January 1997
Volume 38, Issue 1
Free
Articles  |   January 1997
Mechanism of adrenomedullin-induced relaxation in isolated canine retinal arteries.
Author Affiliations
  • T Okamura
    Department of Pharmacology, Shiga University of Medical Science, Ohtsu, Japan.
  • K Ayajiki
    Department of Pharmacology, Shiga University of Medical Science, Ohtsu, Japan.
  • K Kangawa
    Department of Pharmacology, Shiga University of Medical Science, Ohtsu, Japan.
  • N Toda
    Department of Pharmacology, Shiga University of Medical Science, Ohtsu, Japan.
Investigative Ophthalmology & Visual Science January 1997, Vol.38, 56-61. doi:
  • Views
  • PDF
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      T Okamura, K Ayajiki, K Kangawa, N Toda; Mechanism of adrenomedullin-induced relaxation in isolated canine retinal arteries.. Invest. Ophthalmol. Vis. Sci. 1997;38(1):56-61.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract

PURPOSE: To analyze the mechanism of action of adrenomedullin (AM), a peptide recently isolated from human pheochromocytoma, in isolated canine central retinal arteries and to compare the action of calcitonin gene-related peptide (CCRP). METHODS: Changes in isometric tension were recorded in helical strips of the arteries with and without the endothelium. RESULTS: Both AM and CGRP produced relaxation: EC50s were 2.62 and 0.71 x 10(-9) mol/l, respectively, and maximal relaxations were 85.1% and 84.3%, respectively. The AM-induced relaxation was endothelium-independent and unaffected by indomethacin, Ng-nitro-L-arginine, methylene blue, and glibencaalmide. Treatment with [8-37] CGRP markedly inhibited the relaxations caused by AM and CGRP. Treatment with a high concentration of sodium nitroprusside abolished the relaxation caused by nitroglycerin and atrial natriuretic peptide and reduced the relaxation caused by AM and CGRP. A high concentration of beraprost, a stable analog of prostaglandin I2, suppressed the response to AM and CGRP but not to nitroglycerin. CONCLUSIONS: Endothelium-independent relaxations to AM of canine retinal arteries may be mediated primarily by intracellular cyclic adenosine monophosphate by stimulation of CGRP1 receptors and partially by cyclic guanosine monophosphate; cyclic guanosine monophosphate is unlikely ot be produced by methylene blue-sensitive soluble guanylate cyclase. Prostanoids, nitric oxide, and adenosine triphosphate-dependent K+ channel opening do not appear to be involved in the AM-induced relaxation.

×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×