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1. Subpressor calcium infusion for 1 h, which raised calcium levels to the upper limit of normal in normal subjects, increased plasma and urinary levels of atrial natriuretic peptide (ANP). 2. Heart rate fell, presumably due to carotid baroreflex stimulation (supported by the fall in noradrenaline) and the resultant fall in cardiac output prevented the expected rise in blood pressure due to the rise in total peripheral resistance (TPR). Thus the increase in ANP was not explained by an increase in blood pressure or noradrenaline. 3. There was no evidence for increased atrial stretch (no increase in atrial area or early velocity of left ventricular filling) as a mechanism for increased ANP. 4. Isovolumic left ventricular relaxation time increased, early velocity of ventricular filling decreased and TPR increased, consistent with increased tone in left ventricular and arteriolar muscle. 5. This suggests a direct effect of calcium on the atrial myocyte, stimulating ANP either through contractile or secretory mechanisms.

1. Calcium was infused in normal subjects in subpressor dosage to examine the effects of raised calcium levels on atrial natriuretic peptide (ANP) concentrations. 2. Calcium infusion progressively raised serum ionized and total calcium concentrations significantly, without raising mean arterial pressure or heart rate. 3. Plasma ANP concentrations increased significantly by 5 min of infusion and increased further by 15 min (approximately 40%) to levels which were maintained to 60 min. 4. Urinary sodium excretion increased by 140% during calcium infusion. 5. Calcium may affect secretory as well as contractile functions of the atrial myocyte.