Prostaglandin‐mediated inhibition of noradrenaline release
Prostaglandin‐mediated inhibition of noradrenaline release
复制标题
前列腺素介导的去甲肾上腺素释放抑制
DOI:
10.1111/j.1748-1716.1979.tb06339.x
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发表时间:
1979
期刊:
影响因子:
--
通讯作者:
Å. Wennmalm
中科院分区:
文献类型:
--
作者:
Å. Wennmalm
The effect of indomethacin, a prostaglandin (PG) synthesis inhibitor, on some cardiovascular reflexes was studied in healthy subjects. Heart rate (HR) and respiratory sinus arrhythmia (RSA) in the basal state and during carotid stimulation (neck suction), Valsalva ratio, and changes in heart rate and blood pressure (BP) during an orthostatic test were measured before and one hour after administration of indomethacin (1.5 mg/kg). The efficacy of the PG synthesis inhibitor was monitored by analysis of platelet aggregation induced by arachidonic acid. Following indomethacin no change was observed in basal HR. Carotid stimulation depressed the HR and this effect was of the same amplitude before and after indomethacin. The amplitude of RSA was not affected by indomethacin, either in the basal state or during carotid stimulation. The Valsalva ratio and the changes in HR and BP during the orthostatic test were similar before and after the drug. Circulating levels of noradrenaline were unaffected by indomethacin. These data demonstrate that inhibition of PG bioformation in man does not affect major cardiovascular reflexes. Consequently they disfavour the hypothesis that endogenously formed PG would be involved in the normal activity of the afferent, central or efferent pathways for cardiovascular regulation.