|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Departamento de Bioquímica y Biología Molecular y Fisiología. Facultad de Medicina- IBGM. Universidad de Valladolid CSIC, 47005 Valladolid, Spain
2 Instituto de Neurociencias de Alicante Universidad Miguel Hernández CSIC, 03550 San Juan, Alicante, Spain
We have defined Ca2+ channel subtypes expressed in rabbit carotid body (CB) chemoreceptor cells and their participation in the stimulus-evoked catecholamine (CA) release. Ca2+ currents (ICa) activated at 30 mV, peaked at +10 mV and were fully blocked by 200 µM Cd2+. L-type channels (sensitive to 2 µM nisoldipine) activated at 30 mV and carried 21 ± 2% of total ICa. Non-L-type channels activated at potentials positive to 10 mV and carried: N channels (sensitive to 1 µM
-conotoxin-GVIA) 16 ± 1% of total ICa, P/Q channels (sensitive to 3 µM
-conotoxin-MVIIC after nisoldipine plus GVIA) 23 ± 3% of total ICa and R channels (resistant to all blockers combined) 40 ± 3% of total ICa. CA release induced by hypoxia, hypercapnic acidosis, dinitrophenol (DNP) and high K+o in the intact CB was inhibited by 7998% by 200 µM Cd2+. Hypoxia, hypercapnic acidosis and DNP, depolarized chemoreceptor cells and eventually generated repetitive action potential discharge. Nisoldipine plus MVIIC nearly abolished the release of CAs induced by hypoxia and hypercapnic acidosis and reduced by 74% that induced by DNP. All these secretory responses were insensitive to GVIA. 30 and 100 mM K+o brought resting membrane potential (Em) of chemoreceptor cells (48.1 ± 1.2 mV) to 22.5 and +7.2 mV, respectively. Thirty millimolar K+o-evoked release was abolished by nisoldipine but that induced by 100 mM K+o was mediated by activation of L, N, and P/Q channels. Data show that tested stimuli depolarize rabbit CB chemoreceptor cells and elicit CA release through Ca2+ entry via voltage-activated channels. Only L and P/Q channels are tightly coupled to the secretion of CA.
(Received 28 September 2004;
accepted after revision 3 November 2004;
first published online 4 November 2004)
Corresponding author L. Almaraz: Instituto de Neurociencias de Alicante, Universidad Miguel Hernández CSIC, Campus de San Juan, 03550 San Juan, Alicante, Spain. Email: laura.almaraz{at}umh.es
This article has been cited by other articles:
![]() |
J. R. Lopez-Lopez and M. T. Perez-Garcia An ASIC Channel for Acid Chemotransduction Circ. Res., November 9, 2007; 101(10): 965 - 967. [Full Text] [PDF] |
||||
![]() |
A. J. Rico, J. Prieto-Lloret, C. Gonzalez, and R. Rigual Hypoxia and acidosis increase the secretion of catecholamines in the neonatal rat adrenal medulla: an in vitro study Am J Physiol Cell Physiol, December 1, 2005; 289(6): C1417 - C1425. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |