TY - JOUR
T1 - Modulation of noradrenaline release through presynaptic α2-adrenoceptors in congestive heart failure
AU - Minatoguchi, Shinya
AU - Ito, Hiroyasu
AU - Ishimura, Koji
AU - Watanabe, Hiroko
AU - Imai, Yoko
AU - Koshiji, Masatoshi
AU - Asano, Kiyoji
AU - Hirakawa, Senri
AU - Fujiwara, Hisayoshi
PY - 1995/9
Y1 - 1995/9
N2 - Stimulation of presynaptic α2-adrenoceptors inhibits the release of noradrenaline from sympathetic nerve endings; however, the extent to which it operates in patients with congestive heart failure is still unknown. To investigate the degree of negative feedback to the release of noradrenaline via presynaptic α2-adrenoceptors at sympathetic nerve endings, we measured plasma noradrenaline levels before and after the injection of phentolamine (i.e., plasma noradrenaline concentration at rest, plasma noradrenaline concentration after phentolamine injection [NAph], and the phentolamine-induced increase in plasma noradrenaline [ΔNAph]). Plasma noradrenaline concentration at rest, NAph, and ΔNAph increased in a stepwise manner from New York Heart Association class I to class III. A positive correlation was found between the plasma noradrenaline at rest and ΔNAph (n = 123, r = 0.697, p < 0.001). These results suggest that the enhanced release of plasma noradrenaline is substantially buffered by the mechanism of noradrenaline release-inhibitory presynaptic α2-adrenoceptors in patients with congestive heart failure, and this buffer serves to protect organs such as the heart from excess sympathetic stimulation.
AB - Stimulation of presynaptic α2-adrenoceptors inhibits the release of noradrenaline from sympathetic nerve endings; however, the extent to which it operates in patients with congestive heart failure is still unknown. To investigate the degree of negative feedback to the release of noradrenaline via presynaptic α2-adrenoceptors at sympathetic nerve endings, we measured plasma noradrenaline levels before and after the injection of phentolamine (i.e., plasma noradrenaline concentration at rest, plasma noradrenaline concentration after phentolamine injection [NAph], and the phentolamine-induced increase in plasma noradrenaline [ΔNAph]). Plasma noradrenaline concentration at rest, NAph, and ΔNAph increased in a stepwise manner from New York Heart Association class I to class III. A positive correlation was found between the plasma noradrenaline at rest and ΔNAph (n = 123, r = 0.697, p < 0.001). These results suggest that the enhanced release of plasma noradrenaline is substantially buffered by the mechanism of noradrenaline release-inhibitory presynaptic α2-adrenoceptors in patients with congestive heart failure, and this buffer serves to protect organs such as the heart from excess sympathetic stimulation.
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U2 - 10.1016/0002-8703(95)90360-7
DO - 10.1016/0002-8703(95)90360-7
M3 - Article
C2 - 7661069
AN - SCOPUS:0029091395
SN - 0002-8703
VL - 130
SP - 516
EP - 521
JO - American Heart Journal
JF - American Heart Journal
IS - 3 PART 1
ER -