Enhanced Sympathoexcitatory and Pressor Responses to Chronic Central Sodium Loading in Dahl Salt-Sensitive Vs. -Resistent Rats
Increased responsiveness to increases in CSF Na+ by high salt intake may contribute to salt-sensitive hypertension in Dahl S rats. To test this hypothesis, Dahl S and R rats received a chronic icv infusion of artificial CSF (aCSF) or aCSF containing 0.8 M Na+ (5 μl/hr) for 14 days, using osmotic minipumps. On day 14 in conscious rats, CSF was sampled and BP, HR and renal sympathetic nerve activity (RSNA) were recorded at rest and in response to air stress, icv α2-adrenoceptor agonist guanabenz (50 μg), icv ouabain (0.6 μg), and iv phenylephrine and nitropusside to estimate baroreflex function. Data are mean±SEM (n=8-13). *p<0.05 vs others.†p<0.05 vs aCSF. Similar chronic increases in CSF Na+ caused more severe hypertension, larger responses to air stress and guanabenz, and more blunting of the arterial baroreflex gain in S vs R rats. These findings suggest that enhanced neuronal responsiveness to CSF Na+ is one of the mechanisms contributing to salt-sensitive hypertension in Dahl S rats.