An investigation into the α‐adrenoceptor mediating renal nerve‐induced calcium reabsorption by the rat kidney

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Abstract
1 An investigation was undertaken in pentobarbitone-anaesthetized rats to determine the sub-type of α-adrenoceptor responsible for the renal nerve-induced increases in the reabsorption of calcium and sodium by the tubules of the kidney. 2 Stimulation of the renal nerves at low frequencies (0.8-1.5 Hz) did not change either renal blood flow or glomerular filtration rate but significantly reduced urine flow by 32%, calcium excretion by 36% and absolute and fractional sodium excretions by 36% and 22%, respectively. 3 In the presence of the selective α1-adrenoceptor antagonist prazosin, renal nerve stimulation (2–3 Hz) caused a significant reduction in renal blood flow of 7% but did not change either glomerular filtration rate, urine flow, calcium excretion or absolute and fractional sodium excretions. 4 During administration of the selective α1-adrenoceptor antagonist, idazoxan, renal nerve stimulation (1.0–1.5 Hz) significantly reduced renal blood flow by 4% and glomerular filtration rate by 7%; at the same time there were significant falls in urine flow of 43%, calcium excretion of 43% and absolute and fractional sodium excretions of 41% and 37%, respectively. 5 These results show that low frequency renal nerve stimulation causes an anticalciuresis, independent of renal haemodynamics, which represents an increase in tubular reabsorption of calcium. This effect was blocked by prazosin but not idazoxan which is consistent with the mediation of α1-adrenoceptors. The neurally-induced antinatriuresis also appeared to be dependent on the activation of α1-adrenoceptors.