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Different Regulation of Atrial ANP Release through Neuropeptide Y₂ and Y₄ Receptors
Feng Lian Piao,Kuichang Yuan,Guang Yi Bai,한정희,박우현,김선희 대한의학회 2008 Journal of Korean medical science Vol.23 No.6
Neuropeptide Y (NPY) receptors are present in cardiac membranes. However, its physiological roles in the heart are not clear. The aim of this study was to define the direct effects of pancreatic polypeptide (PP) on atrial dynamics and atrial natriuretic peptide (ANP) release in perfused beating atria. Pancreatic polypeptides, a NPY Y₄ receptor agonist, decreased atrial contractility but was not dose-dependent. The ANP release was stimulated by PP in a dose-dependent manner. GR 23118, a NPY Y₄ receptor agonist, also increased the ANP release and the potency was greater than PP. In contrast, peptide YY (3-36) (PYY), an NPY Y2 receptor agonist, suppressed the release of ANP with positive inotropy. NPY, an agonist for Y1, 2, 5 receptor, did not cause any significant changes. The pretreatment of NPY (18-36), an antagonist for NPY Y₃ receptor, markedly attenuated the stimulation of ANP release by PP but did not affect the suppression of ANP release by PYY. BIIE0246, an antagonist for NPY Y₂ receptor, attenuated the suppression of ANP release by PYY. The responsiveness of atrial contractility to PP or PYY was not affected by either of the antagonists. These results suggest that NPY Y₄ and Y₂ receptor differently regulate the release of atrial ANP.
Piao, Feng Lian,Yuan, Kuichang,Bai, Guang Yi,Han, Jeong Hee,Park, Woo Hyun,Kim, Suhn Hee The Korean Academy of Medical Sciences 2008 JOURNAL OF KOREAN MEDICAL SCIENCE Vol.23 No.6
<P>Neuropeptide Y (NPY) receptors are present in cardiac membranes. However, its physiological roles in the heart are not clear. The aim of this study was to define the direct effects of pancreatic polypeptide (PP) on atrial dynamics and atrial natriuretic peptide (ANP) release in perfused beating atria. Pancreatic polypeptides, a NPY Y<SUB>4</SUB> receptor agonist, decreased atrial contractility but was not dose-dependent. The ANP release was stimulated by PP in a dose-dependent manner. GR 23118, a NPY Y<SUB>4</SUB> receptor agonist, also increased the ANP release and the potency was greater than PP. In contrast, peptide YY (3-36) (PYY), an NPY Y<SUB>2</SUB> receptor agonist, suppressed the release of ANP with positive inotropy. NPY, an agonist for Y<SUB>1, 2, 5</SUB> receptor, did not cause any significant changes. The pretreatment of NPY (18-36), an antagonist for NPY Y<SUB>3</SUB> receptor, markedly attenuated the stimulation of ANP release by PP but did not affect the suppression of ANP release by PYY. BIIE0246, an antagonist for NPY Y<SUB>2</SUB> receptor, attenuated the suppression of ANP release by PYY. The responsiveness of atrial contractility to PP or PYY was not affected by either of the antagonists. These results suggest that NPY Y<SUB>4</SUB> and Y<SUB>2</SUB> receptor differently regulate the release of atrial ANP.</P>