Is osmolality a long-term regulator of renal sympathetic nerve activity in conscious water-deprived rats?
Acute increases in osmolality suppress renal sympathetic nerve activity (RSNA). However, it is not known whether prolonged physiological increases in plasma osmolality chronically inhibit RSNA. To address this hypothesis, mean arterial blood pressure (MAP), heart rate (HR), and RSNA were measured during acute normalization of plasma osmolality in conscious rats made hyperosmotic by 48 h of water deprivation. Water deprivation significantly elevated MAP (120 1 vs. 114 3 mmHg, P <0.05) and plasma osmolality (306 1 vs. 293 1 mosmol/kgH20, P < 0.01). When plasma osmolality was subsequently lowered to normal (minus17 1 mosmol/kgH20) with a 2-h (0.12 ml/min) infusion of 5% dextrose in water (5DW), MAP decreased (minus11 1 mmHg), and RSNA increased (25 10% baseline). To assess the role of circulating vasopressin in these changes, rats were pretreated with a V1-vasopressin receptor antagonist before infusion of 5DW. The antagonist lowered MAP (minus4 1 mmHg) and raised RSNA (31 3% baseline
