Altered hepatic vasopressin and alpha 1-adrenergic receptors after chronic endotoxin infusion.
Sepsis and septic shock are complicated by a number of hemodynamic and metabolic aberrations. These include catecholamine refractoriness and altered glucose metabolism. Recently, a nonshock rat model of continuous endotoxin infusion via an implanted osmotic pump was developed that reproduces some of the metabolic and cardiovascular findings of human sepsis. By using this model, we have found a decreased number of hepatic plasma membrane alpha 1-adrenergic and [Arg8]vasopressin receptors in rats continuously infused with endotoxin. There was a significant decrease in [3H]prazosin (35 +/- 7%) and [3H] [Arg8]vasopressin (43 +/- 8%) receptors after 30 h of continuous endotoxin infusion with no change in affinity. The ability of norepinephrine to form the high-affinity complex with alpha 1-adrenergic receptors was not altered after chronic endotoxin infusion. The results are consistent with the concept that alterations in receptor number might underlie certain of the metabolic consequences of chronic sepsis.
D000818:Animals; D004731:Endotoxins / Q000494:pharmacology*; D004926:Escherichia coli; D008099:Liver / Q000378:metabolism*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects* / Q000378:metabolism; D011945:Receptors, Angiotensin / Q000378:metabolism; D017483:Receptors, Vasopressin; D013997:Time Factors; D014316:Tritium; D014667:Vasopressins / Q000378:metabolism*
D004731:Endotoxins; D011942:Receptors, Adrenergic, alpha; D011945:Receptors, Angiotensin; D017483:Receptors, Vasopressin; D014316:Tritium; D014667:Vasopressins