Osmolality: a physiological long-term regulator of lumbar sympathetic nerve activity and arterial pressure

Acute infusion of hypertonic fluid increases mean arterial pressure (MAP) in part by elevating nonrenal sympathetic activity. However, it is not known whether chronic, physiological increases in osmolality also increase sympathetic activity. To test this hypothesis, MAP, heart rate (HR), and lumbar sympathetic nerve activity (LSNA) were measured in conscious, 48-h water-deprived rats (WD) during a progressive reduction in osmolality produced by a 2-h systemic infusion (0.12 ml/min) of 5% dextrose in water (5DW). Water deprivation significantly increased osmolality (308 +/- 2 vs. 290 +/- 2 mosmol/kgH2O, P < 0.001), HR (453 +/- 7 vs. 421 +/- 10 beats/min, P < 0.05), and LSNA (63.5 +/- 1.8 vs. 51.9 +/- 3.8% baroreflex maximum, P < 0.01). Two hours of 5DW infusion reduced osmolality (-15 +/- 5 mosmol/kgH2O), LSNA (-23 +/- 3% baseline), and MAP (-10 +/- 1 mmHg). To evaluate the role of vasopressin in these changes, rats were pretreated with a V1-vasopressin receptor antagonist. The antagonist lowered MAP (-5 +/- 1 mmHg) and elevated HR (32 +/- 7 beats/min) and LSNA (11 +/- 3% baseline) in WD (P < 0. 05), but not in water-replete, rats. 5DW infusion had a similar cumulative effect on all variables in V1-blocked WD rats, but had no effect in water-replete rats. Infusion of the same volume of normal saline in WD rats did not change osmolality, LSNA or MAP. Together these data indicate that, in dehydrated rats, vasopressin supports MAP and suppresses LSNA and HR and that physiological changes in osmolality directly influence sympathetic activity and blood pressure independently of changes in vasopressin and blood volume.