Characteristics of vasopressin release during controlled reduction in arterial pressure.

Because of the interruption of the descending sympathetic nervous pathways, individuals with cervical spinal cord injury experience orthostatic hypotension when in an upright posture. The changes in hemodynamic parameters that occur during upright posture can be closely monitored and quantitated during progressive head-up tilting on a tilt table. We have utilized this method to assess the response of vasopressin and other vasoactive hormones to gradual, progressive reductions in arterial pressure and to identify possible threshold responses to baroreceptor stimulation in human subjects. Studies were performed in 12 quadriplegic subjects, 3 paraplegic subjects, and 3 normal control subjects. Data from the studies in paraplegic and normal subjects did not differ and were pooled as control data. In quadriplegic subjects, mean arterial pressure (MAP) decreased from 93 +/- 4 mm Hg to 60 +/- 3 mm Hg in a closely correlated (r = 0.948, p < 0.002) linear relationship with increasing degrees of tilt, whereas in control subjects, MAP increased from 81 +/- 4 to 88 +/- 3 mm Hg. Plasma vasopressin concentrations (Pavp) increased minimally in quadriplegic subjects until MAP was reduced to levels that were 25% to 30% lower than MAP with subjects in the supine posture. Beyond this level of hypotension, Pavp increased markedly. Log-linear regression analysis of these data showed a highly significant correlation (r = 0.85, p < 0.0002) between in Pavp and MAP, which defines Pavp as an exponential function of decreasing MAP. Changes in Pavp in control subjects were minimal during incremental head-up tilting. In contrast, plasma renin activity (PRA) increased in both quadriplegic and control subjects. Log-linear regression analysis of these data showed highly significant correlates between in PRA and degree of tilt in both quadriplegic (r = 0.958, p < 0.0002) and control (r = 0.873, p < 0.0002) subjects. Plasma atrial natriuretic peptide concentrations decreased linearly with increasing degrees of tilt. The rate of decline in Panp was greater in quadriplegic than in control subjects. These studies provide additional evidence that Pavp increases exponentially as a function of decreasing MAP and suggest that a critical threshold level of hypotension exists at which vasopressin release accelerates rapidly in response to baroreceptor stimulation. At this level of reduced MAP, Pavp reaches levels that are potentially capable of exerting a pressor effect.