Display options
Share it on

Mediators Inflamm. 1995;4(1):55-9. doi: 10.1155/S096293519500010X.

Possible bi-directional link between ET(A) receptors and protein kinase C in rat blood vessels.

Mediators of inflammation

A M Northover, B J Northover

Affiliations

  1. Department of Pharmaceutical Sciences School of Applied Sciences De Montfort University Leicester LE1 9BH UK.

PMID: 18475617 PMCID: PMC2365604 DOI: 10.1155/S096293519500010X

Abstract

Possible links have been investigated between activation of protein kinase C (PKC) and endothelin (ET) production by small blood vessels. Perfusion pressures were recorded from rat isolated mesenteric artery, with or without the small intestine attached, before and after addition to the perfusate of either ET-1, ET-3 or the PKC activator 12-deoxyphorbol 13-phenylacetate (DOPPA). Rises in perfusion pressure in response to ET-1 (10(-8) M)or DOPPA (10(-6) M) were reduced significantly by pre-treatment with either the ET(A) receptor antagonist PD151242 (10(-6) M) or the PKC inhibitor Ro 31-8220 (10(-6) M). ET-3 (10(-8) M) had a significant, albeit small, effect only when the gut was still attached to the mesentery. Inthis latter preparation ET-1 and DOPPA increased the permeability of villi microvessels to colloidal carbon in the perfusate. This effect of DOPPA was reduced by pre-treatment with either PD151242 or Ro 31-8220, but the effects of ET-1 were reduced significantly only by Ro 31-8220. ET-3 (10(-8) M) was without effect. The results suggest a possible bi-directional link between ET(A) receptors and PKC in the intestinal vasculature.

References

  1. J Biol Chem. 1989 May 15;264(14):8237-40 - PubMed
  2. FEBS Lett. 1989 Dec 18;259(1):61-3 - PubMed
  3. Biochem Biophys Res Commun. 1993 Sep 15;195(2):1050-6 - PubMed
  4. Br J Exp Pathol. 1975 Feb;56(1):52-61 - PubMed
  5. Am J Physiol. 1994 Mar;266(3 Pt 2):H959-66 - PubMed
  6. Life Sci. 1989;45(21):2051-9 - PubMed
  7. J Pharmacol Exp Ther. 1990 Aug;254(2):393-9 - PubMed
  8. Hypertension. 1991 Aug;18(2):165-70 - PubMed
  9. Nature. 1988 Mar 31;332(6163):411-5 - PubMed
  10. J Mol Cell Cardiol. 1990 Sep;22(9):1017-23 - PubMed
  11. Jpn J Pharmacol. 1991 Nov;57(3):431-5 - PubMed
  12. Eur J Pharmacol. 1994 May 23;257(3):307-10 - PubMed
  13. J Biol Chem. 1989 Sep 5;264(25):14954-9 - PubMed
  14. Circ Res. 1992 Oct;71(4):951-9 - PubMed
  15. Br J Pharmacol. 1994 Apr;111(4):989-96 - PubMed
  16. FEBS Lett. 1988 Apr 25;231(2):440-4 - PubMed
  17. J Pharmacol Toxicol Methods. 1993 Aug;29(4):227-32 - PubMed
  18. Proc Natl Acad Sci U S A. 1989 Apr;86(8):2863-7 - PubMed
  19. Biochem Biophys Res Commun. 1985 Oct 15;132(1):56-62 - PubMed
  20. Br J Pharmacol. 1994 Sep;113(1):49-54 - PubMed
  21. Br J Pharmacol. 1994 Jun;112(2):704-8 - PubMed
  22. J Biol Chem. 1983 Oct 10;258(19):11442-5 - PubMed
  23. Circ Res. 1987 Nov;61(5):632-40 - PubMed
  24. J Hypertens. 1990 Sep;8(9):843-9 - PubMed
  25. Nature. 1990 Dec 20-27;348(6303):732-5 - PubMed
  26. Pharmacol Rev. 1994 Jun;46(2):137-42 - PubMed
  27. Br J Pharmacol. 1991 Dec;104(4):797-804 - PubMed
  28. Agents Actions. 1989 Mar;26(3-4):367-71 - PubMed
  29. Pharmacol Rev. 1986 Sep;38(3):227-72 - PubMed
  30. Inflammation. 1994 Oct;18(5):481-7 - PubMed
  31. J Biol Chem. 1985 Apr 25;260(8):4547-50 - PubMed
  32. Eur J Pharmacol. 1993 Nov 30;250(1):85-94 - PubMed
  33. Am J Physiol. 1993 Jan;264(1 Pt 2):H150-6 - PubMed

Publication Types