Abstract
Angiotensin II (ANG II) and atrial natriuretic peptide (ANP) play important roles in the regulation of cardiovascular function and fluid balance (1,2). Circulating ANG II stimulates specific receptors to induce vasoconstriction, aldosterone production, vasopressin release, and sodium retention (2). There are alterations in the peripheral renin-angiotensin system in genetic and experimental hypertension (3). The renin-angiotensin system is also important in human hypertension, and blockade of the last step of ANG II formation by inhibition of the angiotensin converting enzyme (ACE) is one of the standard therapies. ANP, produced in the heart, is released to the circulation and is involved in the control of fluid volume and cardiovascular function (1). ANP metabolism is altered in hypertension (4). The peripheral effects of ANP, increased sodium and water excretion by the kidneys, decreased aldosterone production, vasodilation and antihypertensive actions are antithetical to those of the water conservation peptides, vasopressin, and ANG II (1). For these reasons peripheral ANP and ANG II are considered to be part of physiologically antagonistic regulatory systems.
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