Purchase this article with an account.
Rong Liu, Josef Flammer, Ivan O. Haefliger; Isoproterenol, Forskolin, and cAMP-Induced Nitric Oxide Production in Pig Ciliary Processes. Invest. Ophthalmol. Vis. Sci. 1999;40(8):1833-1837.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
purpose. To investigate whether isoproterenol and forskolin, two adenylylcyclase
activators, or 8-bromo-cAMP, an adenosine 3′,5′-cyclic monophosphate
(cAMP) analog, increase nitric oxide (NO) production in isolated
porcine ciliary processes.
methods. Nitrite (an NO metabolite) was measured (Griess reaction) before and 2
hours after exposure to 0.1 to 100 μM isoproterenol (aβ
-adrenoreceptor agonist), 0.01 to 100 μM forskolin, or 0.1 to 1000μ
M 8-bromo-cAMP. Some experiments were conducted in the presence of
0.5 mM NG-nitro-l-arginine methyl ester
(l-NAME; a nitric oxide synthase [NOS] inhibitor), 10μ
M propranolol (a β-adrenoreceptor antagonist), or 1 μM KT 5720
(a cAMP-dependent protein kinase inhibitor). cAMP production was also
measured (by immunoassay).
results. Nitrite production was increased by isoproterenol (maximum, 10 μM:
164%; P < 0.001), forskolin (maximum, 10 μM:
254%; P < 0.001), and 8-bromo-cAMP (maximum, 100μ
M: 184%; P < 0.001), an effect prevented by l-NAME (P < 0.05–0.001). Propranolol
inhibited only isoproterenol-induced (10 μM) nitrite production
(P < 0.05), whereas KT 5720 (P < 0.05) inhibited isoproterenol- (10 μM) and 8-bromo-cAMP–induced
(10 μM) nitrite production. Furthermore, cAMP production evoked by
isoproterenol (10 μM, P < 0.05) but not by
forskolin (10 μM, P < 0.001) was inhibited by
propranolol (P < 0.05).
conclusions. In isolated porcine ciliary processes, drugs activating adenylylcyclase
or mimicking cAMP increase the production of NO by a mechanism that
appears to involve both a cAMP-dependent protein kinase and
This PDF is available to Subscribers Only