Epidemiological studies have indicated that
hypertension enhances the development of
atherosclerosis in patients with
lipid disorders. However, it was still unclear whether this promoting effect resulted only from hemodynamic changes or whether part of it was mediated by humoral or neurogenic factors independent of blood pressure alteration. The aim of this study was to determine whether
mineralocorticoids, which are known to be involved in the pathogenesis of
hypertension, could be implicated in the atherosclerotic process independent of pressure changes. For this purpose, the effect of
deoxycorticosterone (
DOCA, 200 mg/kg s.c.) on aortic
atherosclerosis was studied in Watanabe heritable hyperlipidemic (WHHL) rabbits in comparison with New Zealand rabbits. After 4 weeks of treatment,
DOCA significantly increased the size of atherosclerotic lesions in the arch and thoracic aorta (+115%) in parallel with the aortic
cholesterol ester content (+83%). The vascular free
cholesterol and
triglyceride content remained unchanged on
DOCA treatment, as were arterial pressure and plasma
cholesterol levels. None of these effects was observed in New Zealand rabbits.
DOCA did not accentuate the alteration of endothelial function usually found in WHHL rabbits. The sensitivity to
serotonin was not altered, but the maximal contraction to this agonist was decreased in both strains by
mineralocorticoid treatment.