Gap junction-dependent increases in smooth muscle cAMP underpin the EDHF phenomenon in rabbit arteries

Biochemical and Biophysical Research Communications
Hannah J TaylorTudor M Griffith

Abstract

We have investigated the role of cAMP in nitric oxide (NO)- and prostanoid-independent vascular relaxations evoked by acetylcholine (ACh) in isolated arteries and perfused ear preparations from the rabbit. These EDHF-type responses are shown to be associated with elevated cAMP levels specifically in smooth muscle and are attenuated by blocking adenylyl cyclase or protein kinase A (PKA). Relaxations are amplified by 3-isobutyl-1-methylxanthine, which prevents cAMP hydrolysis, while remaining susceptible to inhibition by the combination of two K(Ca) channel blockers, apamin and charybdotoxin. Analogous endothelium- and cAMP-dependent relaxations were evoked by cyclopiazonic acid (CPA) which stimulates Ca(2+) influx via channels linked to the depletion of Ca(2+) stores. Responses to ACh and CPA were both inhibited by interrupting cell-to-cell coupling via gap junctions with 18alpha-glycyrrhetinic acid and a connexin-specific Gap 27 peptide. The findings suggest that EDHF-type responses are initiated by capacitative Ca(2+) influx into the endothelium and propagated by direct intercellular communication to effect relaxation via cAMP/PKA-dependent phosphorylation events in smooth muscle.

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Citations

Jan 11, 2003·British Journal of Pharmacology·Ragnhild StøenJan Olof G Karlsson
Jun 12, 2013·Pflügers Archiv : European journal of physiology·David C EllinsworthShaun L Sandow
Apr 25, 2002·Proceedings of the National Academy of Sciences of the United States of America·Tudor M GriffithDavid H Edwards
Apr 10, 2010·Pflügers Archiv : European journal of physiology·Cor de Wit, Tudor M Griffith
May 4, 2005·Proceedings of the National Academy of Sciences of the United States of America·Tudor M GriffithDavid H Edwards
Dec 3, 2003·Proceedings of the National Academy of Sciences of the United States of America·Andrew T ChaytorTudor M Griffith
Jan 9, 2007·Trends in Pharmacological Sciences·Shaun L Sandow, Marianne Tare
May 8, 2004·British Journal of Pharmacology·Tudor M GriffithChristopher McGuigan
Aug 10, 2006·Clinical and Experimental Pharmacology & Physiology·Andrei SibaevMartin Storr
Sep 2, 2005·European Journal of Pharmacology·Rika EgamiHitoo Nakano
Mar 16, 2004·American Journal of Physiology. Heart and Circulatory Physiology·Yasuo KansuiMitsuo Iida
May 24, 2005·American Journal of Physiology. Heart and Circulatory Physiology·Takayuki MatsumotoKatsuo Kamata
Mar 29, 2014·Pharmacological Reviews·Marie BillaudBrant E Isakson
May 17, 2005·American Journal of Physiology. Heart and Circulatory Physiology·Takayuki MatsumotoKatsuo Kamata
May 8, 2004·American Journal of Physiology. Heart and Circulatory Physiology·Takayuki MatsumotoKatsuo Kamata
Aug 16, 2002·American Journal of Physiology. Heart and Circulatory Physiology·H L XuD A Pelligrino
Jun 10, 2003·American Journal of Physiology. Heart and Circulatory Physiology·Takayuki MatsumotoKatsuo Kamata
Jun 26, 2007·Journal of Vascular Research·David H EdwardsTudor M Griffith
Jan 31, 2004·American Journal of Physiology. Regulatory, Integrative and Comparative Physiology·Leonid LukshaKarolina Kublickiene
May 26, 2005·Anesthesiology·Robert M BryanSean P Marrelli
Jan 11, 2003·American Journal of Physiology. Heart and Circulatory Physiology·Yoshiteru MorioIvan F McMurtry
Mar 15, 2002·American Journal of Physiology. Heart and Circulatory Physiology·Andrew T ChaytorTudor M Griffith

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