To define the relation between atrial pressures and the release of atrial natriuretic peptide, we measured plasma concentrations of the peptide in 26 patients with cardiac disease--11 with normal atrial pressures and 15 with elevated atrial pressures (11 of these 15 had elevated pressures in both atria). Mean peptide levels (+/- SEM) in the peripheral venous blood were increased in the 11 patients with cardiac disease and normal atrial pressures, as compared with 60 healthy controls (48 +/- 14 vs. 17 +/- 2 pmol per liter). In the patients with elevated atrial pressures, peptide concentrations were increased twofold in peripheral venous, right atrial, pulmonary arterial, and systemic arterial plasma, as compared with the concentrations in the patients with normal atrial pressures. A step-up in peptide concentration was seen between the venous and right atrial plasma (P less than 0.002) and between the pulmonary and systemic arterial plasma (P less than 0.01), suggesting release of the peptide from the atria. A linear relation was found between right atrial pressure and right atrial peptide concentration (r = 0.835, P less than 0.001) and between pulmonary wedge pressure and the systemic arterial peptide concentration (r = 0.866, P less than 0.001). Right atrial pressure and the peptide concentration both increased with exercise testing in the nine patients evaluated. We conclude that the release of atrial natriuretic peptide is at least partly regulated by right and left atrial pressures. Distinguishing the relative contributions of the two atria and defining the role of peptide release in the pathogenesis of heart failure will require further investigation.

No abstract

Circulating levels of the calcium-regulating hormones, calcitonin, calcitriol, and parathyroid hormone, were analyzed in relation to plasma renin activity in 10 persons with normal blood pressure and in 51 persons with essential hypertension. Calcitriol (p less than 0.008) and parathyroid hormone (p less than 0.01) levels were elevated in hypertensives with low renin activity, whereas calcitonin levels were higher in patients with high renin activity (p less than 0.008), compared with normotensive controls and other hypertensive patients. Continuous relationships were observed between calcitriol levels and plasma renin activity in all patients (r = -0.65, p less than 0.001) and between parathyroid hormone levels and urinary sodium excretion in hypertensive patients with low renin activity (r = -0.63, p less than 0.01). Together, these results support a linkage between calcium metabolism and renin-sodium factors in essential hypertension. Calcium-regulating hormones and the renin-aldosterone system may coordinately mediate the blood pressure effects of differing dietary calcium and sodium intakes at the cellular level by altering cellular handling of monovalent and divalent ions.

The vasodilating potency of a-human atrial natriuretic peptide (a-hANP) was investigated in the forearms of 16 normotensive subjects, 22 to 48 (mean 28) years old, with the use of venous occlusion plethysmography. a-hANP, 0.005 to 1.5 ,ug/min/100 ml forearm volume (FAV), infused in nine dose steps into the brachial artery increased forearm blood flow (FAF; ml/min/100 ml FAV) from 2.8 ± 0.4 (SEM) to a maximum of 9.6 ± 1.1. Forearm vascular resistance (mean arterial pressure/ FAF) decreased by 72%. The a-hANP dose that produced a 50% vasodilator response was 0.093 0.0 16 gg/min/100 ml FAV (n = 11) and it resulted in a venous plasma concentration of ANP (pANP) of 115 ± 7 pmol/liter (normal 2 to 80; radioreceptor assay). Intraindividually, the maximum dose of ahANP induced an increase in FAF that was 60% of the maximum response to sodium nitroprusside (14.1 ± 1.8). Combined infusions (n = 9) of maximum forearm vasodilator doses of a-hANP and nitroprusside increased FAF to 22.7 ± 3.4; this additive vasodilator effect of a-hANP and nitroprusside is consistent with their different actions on the guanylate cyclase system. In man, the direct vasorelaxant effect of a-hANP occurs at concentrations within the upper normal range of pANP, suggesting a physiologic vasodilator role for a-hANP. Circulation 75, No. 1, 221-228, 1987. ATRIAL PEPTIDES1 contained in specific granules of the mammalian atria5-9 and released into the circulation on atrial distention"'-2 may play a physiologic role in circulatory homeostasis because they exhibit potent vasorelaxant,'3 natriuretic, 7 8 14 and aldosterone-inhibiting effects.'5' 16 Atrial peptides oppose the vascular smooth muscle contraction induced by norepinephrine, angiotensin JJ,17 18 and serotonin, histamine, and methoxamine.'9 They have been shown to bind to specific high-affinity receptors in adrenal,20 renal, and