Norepinephrine release from sympathetic nerves in human right atria can be inhibited by activation of prejunctional D2-receptors and α2-adrenergic receptors.
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D2-receptor agonism may inhibit atrial norepinephrine release; leaves open translation to human sympathetic regulation or therapy.
Summary: The aim of the present study was to investigate dopamine receptor- and α-adrenergic receptor-mediated modulation of norepinephrine release in human atria. Right atrial appendages were incubated with 3H-norepinephrine, placed in superfusion chambers, and field-stimulated by platinum electrodes at a frequency of 5 Hz. The stimulation-induced (S-I) outflow of radioactivity was taken as an index of norepinephrine release. The dopamine D2-receptor agonist quinpirole (0.03–3 μM) concentration dependently inhibited the S-I outflow of radioactivity with an EC50 of 0.03 μM. The concentration-response curve of quinpirole was potently shifted to the right by the D2-receptor antagonists domperidone (0.003 μM, pKB ∼9.2) and S(–)-sulpiride (0.1 μM, pKB ∼8.6). The D1-receptor antagonist SCH 23390 (1 μM) slightly (pKB $6.9) shifted the concentration-response curve of quinpirole, whereas the α2-adrenergic antagonist rauwolscine (0.01 μM) and the α1-adrenergic antagonist prazosin (1 μM) had no effect. The D1-receptor agonist did not affect fenoldopam (0.03 and 0.3 μM), but fenoldopam (3 μM) enhanced the S-I outflow of radioactivity. The facilitatory effect of fenoldopam (3 μM) was unaltered by SCH 23390 (0.1 μM) but prevented by rauwolscine (0.01 μM). The α2 adrenergic agonist UK 14304 (0.01–1 μM) (EC50: 0.06 μM), but not the α1-adrenergic agonist methoxamine (0.3–30 μM), inhibited S-I outflow of radioactivity. The concentration-response curve of UK 14304 was shifted to the right by rauwolscine (0.01 μM, pKB ∼8.6). SCH 23390 (1 μM), S(–)-sulpiride (1 μM), and the α1-adrenergic antagonist prazosin (1 μM) did not shift the concentration-response curve of UK 14304. Rauwolscine (0.01–1 μM) by itself, in contrast to sulpiride (0.1–10 μM) by itself, enhanced S-I outflow of radioactivity. The data suggest that norepinephrine release from sympathetic nerves in human right atria can be inhibited by activation of prejunctional D2-receptors and α2-adrenergic receptors. Prejunctional α2 adrenergic receptors, in contrast to dopamine D2receptors, seem to be activated by their respective endogenous ligand in human atria.
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Rump et al. (1995) studied this question.
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