Abstract
In NaCl-sensitive spontaneously hypertensive rats, diets high in NaCl increase arterial pressure and peripheral sympathetic nervous system activity and decrease the sympatho-inhibition mediated by the anterior hypothalamic area. To test the importance of the defect in anterior hypothalamic area-mediated sympatho-inhibition in the pathogenesis of NaCl-sensitive hypertension, bilateral ibotenic acid lesions of the anterior hypothalamic area were made in NaCl-sensitive spontaneous hypertensive rats, in NaCl-resistant spontaneously hypertensive rats and in normotensive, NaCl-resistant Wistar Kyoto rats. In NaCl-sensitive spontaneous hypertensive rats on a basal NaCl diet, the anterior hypothalamic area lesions caused a rapid rise in arterial pressure within the first week after surgery; by 21 days after surgery, mean systolic arterial pressure of the lesion group was 24 mmHg higher than that of the sham-operated group. In a second experiment, NaCl-sensitive spontaneous hypertensive rats were placed on an 8% NaCl diet 1 day after the lesion of the anterior hypothalamic area. 5 days after the operation, the lesion group of NaCl-sensitive spontaneous hypertensive rats on the 8% NaCl diet had a significantly higher arterial pressure than the sham-operated group, but by 1 week after the lesion, arterial pressures were not significantly different between the lesion and sham-operated NaCl-sensitive spontaneous hypertensive rats on the high NaCl diet. In Wistar Kyoto rats on a basal NaCl diet, lesions of the anterior hypothalamic area resulted in a small, transient elevation of arterial pressure, but no sustained effect. In NaCl-resistant spontaneous hypertensive rats, the anterior hypothalamic area lesions did not affect arterial pressure. These results support the hypothesis that in NaCl-sensitive spontaneous hypertensive rats the anterior hypothalamic area contributes importantly to arterial pressure regulation and the data suggest that both the lesion of the anterior hypothalamic area and the high-NaCl diet may affect arterial pressure regulation through the same mechanism.
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