EFFECTS OF VASOPRESSIN V-1-RECEPTOR BLOCKADE DURING ACUTE AND SUSTAINED HYPOVOLEMIC HYPOTENSION

Citation
Bm. Wall et al., EFFECTS OF VASOPRESSIN V-1-RECEPTOR BLOCKADE DURING ACUTE AND SUSTAINED HYPOVOLEMIC HYPOTENSION, American journal of physiology. Regulatory, integrative and comparative physiology, 39(2), 1996, pp. 356-364
Citations number
42
Categorie Soggetti
Physiology
ISSN journal
03636119
Volume
39
Issue
2
Year of publication
1996
Pages
356 - 364
Database
ISI
SICI code
0363-6119(1996)39:2<356:EOVVBD>2.0.ZU;2-L
Abstract
The response of vasopressin and its role in the maintenance of arteria l pressure during and after development of hypotensive central hypovol emia were studied in tilt table studies in quadriplegic subjects. The studies were performed during acute head-up tilting to a maximally tol erated degree of tilt (8 subjects) and during sustained head-up tilt f ollowing a 20% reduction in mean arterial pressure (MAP) (11 subjects) . Studies in all subjects were performed on two separate days, once wi th and once without administration of a selective vasopressin V-1-rece ptor antagonist. During acute head-up tilting, plasma vasopressin conc entrations (P-AVP) did not increase significantly until MAP decreased to similar to 60 mmHg at maximal tilt. There was no difference in the degree of hypotension produced in the presence compared with the absen ce of V-1-receptor blockade. There was also no difference in plasma re nin activity (PRA) or in plasma cortisol or aldosterone concentrations at maximal tilt. In contrast, during sustained head-up tilt following a 20% reduction in arterial pressures, systolic and mean arterial pre ssures were significantly lower and PRA was significantly higher in th e presence than in the absence of V-1-receptor blockade. P-AVP increas ed and was significantly higher after 30 min of sustained tilt than pr etilt P-AVP in supine posture. These studies do not provide evidence o f a role for vasopressin in the maintenance of arterial pressure durin g the acute development of hypotensive hypovolemia in human subjects, but they do provide evidence of a modest role for vasopressin in the m aintenance of arterial pressure when the effect of hypovolemia is more moderate and sustained.