Oral contraceptive-induced high blood pressure is prevented by renin-angiotensin suppression in female rats but not by sympathetic nervous system blockade.

The use of oral contraceptive (OC) steroids is associated with high blood pressure, although mechanisms responsible are still unclear. This study sought to investigate the possible roles that renin-angiotensin system (RAS) and sympathetic nervous system (SNS) may play in the development of OC-induced hypertension. Administration of OC led to significant increases in blood pressure, heart weight and significant decrease in urinary output in OC-treated and OC+clonidine-treated groups but not in OC+captopril-treated group. The pressor response to angiostensin II was significantly greater in the OC-treated rats than in the control rats. However, the pressor responses induced by norepinephrine were not significantly affected by OC administration. The results of the present study demonstrate that OC-induced high blood pressure is associated with cardiac hypertrophy, enhanced pressor response to angiotensin II and preserved pressor response to sympathetic activation. The study also suggests that the development of the OC-induced hypertension and cardiac hypertrophy is mediated by RAS, but not by SNS.

Effect of increased calcium intake on cardiac and vascular Na(+)-K(+)-ATPase activity in oral contraceptive-treated female Sprague-Dawley rats.

The present study aimed at investigating the influence of increased dietary calcium on Na(+)-K(+)-ATPase activity in heart and aorta of female Sprague-Dawley rats treated with oral contraceptive (OC) steroids. Rats were grouped as control (CR), OC-treated and OC+calcium-treated. OC-treated and OC+calcium-treated received a combination of OC steriods (ethinyloestradiol and norgestrel; ig). OC+calcium-treated rats were fed with 2.5% calcium diet, while OC-treated and CR groups were fed on 0.9% calcium diet. The activity of Na(+)-K(+)-ATPase in heart and aorta was significantly lower in OC-treated rats than those in the other groups. OC treatment caused significant increase in plasma glucose and significant decrease in plasma K+ as compared to control group. Decrease in Na(+)-K(+)-ATPase activity and plasma K+ was abrogated by increased calcium intake, while increase in plasma glucose was not normalized by calcium supplementation. Plasma levels of Na+, lipid peroxidation index and ascorbic acid were comparable among the three groups. These results showed that OC treatment could lead to impaired activity of cardiac and vascular Na(+)-K(+)-ATPase, possibly due to reduced plasma K+ level and these effects could be abolished by high calcium diet.