Vasopressin release during endotoxaemic shock in mice lacking inducible nitric oxide synthase.
We tested the hypothesis that nitric oxide (NO) arising from the action of inducible nitric oxide synthase (iNOS) is responsible for the deficiency in vasopressin (AVP) release and consequent hypotension during endotoxaemic shock. Wild-type (WT) and iNOS knockout mice (iNOS(-/-)) were given either saline or Escherichia coli lipopolysaccharide (LPS, 1.0 mg/kg i.v., final volume 0.03 ml). Mean arterial blood pressure (MAP) was measured and plasma AVP levels determined before and after LPS or saline injection. In WT mice, MAP was significantly lower 2 h after LPS administration and remained low for the remainder of the 6-h observation period. AVP plasma levels were increased at the 2nd and 4th h of the experiment, returning thereafter to basal levels. Conversely, LPS injection in iNOS iNOS(-/-) mice elicited a sustained increase in plasma AVP concentration and attenuated the fall in blood pressure. These data indicate that NO arising from the iNOS plays an important inhibitory role in AVP release during endotoxaemia and may be responsible for the hypotension occurring during this vasodilatory shock.
Carnio
Evelin C
EC
Escola de Enfermagem de Ribeirão Preto, Universidade de São Paulo, 14040-902-Ribeirão Preto, São Paulo, Brazil. carnioec@eerp.usp.br
Stabile
Angelita M
AM
Batalhão
Marcelo E
ME
Silva
João Santana
JS
Antunes-Rodrigues
José
J
Branco
Luiz G S
LG
Magder
Sheldon
S
D000818:Animals; D001127:Arginine Vasopressin / Q000378:metabolism*; D001794:Blood Pressure / Q000187:drug effects; D005260:Female; D008070:Lipopolysaccharides; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009569:Nitric Oxide / Q000502:physiology; D052247:Nitric Oxide Synthase Type II / Q000096:biosynthesis / Q000172:deficiency; D012772:Shock, Septic / Q000503:physiopathology*
D008070:Lipopolysaccharides; D001127:Arginine Vasopressin; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II