An investigation into the neural regulation of calcium excretion by the rat kidney.

1. An investigation was undertaken to examine the action of the renal nerves on the reabsorption of calcium ions from the left kidney of sodium pentobarbitone anaesthetized rats. 2. Renal denervation had no effect on renal haemodynamics but increased urine flow, calcium excretion, absolute and fractional sodium excretions by 26% (P less than 0.02), 73% (P less than 0.02), 90% (P less than 0.001) and 82% (P less than 0.01), respectively, without affecting the calcium to sodium excretion ratio. In a group of animals which were similarly prepared but the renal nerves were not sectioned, neither renal blood flow, nor the excretion of water, calcium or sodium changed during the time course of the experiment although glomerular filtration rate increased significantly (P less than 0.05) by 19%. 3. Low rates (0.8-1.5 Hz at 15 V, 0.2 ms) of renal nerve stimulation did not change renal haemodynamics but reduced urine flow by 31% (P less than 0.001), calcium excretion by 32% (P less than 0.001), sodium excretion by 32% (P less than 0.001) and fractional sodium excretion by 32% (P less than 0.01) while the calcium to sodium excretion ratio was unaffected. Renal nerve stimulation at 3-5 Hz reduced renal blood flow by 15% (P less than 0.02), did not change glomerular filtration rate and reduced urine flow, calcium excretion, absolute and fractional sodium excretions by 35% (P less than 0.01), 30% (P less than 0.01), 32% (P less than 0.01) and 32% (P less than 0.05), respectively, while the calcium to sodium excretion ratio remained unchanged. 4. These data show that the renal nerves can modulate the excretion of calcium by a mechanism which is independent of renal haemodynamics and which may represent a direct action of the nerves on the calcium reabsorptive processes of the tubular cells. It remains to be determined whether this neural control of calcium reabsorption is a direct one or indirect via changes in sodium reabsorption.