Our group has previously shown in pithed rats that the cardiac sympathetic drive, which produces tachycardic responses, is inhibited by 5‐HT via the activation of prejunctional 5‐HT1B/1D/5 receptors. Interestingly, when 5‐HT2 receptors are chron...
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https://www.riss.kr/link?id=O112706764
2020년
-
0305-1870
1440-1681
SCI;SCIE;SCOPUS
학술저널
403-411 [※수록면이 p5 이하이면, Review, Columns, Editor's Note, Abstract 등일 경우가 있습니다.]
0
상세조회0
다운로드다국어 초록 (Multilingual Abstract)
Our group has previously shown in pithed rats that the cardiac sympathetic drive, which produces tachycardic responses, is inhibited by 5‐HT via the activation of prejunctional 5‐HT1B/1D/5 receptors. Interestingly, when 5‐HT2 receptors are chron...
Our group has previously shown in pithed rats that the cardiac sympathetic drive, which produces tachycardic responses, is inhibited by 5‐HT via the activation of prejunctional 5‐HT1B/1D/5 receptors. Interestingly, when 5‐HT2 receptors are chronically blocked with sarpogrelate, the additional role of cardiac sympatho‐inhibitory 5‐HT1F receptors is unmasked. Although 5‐HT2 receptors mediate tachycardia in rats, and the chronic blockade of 5‐HT2 receptors unmasked 5‐HT7 receptors mediating cardiac vagal inhibition, the role of 5‐HT7 receptors in the modulation of the cardiac sympathetic tone remains virtually unexplored. On this basis, male Wistar rats were pretreated during 14 days with sarpogrelate (a 5‐HT2 receptor antagonist) in drinking water (30 mg/kg/day; sarpogrelate‐pretreated group) or equivalent volumes of drinking water (control group). Subsequently, the rats were pithed to produce increases in heart rate by either electrical preganglionic spinal (C7‐T1) stimulation of the cardiac sympathetic drive or iv administration of exogenous noradrenaline. The iv continuous infusion of AS‐19 (a 5‐HT7 receptor agonist; 10 µg/kg/min) (i) inhibited the tachycardic responses to sympathetic stimulation, but not those to exogenous noradrenaline only in sarpogrelate‐pretreated rats. This inhibition was completely reversed by SB258719 (a selective 5‐HT7 receptor antagonist; 1 mg/kg, iv) or glibenclamide (an ATP‐sensitive K+ channel blocker; 20 mg/kg, iv). These results suggest that chronic 5‐HT2 receptor blockade uncovers a cardiac sympatho‐inhibitory mechanism mediated by 5‐HT7 receptors, involving a hyperpolarization due to the opening of ATP‐sensitive K+ channels. Thus, these findings support the role of 5‐HT7 receptors in the modulation of the cardiac sympathetic neurotransmission.