Dual effects of angiotensin II on calcium currents in neonatal rat nodose neurons

Angiotensin II (AII) reversibly modulates calcium current in isolated neonatal rat nodose ganglion cells by two different pathways. A maximum inhibitory effect of 43 +/- 6% (n = 25) of the peak calcium current at -10 mV was observed at 10 nM AII. The IC50 of the inhibitory response was 100 pM. Losar...

Full description

Saved in:
Bibliographic Details
Published in:The Journal of neuroscience 1994-11, Vol.14 (11), p.7159-7167
Main Authors: Bacal, K, Kunze, DL
Format: Article
Language:English
Subjects:
Angiotensin II - antagonists & inhibitors
Angiotensin II - physiology
Animals
Animals, Newborn
Biphenyl Compounds - pharmacology
Calcium Channel Blockers - pharmacology
Calcium Channels - drug effects
Calcium Channels - physiology
Female
Imidazoles - pharmacology
In Vitro Techniques
Losartan
Male
Neurons - physiology
Nodose Ganglion - physiology
omega-Conotoxin GVIA
Peptides - pharmacology
Pertussis Toxin
Rats
Rats, Sprague-Dawley
Tetrazoles - pharmacology
Virulence Factors, Bordetella - pharmacology
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Angiotensin II (AII) reversibly modulates calcium current in isolated neonatal rat nodose ganglion cells by two different pathways. A maximum inhibitory effect of 43 +/- 6% (n = 25) of the peak calcium current at -10 mV was observed at 10 nM AII. The IC50 of the inhibitory response was 100 pM. Losartan, a specific antagonist for the AT1 type of AII receptor, abolished the AII-induced inhibition, as did preincubation with pertussis toxin (PTX). When omega-conotoxin GVIA (CTX) was added to the bath solution, AII produced no inhibition of the remaining calcium current, indicating that the AII inhibition was mediated through CTX-sensitive calcium channels. Reversible facilitation of calcium current was seen more rarely. The AII-induced facilitation was unaffected by losartan and PTX, indicating that the effect is mediated by a non-AT1 receptor and does not depend upon a PTX-sensitive G-protein. The facilitation is present when the CTX-sensitive current has been blocked and involves activation of a reserve pool of dihydropyridine (DHP)-sensitive channels. In general, a particular neuron exhibited either inhibition or facilitation. However, in some neurons both inhibition and facilitation could be demonstrated in the presence of the appropriate blocking agents.
ISSN:0270-6474
1529-2401
DOI:10.1523/jneurosci.14-11-07159.1994