Effect of natriuretic peptide receptor antagonist on lipopolysaccharide-induced fever in rats: is natriuretic peptide an endogenous antipyretic?

Item request has been placed! ×
Item request cannot be made. ×
loading   Processing Request
Read More Add to Saved list
  • Author(s): Miyoshi M;Miyoshi M; Kitagawa Y; Imoto T; Watanabe T
  • Source:
    The Journal of pharmacology and experimental therapeutics [J Pharmacol Exp Ther] 2006 Sep; Vol. 318 (3), pp. 1163-70. Date of Electronic Publication: 2006 Jun 02.
  • Publication Type:
    Journal Article; Research Support, Non-U.S. Gov't
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: American Society for Pharmacology and Experimental Therapeutics Country of Publication: United States NLM ID: 0376362 Publication Model: Print-Electronic Cited Medium: Print ISSN: 0022-3565 (Print) Linking ISSN: 00223565 NLM ISO Abbreviation: J Pharmacol Exp Ther Subsets: MEDLINE
    • Publication Information:
      Publication: 1999- : Bethesda, MD : American Society for Pharmacology and Experimental Therapeutics
      Original Publication: Baltimore : Williams & Wilkins
    • Subject Terms:
      Fever/*prevention & control ; Guanylate Cyclase/*antagonists & inhibitors ; Lipopolysaccharides/*toxicity ; Natriuretic Peptides/*physiology ; Polysaccharides/*pharmacology ; Receptors, Atrial Natriuretic Factor/*antagonists & inhibitors; Animals ; Atrial Natriuretic Factor/pharmacology ; Body Temperature/drug effects ; Fever/chemically induced ; Interleukin-1/pharmacology ; Male ; Rats ; Rats, Wistar
    • Abstract:
      We investigated whether natriuretic peptide (NP) acts as an endogenous antipyretic inside and/or outside the blood-brain barrier in rats made febrile by systemic administration of bacterial endotoxin (lipopolysaccharide; LPS). Intravenous (i.v.) injection of LPS induced a triphasic fever, the second phase of which was significantly enhanced by an i.v. injection of the NP receptor (A-type and B-type) antagonist HS-142-1, a glucose-caproic acid polymer. In contrast, the same antagonist (i.v.) had no effect on the fever induced by i.v. injection of interleukin (IL)-1beta. An i.v. administration of HS-142-1 enhanced the LPS (i.v.)-induced IL-1beta response in the rat spleen. An i.v. treatment with atrial NP (ANP) significantly attenuated the second phase of the LPS-induced fever. On the other hand, i.c.v. injection of the above-mentioned NP receptor antagonist resulted in an augmentation of the third phase of the fever induced by i.v. administration of LPS, the same phase that was attenuated by ANP given i.c.v. When given intracerebro-ventricularly (i.c.v.), the antagonist had no effect on the fever induced by i.v. IL-1beta. Finally, the fever induced by i.c.v. injection of LPS was not affected even by an i.c.v. administration of the antagonist. These results suggest that the production of pyrogenic cytokines (such as IL-1beta) that follows i.v. LPS injection may be inhibited by NP acting outside the blood-brain barrier, leading to an inhibition of the fever. In contrast, inside the blood-brain barrier NP may inhibit cytokine-independent mechanisms present within the rat brain that mediate LPS (i.v.)-induced fever.
    • Accession Number:
      0 (HS 142-1)
      0 (Interleukin-1)
      0 (Lipopolysaccharides)
      0 (Natriuretic Peptides)
      0 (Polysaccharides)
      85637-73-6 (Atrial Natriuretic Factor)
      EC 4.6.1.2 (Guanylate Cyclase)
      EC 4.6.1.2 (Receptors, Atrial Natriuretic Factor)
      EC 4.6.1.2 (atrial natriuretic factor receptor A)
      EC 4.6.1.2 (atrial natriuretic factor receptor B)
    • Publication Date:
      Date Created: 20060606 Date Completed: 20061010 Latest Revision: 20061115
    • Publication Date:
      20240829
    • Accession Number:
      10.1124/jpet.106.102731
    • Accession Number:
      16751254