Abstract

Previous studies showed that neonatal thymectomy prevented the spontaneous increase in blood pressure in genetically hypertensive rats (LH) of the Lyon strain, leaving untouched that of their normotensive controls (LN). As the thymus is connected to the neuroendocrine system through secretion of hormonal factors, we investigated the possible role played by these factors in hypertension of LH rats. To that end we studied, in sham-operated and neonatally thymectomized LH rats, the blood pressure effects of thymostimulin, a partially purified thymus extract and examined whether changes in major neuroendocrine factors of blood pressure regulation occurred in thymectomized LH rats. Thymostimulin (1 or 10 mg/kg/48 h) did not modify blood pressure in sham-operated LH rats and failed to consistently increase it in neonatally thymectomized animals. Urinary mineralocorticoids, catecholamines and their metabolites, and plasma renin levels were not altered by neonatal thymectomy. Plasma testosterone was decreased to a similar degree by neonatal thymectomy in LH and normotensive controls. These results do not favor a pressor role of thymic hormonal factors in LH rats and show that the antihypertensive effect of neonatal thymectomy is not secondary to a decreased secretion of catecholamines, renin, mineralocorticoids, and testosterone. They therefore suggest that the role of the thymus in genetically hypertensive LH rats is more likely mediated by cellular immune mechanisms than by hormonal processes.

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