HEMODYNAMICS, FLUID VOLUME, AND HORMONAL RESPONSES TO CHRONIC HIGH-SALT INTAKE IN DOGS

被引:53
作者
KRIEGER, JE [1 ]
LIARD, JF [1 ]
COWLEY, AW [1 ]
机构
[1] MED COLL WISCONSIN, DEPT PHYSIOL, 8701 WATERTOWN PLANK RD, MILWAUKEE, WI 53226 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY | 1990年 / 259卷 / 06期
关键词
BLOOD PRESSURE; CARDIAC OUTPUT; TOTAL PERIPHERAL RESISTANCE; SODIUM CHLORIDE;
D O I
10.1152/ajpheart.1990.259.6.H1629
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The sequential hemodynamics, fluid and electrolyte balances, and the hormonal responses to a 7-day high-salt (NaCl) intake were investigated in sodium-depleted conscious dogs (n = 6). Studies were carried out in metabolic cages mounted on sensitive load cells, which enabled continuous 24 h/day monitoring of total body weight (TBW) as an index of changes in body water. Beat-by-beat hemodynamics were determined 24 h/day. Water (700 ml/day iv) intake was maintained constant. Daily fluid and electrolyte balances and hormonal analyses were performed. An increase of daily salt intake from 8 to 120 meq increased TBW 251 +/- 44 g (P < 0.05), which was sustained thereafter. Average 24-h mean arterial pressure (MAP) and heart rate (HR) remained unchanged. Average cardiac output (CO) increased 11% (P < 0.05) above control values by day 2, while total peripheral resistance (TPR) decreased proportionally. CO and TPR returned to control values only when low salt was resumed. Blood volume (BV) was unchanged on day 2 as indicated by direct measurement of BV (Cr-51-labeled red blood cells) or by analysis of plasma protein concentration. A 92-meq (P < 0.05) sodium retention was observed initially, and plasma sodium concentration increased slightly. Plasma renin activity, angiotensin II, and aldosterone levels decreased significantly, whereas vasopressin and atrial natriuretic peptide levels remained unchanged. In summary, chronic high-salt intake resulted in a net retention of water and sodium with no changes in MAP, HR, or BV. The rise in CO was offset by a reduction in TPR, which appeared at least in part related to angiotensin II suppression.
引用
收藏
页码:H1629 / H1636
页数:8
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