An investigation was undertaken in the pentobarbitone anaesthetized rat to determine the influence of calcium entry blockade on the haemodynamic and tubular responses of the kidney to renal sympathetic nerve stimulation. Electrical activation of the nerves, at rates causing a 12% reduction in renal blood flow, did not change glomerular filtration rate but significantly reduced urine flow (32%) and absolute (34%) and fractional sodium excretion (33%). Intravenous administration of diltiazem (10 and 20 micrograms/kg/min) and nifedipine (1.0 and 2.0 micrograms/kg/min) caused significant reductions of systemic blood pressure. Stimulation of the renal nerves, to reduce renal blood flow between 15% and 18% in the presence of both low and high doses of diltiazem, caused significant falls in glomerular filtration rate of 9% and 23%, respectively. During the low dose of nifedipine glomerular filtration rate did not change but in animals receiving the higher dose it fell by 17%. The magnitude of the neurally induced changes in urine flow, absolute and fractional sodium excretions were not different at either dose level of diltiazem or nifedipine from that observed in the absence of drugs. Stimulation of the renal nerves at low rates, which did not change renal blood flow, had no effect on glomerular filtration rate but significantly reduced urine flow (38%) and absolute (39%) and fractional sodium excretion (35%). At these low rates of nerve stimulation glomerular filtration rate remained unchanged during the infusion of either dose level of diltiazem. However, during administration of both the low and high doses of nifedipine there were significant reductions of glomerular filtration rate of 20% and 17%, respectively. The magnitude of the neurally induced changes in urine flow, absolute and fractional sodium excretions in the presence of both low and high doses of diltiazem and nifedipine were the same as those observed in the absence of drugs. The results of this study provide no evidence to indicate that the nerve mediated increases in tubular sodium reabsorption, a response involving alpha-adrenoreceptors, is dependent on the movement of calcium into the epithelial cells. The data did not indicate that blockade of calcium entry into cells impaired the ability of the kidney to regulate glomerular filtration rate which appeared to be due to a lack of renal efferent arteriolar vasoconstriction.