Effect of serum autoantibodies against the M2 muscarinic acetylcholine receptors from patients with heart failure on L-Type Ca2+ channel activity in guinea pig cardiac myocytes.
- Author:
Guo-bin MIAO
1
;
Jin-chun LIU
;
Shu-yan WANG
;
Xiu-lan LIU
;
Jian ZHANG
;
Lin ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Adult; Aged; Animals; Autoantibodies; pharmacology; Calcium Channels, L-Type; drug effects; Female; Guinea Pigs; Heart Failure; immunology; Humans; Male; Middle Aged; Myocytes, Cardiac; drug effects; metabolism; Patch-Clamp Techniques; Receptor, Muscarinic M2; immunology; Serum; immunology
- From: Chinese Journal of Cardiology 2006;34(6):537-540
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of serum autoantibodies against the human M(2) muscarinic acetylcholine receptors (M(2)-receptors, Abs) from patients with congestive heart failure on L-Type Ca(2+) channel activity in guinea pig cardiac myocytes.
METHODUsing whole cell patch-clamp technique, we quantitatively measured the ionic intensity and density of L-Type Ca(2+) channel (I(Ca-L)).
RESULTSThe M(2)-receptors agonist (carbachol) could decrease the I(Ca-L) peak intensity and density stimulated by isoprenaline from (2111.65 +/- 203.13) pA and (18.83 +/- 1.14) pA/pF to (1230.87 +/- 208.14) pA (P < 0.01) and (10.72 +/- 1.06) pA/pF (P < 0.01). The serum Abs could also decrease I(Ca-L) peak intensity and density [from (1995.21 +/- 195.13) pA and (18.13 +/- 1.03) pA/pF to (636.42 +/- 110.07) pA (P < 0.01) and (5.54 +/- 0.81) pA/pF, P < 0.01]. The M(2)-receptors antagonist, atropine was able to block these effects of carbachol and Abs.
CONCLUSIONSThe circulating serum autoantibodies against the M(2)-receptors has similar effect as M(2)-receptors agonist on decreasing the isoprenaline stimulated I(Ca-L) in guinea pig cardiac myocytes and possess negative inotropic effect. These results further suggest that serum autoantibodies against the human M(2) muscarinic acetylcholine receptors may participate in the pathophysiological processes in patients with heart failure.
