Nitric oxide modulation of body fluid and blood pressure homeostases during stress

Brain-derived nitric oxide (NO) modulates the hypothalamo-neurohypophysial system, cardiovascular function and drinking behavior. Under normovolemic isosmotic conditions, NO tonically inhibits the basal release of vasopressin (VP) and oxytocin (OT) from the magnocellular neuroendocrine system. When both intracellular and intravascular volumes decrease during water deprivation, or independently during osmotic stimulation and hemorrhage, the NO inhibitory action on VP secretion is removed while on OT it is enhanced. This results in a preferential release of VP, a mechanism dependent on prostaglandin. NO facilitates drinking behavior, which is stimulated by decreases in intracellular and intravascular volume, and by a mechanism independent of prostaglandin and angiotensin II (ANG II). NO also maintains resting arterial blood pressure. Inhibiting NO synthase (NOS) with L-NAME (icv) increases blood pressure in a biphasic pattern: initially there is a transient increase within 5 min, followed by a long-lasting presser response from 30-120 min. The initial rise in blood pressure results from removing NO attenuation of an ANG LT presser response dependent on prostaglandin, as the peptide-induced elevation in blood pressure is prevented by indomethacin, a cyclooxygenase inhibitor. Vasodilation produced by NO counter-balances osmotic and ANG IT-induced presser responses. Paradoxically, during hemorrhage, vasodilation via brain-derived NO also increases, presumably to maintain peripheral vasodilation and blood flow to vital organs.