Dietary salt loading exacerbates the increase in sympathetic nerve activity caused by intravenous insulin infusion in rats.

Obesity and type 2 diabetes mellitus frequently produce chronic elevations in blood insulin levels. Importantly, hyperinsulinemia stimulates increases in sympathetic nerve activity that may predispose to hypertension, atherosclerosis, and end-organ damage. Because depletion of dietary salt (NaCl) increases angiotensin II levels, which has been shown to enhance sympathetic responses to excitatory stimuli such as thermal stimulation and bicuculline in the hypothalamus, we predicted that insulin-induced elevations in lumbar sympathetic activity would be augmented by low NaCl and suppressed by high dietary NaCl. Adult male Sprague-Dawley rats were randomized into groups receiving low (0.0 mEq/d, n = 10), normal (2.0 mEq/d, n = 10), and high (5.7 mEq/d, n = 10) NaCl for a period of 8 days. After this, the animals were anesthetized for measurement of heart rate, mean arterial pressure, and lumbar sympathetic nerve activity during 110 minutes of intravenous insulin infusion (15 mU/kg per minute) with euglycemic clamp. Insulin administration caused modest blood pressure decreases accompanied by heart rate increases that were similar across the 3 dietary groups. Unexpectedly, sympathetic increases to insulin were lowest in the low-NaCl group (100%-135% +/- 24%), moderate in the normal-NaCl group (100%-170% +/- 23%), and greatest in the high-NaCl group (100%-252% +/- 39%). Dietary NaCl level did not affect baseline blood glucose or insulin sensitivity as assessed by euglycemic clamp. These findings indicate that dietary salt loading exacerbates the lumbar sympathoexcitatory response to intravenous insulin infusion in rats.