Reflex control of osmotically stimulated vasopressin in normal humans.

Previous studies have shown that in normal humans plasma arginine vasopressin (AVP) does not increase in response to unloading of cardiopulmonary and sinoaortic baroreceptors produced by lower body negative pressure (LBNP) unless hypotension occurs. To assess whether prior osmotic stimulation of AVP might bring out latent sensitivity to nonosmotic control mechanisms in humans we studied the response of plasma AVP to graded LBNP after a 105-min infusion of 5% saline in a group of eight normal individuals. During the infusion and before LBNP, serum osmolality increased from 288 +/- 9 to 300 +/- 10 mosmol/kg, and plasma AVP increased from 4.4 +/- 1.7 to 8.0 +/- 2.5 pg/ml. Neither osmolality nor AVP changed significantly during two stages of LBNP that first reduced central venous pressure alone and then reduced central venous pressure with accompanying tachycardia and narrowing of the pulse pressure. Time control studies performed in five individuals subjected to central venous catheterization and an identical hypertonic saline infusion failed to show significant spontaneous changes in AVP during a comparable interval after the infusions but without LBNP. Thus osmotic stimulation with hypertonic saline did not render AVP more sensitive to nonhypotensive unloading of cardiopulmonary and sinoaortic baroreceptors in normal humans.