Possible mechanisms of salt-induced hypertension in Dahl salt-sensitive rats

被引:20
作者
Bayorh, MA [1 ]
Ogbolu, EC
Williams, E
Thierry-Palmer, M
Sanford, G
Emmett, N
Harris-Hooker, S
Socci, RR
Chu, TC
Chenault, VM
机构
[1] Morehouse Sch Med, Dept Pharmacol Toxicol, 720 Westview Dr SW, Atlanta, GA 30310 USA
[2] Morehouse Sch Med, Dept Biochem, Atlanta, GA 30310 USA
[3] Morehouse Sch Med, Dept Physiol, Atlanta, GA 30310 USA
[4] Morehouse Sch Med, Dept Med, Atlanta, GA 30310 USA
[5] US FDA, CDRH, ODE, DCLD, Rockville, MD 20850 USA
关键词
Dahl rats; blood flow; blood pressure; cyclic GMP; norepinephrine release;
D O I
10.1016/S0031-9384(98)00194-2
中图分类号
B84 [心理学];
学科分类号
04 ; 0402 ;
摘要
Genetic factors, diet, and salt sensitivity have all been implicated in hypertension. To further understand the mechanisms involved in salt-induced hypertension, cardiovascular, hemodynamics, and biochemical parameters in Dahl salt-sensitive rats were evaluated in animals on high- and low-sodium diets. During a 4-week treatment period, blood pressure was significantly elevated in the high (8.0%) salt group compared to the low (0.3%) salt group (p less than or equal to 0.05 for weeks 2 and 4, respectively). No significant changes were observed in heart rate. The increase in blood pressure was associated with significant increases in lower abdominal aortic and renal vascular resistance, along with a reduction in blood flow. A fourfold increase in arginine vasopressin was observed in animals on the high-salt diet. In contrast, there was no effect on plasma sodium, potassium, or aldosterone levels during the treatment period. As measured in isolated aortic rings, the high-salt diet also caused a significant elevation in stimulated norepinephrine release and a reduction in cyclic GMP levels. These data suggest that salt-induced elevation in blood pressure is due to activation of both the sympathetic and arginine vasopressin systems via mechanisms involving decreased cyclic GMP generation in vascular smooth muscle. (C) 1998 Elsevier Science Inc.
引用
收藏
页码:563 / 568
页数:6
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