 0.05). The same 6 subjects in balance at 300 meq Na intake (UNaV 287 .+-. 18 meq/24 h) had no difference in aldosterone response or slope of the angiotensin II-aldosterone dose-response curve with dopamine or vehicle. Serum prolactin concentrations were lower with dopamine (5.4 .+-. 1.2 ng/ml) than with vehicle (9.3 .+-. 1.4 ng/ml, P < 0.05) by 90 min of infusion and remained suppressed for the rest of the study. Cortisol levels were significantly higher with dopamine than with vehicle from 120-150 min of infusion (P < 0.05). In conclusion, dopamine inhibits angiotensin II-stimulated aldosterone secretion during Na deficiency in man.