Progressive increments of dietary sodium markedly exaggerated the liberation of catecholamines following renal nerve stimulation and the hemodynamic response of the kidney in dogs.
For 10 days, dogs were fed a normal salt diet containing 70 mequiv. Na+/day (NSD) followed by a high salt diet containing 170 mequiv. Na+/day (HSD) or 240 mequiv. Na+/day (VHSD), or the order was reversed. K+ in these diets was fixed at 40 mequiv./day. The different diets did not influence the basal level of serum catecholamines (CA). Intravenous angiotensin II (ATII) in subpressor doses produced, under NSD and HSD, an increase in serum CA accompanied by reductions in total renal blood flow as well as regional blood flow rates (microspheres), mostly in the deeper regions of the cortex. Under VHSD, ATII did not affect serum CA and barely decreased total renal blood flow, reducing regional blood flow rate in C3 and C4 only. The increase in renal vein serum CA produced by renal nerve stimulation was potentiated by ATII but under constant plasma levels of the latter, progressive increments of Na+ in the diet markedly exaggerated the liberation of CA following renal nerve stimulation and the hemodynamic response of the kidney. We conclude that the Na+ content in the diet markedly influences the increase in serum CA after renal nerve stimulation and greatly influences the response of that organ to renal nerve stimulation.
Carrière et al. (Mon,) reported a other. High salt diet vs. Normal salt diet (70 mequiv. Na+/day) was evaluated on Serum catecholamine release and renal blood flow response to angiotensin II and renal nerve stimulation. Progressive increments of dietary sodium markedly exaggerated the liberation of catecholamines following renal nerve stimulation and the hemodynamic response of the kidney in dogs.
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