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 / 中华心血管病杂志
Chinese Journal of Cardiology
;
(12): 537-540, 2006.
Artigo
em Chinês
| WPRIM
| ID: wpr-295280
ABSTRACT
<p><b>OBJECTIVE</b>To 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.</p><p><b>METHOD</b>Using whole cell patch-clamp technique, we quantitatively measured the ionic intensity and density of L-Type Ca(2+) channel (I(Ca-L)).</p><p><b>RESULTS</b>The 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.</p><p><b>CONCLUSIONS</b>The 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.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Farmacologia
/
Autoanticorpos
/
Técnicas de Patch-Clamp
/
Canais de Cálcio Tipo L
/
Miócitos Cardíacos
/
Soro
/
Receptor Muscarínico M2
/
Alergia e Imunologia
/
Cobaias
/
Insuficiência Cardíaca
Limite:
Animais
/
Feminino
/
Humanos
/
Masculino
Idioma:
Chinês
Revista:
Chinese Journal of Cardiology
Ano de publicação:
2006
Tipo de documento:
Artigo
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