[Changes of the renin-angiotensin-aldosterone system under contraceptive steroids. Contribution to the etiology of hypertension under hormonal contraceptives]

Abstract

Treatment with hormonal contraceptives leads to a considerable stimulation of the renin-angiotensin-aldosterone-system. First of all, there is a 2,5- to 4fold increase of renin substrate synthesis in the liver. As a consequence, more angiotensin I and angiotensin II are released. Angiotensin II stimulates the secretion of aldosterone in the adrenals, thus producing a higher aldosterone concentration in plasma. The urinary excretion of aldosterone is elevated to a lesser degree, probably because of the simultaneously increased binding of aldosterone to plasma proteins. The release of renin is suppressed to 50% by negative feedback mechanisms. Some possible factors in the etiology of hypertension induced by oral contraceptives are discussed.

PIP: Hormonal contraceptive treatment results in considerable stimulation of the renin-angiotensin-aldosterone system. Hepatic synthesis of renin substrate increases by a factor of 2.5-4. As a result, more angiotensin I an angiotensin II are released. Angiotensin II stimulates adrenal aldosterone production, producing a higher plasma aldosterone concentration. Urinary aldosterone secretion rises less, probably because binding of aldosterone to plasma proteins is increased at the same time. Renin release is suppressed to 50% by negative feedback mechanisms. Other factors in the etiology of hypertension may include effects on sodium balance and on the sensitivity of the blood vessels to pressure-regulating substances.