A substantial proportion of patients with essential hypertension have raised circulating atrial natriuretic peptide levels, pointing to important compensatory mechanisms for sodium balance.
This review highlights the compensatory role of elevated atrial natriuretic peptides in essential hypertension and the potential therapeutic value of manipulating endogenous ANP levels.
The identification of the atrial natriuretic peptides (ANP) as a new hormonal system has provided a new perspective on the mechanisms controlling renal sodium excretion and abnormalities in sodium homeostasis. The present article focuses on the potential importance of ANP (ANF 99-126) in essential hypertension with particular reference to circulating ANP levels and the relationship between the ANP and the renin-angiotensin system in the control of sodium balance and blood pressure. There is now considerable evidence demonstrating that a substantial proportion of patients with essential hypertension have raised circulating ANP levels. Given the known biological actions of ANP, these raised levels point to important compensatory mechanisms. This is further supported by studies during alterations in dietary sodium intake, as sodium restriction high-lighted important relationships between ANP and the renin angiotensin system. The potential importance of ANP in essential hypertension is strengthened by recent demonstration of natriuretic and antihypertensive actions associated with small increases in circulating ANP as induced by administration of exogenous ANP. Furthermore, the recent development of orally active inhibitors of ANP metabolism now provides a basis to determine the therapeutic importance of specific manipulation of endogenous ANP levels in patients with essential hypertension.
Sagnella et al. (Tue,) conducted a review in essential hypertension. Atrial natriuretic peptides (ANP) was evaluated. A substantial proportion of patients with essential hypertension have raised circulating atrial natriuretic peptide levels, pointing to important compensatory mechanisms for sodium balance.