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Salt increases blood pressure with biphasic changes in hypothalamic responsiveness in rats
1Second Department of Medicine, Kyoto Prefectural University of Medicine, Japan.
Journal of Cardiovascular Pharmacology
|August 1, 1988
Summary
Chronic high salt intake initially reduces, then increases, brain responses controlling blood pressure. This biphasic effect in the ventromedial hypothalamus may lead to salt-induced hypertension.
Area of Science:
- Cardiovascular Physiology
- Neuroendocrinology
- Renal and Electrolyte Physiology
Background:
- Dietary salt intake is a major factor in hypertension development.
- The ventromedial hypothalamus plays a role in regulating sympathetic activity and blood pressure.
Purpose of the Study:
- To investigate the biphasic effects of chronic salt loading on the ventromedial hypothalamus's control of sympathetic activity and blood pressure.
- To determine the role of baroreflexes in mediating these effects.
Main Methods:
- Male Wistar rats were fed a high-salt (8% NaCl) diet for 1 or 4 weeks.
- Tail-cuff systolic pressures were measured.
- Pressor and sympathetic responses to ventromedial hypothalamic stimulation were assessed.
- Experiments were repeated after sinoaortic denervation and bilateral vagotomy.
Main Results:
- Four weeks of salt loading elevated systolic pressure and enhanced pressor/sympathetic responses to hypothalamic stimulation, effects that persisted after sinoaortic denervation.
- One week of salt loading reduced these responses, an effect reversed by vagotomy, suggesting cardiopulmonary baroreflex involvement.
- Circulating plasma volume increased after 1 week of salt loading.
Conclusions:
- Chronic dietary salt loading exerts biphasic effects on the ventromedial hypothalamus, initially inhibiting then stimulating sympathetic activity.
- These changes in hypothalamic responsiveness may contribute to the development of salt-induced hypertension.
- Cardiopulmonary baroreflexes modulate the initial inhibitory phase of salt loading on hypothalamic function.