Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2008 Apr;131(4):349–364. doi: 10.1085/jgp.200709881

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2008, The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

PMC Copyright notice

Figure 6. — Mathematical simulations of the system described by the schematic in Fig. 5. Panels on left depict the signal being measured, panels on right depict the underlying cAMP signals. (A and B) Simulations of normalized current through CNG channels (I/I _max) due to isoproterenol-induced cAMP signals under control conditions. (C and D) Simulations of isoproterenol-induced currents and cAMP signals in the presence of 20 nM PKI (included in the pipette solution). Including PKI in the pipette solution inhibits PKA-mediated stimulation of PDE activity, allowing increased cAMP levels, but the signal is still transient due to basal PDE4 activity and GRK-mediated receptor desensitization. (E and F) Simulations describing the effect of GRK inhibition (3 μM 59-74E) on isoproterenol-induced signals. The signals are still transient due to PKA-mediated stimulation of PDE4 activity. (G and H) Simulations of currents and cAMP signals when both PKA and GRK activity are inhibited (with PKI and 59-74E). Inhibiting receptor desensitization and the stimulation of PDE4 activity prevents the decay of isoproterenol-induced signals.