Muscarinic inhibition of cardiac norepinephrine and neuropeptide Y release during ischemia and reperfusion

• Verfasst von: Haunstetter, Armin [VerfasserIn]
• Verfasst von: Haass, Markus [VerfasserIn]
• Verfasst von: Yi, Xiaozhong [VerfasserIn]
• Verfasst von: Krüger, Carsten [VerfasserIn]
• Verfasst von: Kübler, Wolfgang [VerfasserIn]
• Titel: Muscarinic inhibition of cardiac norepinephrine and neuropeptide Y release during ischemia and reperfusion
• Verf.angabe: Armin Haunstetter, Markus Haass, Xiaozhong Yi, Carsten Krüger and Wolfgang Kübler
• E-Jahr: 1994
• Jahr: December 1, 1994
• Umfang: 7 S.
• Fussnoten: Gesehen am 12.05.2025
• Titel Quelle: Enthalten in: American journal of physiology. Regulatory, integrative and comparative physiology
• Ort Quelle: Bethesda, Md. : American Physiological Society, 1977
• Jahr Quelle: 1994
• Band/Heft Quelle: 267(1994), 6, Seite R1552-R1558
• ISSN Quelle: 1522-1490
• DOI: doi:10.1152/ajpregu.1994.267.6.R1552
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1925313778

Abstract

It was the aim of the present study to characterize the modulatory effect of muscarinic agonists on the overflow of norepinephrine and neuropeptide Y (NPY) from the in situ perfused guinea pig heart, induced by electrical stimulation of the left stellate ganglion (6 Hz, 5 V, 1 min). The muscarinic agonists oxotremorine (0.01-1 microM) and carbachol (0.1-10 microM) reduced norepinephrine and NPY overflow in a concentration-dependent manner to approximately 30% of control. The inhibitory effect of carbachol was antagonized by the unspecific muscarinic antagonist atropine (1 microM) but not by the nicotinic antagonist hexamethonium (100 microM). The M2-specific antagonist AF-DX-116BS was 25 times more potent than the M1-specific antagonist pirenzepine in antagonizing the inhibitory effect of carbachol [50% inhibitory concentration (IC50) = 0.2 microM for AF-DX-116BS; IC50 = 5.0 microM for pirenzepine]. These findings indicate that presynaptic muscarinic inhibition of stimulated norepinephrine and NPY release from the guinea pig heart is mediated mainly by activation of M2 receptors. As early as 2 min after stop-flow ischemia, the inhibitory effect of carbachol (10 microM) on the stimulation-evoked overflow of norepinephrine and NPY was lost. On reperfusion with oxygenated buffer after 10 min of stop-flow ischemia the inhibitory effect of carbachol (10 microM) on stimulation-induced norepinephrine and NPY overflow recovered within 3 min.