In a rat model, NTS lesions cause systemic hypertension and increased peripheral resistance, with spontaneously hypertensive rats exhibiting distinct regional vasoconstriction patterns.
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NTS lesion findings in rats remain hypothesis-generating; leaves open any role in human hypertension pathogenesis or therapy.
Systemic and regional hemodynamic responses to bilateral lesions of the nucleus tractus solitarii (NTS) were studied in alpha-chloralose-urethane anesthetized American Wistar rats (NR), Wistar-Kyoto rats (WKY), and spontaneously hypertensive rats (SHR) by microsphere methods. After NTS lesions, arterial pressure rose by virtue of increased total peripheral resistance in each strain. Cardiac output was lower in NR and WKY, but not in SHR. In all strains, vasoconstriction was nonuniformly distributed among the systemic vasculatures: hepatosplanchnic, renal, and carcass (i.e. skin, skeletal muscle, bone, fat) vascular resistances were higher, but cerebral and coronary vascular resistance remained unchanged. There were some differences, however, in regional vascular responses to NTS lesions among these strains: carcass vasoconstriction was predominant in NR; it was less evident in SHR; and the WKY responses were intermediate. These results indicate that, although systemic hemodynamic responses were similar in these strains, and the reflex inhibition of central sympathetic outflow is not evidently deteriorated in SHR, the regional hemodynamics (i.e., hepatosplanchnic and renal vasculatures) in the SHR demonstrated greater arteriolar constriction.
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Kitamura et al. (1981) studied this question.
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