1. In experimental studies, activation of renal sympathetic nerves attenuates the natriuretic response to atrial natriuretic factor. We therefore investigated the response to low-dose infusion of atrial natriuretic factor in renal transplant recipients.
2. Eight male cyclosporin-treated renal transplant recipients received human-α atrial natriuretic factor (1–28) at a dose of 1.2 pmol min−1 kg−1 or placebo for 2 h in a placebo-controlled, randomized, cross-over study. The plasma atrial natriuretic factor concentration rose from 18.5 to 49.2 pmol/l in association with an immediate natriuresis (a rise of 49.1 μmol/min in the first 30 min, P<0.05; peaking at a 61% increase from baseline, P<0.01), diuresis (from 3.37 to 7.46 ml/min) and a threefold rise in urinary cyclic GMP excretion.
3. In response to infusion of atrial natriuretic factor, the packed cell volume rose by 4.2% (P < 0.001) and the filtration fraction by 5% (from 22 to 27%, P<0.05), but there was no significant change in renal plasma flow, glomerular filtration rate or mean arterial blood pressure. Likewise, the plasma catecholamine concentrations, plasma renin activity and serum erythropoietin concentration remained unchanged.
4. The sensitivity of the renal allograft to plasma atrial natriuretic factor concentrations in the high physiological range suggests a role for endogenous atrial natriuretic factor in the modulation of graft function. Furthermore, the immediate natriuretic response to atrial natriuretic factor in the effectively denervated transplant kidney, in contrast to the delayed response seen in normal subjects, may imply that sympathetic nerves have an inhibitory effect on the renal response to atrial natriuretic factor in normal man.
5. In contrast to the findings of studies in vitro, infusion of atrial natriuretic factor had no effect on the serum erythropoietin concentration.