Vanadate가 사람의 제대혈관의 장력에 미치는 효과 = Effect of Vanadate on Vascular Tension in the Isolated Human Umbilical Blood Vessel

국문 초록 (Abstract)

혈관작용성 물질의 연구에 이상적이라고 알려진 제대혈관의 장력에 미치는 vanadate의 효과와 그 작용기작을 규명하기 위하여 실험하였다.
Vanadate는 사람의 제대정맥과 동맥 모두에서 농도의존적인 수축을 일으켰으며, 모든 농도에서 제대정맥이 제대동맥보다 더 큰 수축반응을 나타내었고, Methylene blue ( )를 혈관 절편에 전처리하거나 화학적으로 제대혈관을 탈내피 시킨 후 (saponin 0.03㎎/ml, 45min) verapamil ( )으로 전처리한 경우 vanadate의 수축반응은 제대정맥과 동맥 모두에서 유의한 차이가 없었으며, Indomethacin ( )으로 혈관 단편을 전처리한 후에는 vanadate에 의한 수축반응은 제대정맥과 동맥 모두에서 현저히 억제 (각각 97.6±0.02%, 97.3±0.01%)되었고 제대혈관 절편을 OKY046 ( )으로 전처리시킨 후 vanadate,의 수축 효과를 관찰한 결과 전처리 전과 유의한 반응의 차이를 볼 수 없었다.
사람의 제대혈관에서 vanadate에 의해 유발된 수축은 내피세포 비의존성 수축으로 제대동맥보다 정맥에서 수축 반응이 더 컷으며 ,vanadate에 의한 수축은 TXA₂가 아닌 prostanoid계의 다른 수축 물질에 의해 일어남을 알 수 있었다.

다국어 초록 (Multilingual Abstract)

Vanadium is a trace element essential for the normal development and growth of the human and animals. Under physiological conditions, it is present in small concentrations in serum and tissues of the different animals. This anion is able to inhibit ATPase and ATPase of different tissues, including the cardiac and vascular smooth muscle. These enzymes play an important role in the regulation of the vascular tone. In fact, it was recently reported that vanadate induced contractions of the vascular and non vascular smooth muscles. On the other hand, human umbilical vessels are known to be ideal for the study of vasoactive substances because of poor innervation of autonomic nerves to these vessels.
The aim of present study was to investigate effect of vanadate on the vascular tension of the isolated human umbilical vein (HUV) and artery (HUA) obtained from full-term deliveries after cesarean section and to elucidate the mechanism of these vanadate-induced vascular response.
Vanadate ( ) induced concentration-dependent contraction of HUV and HUA preparations. At all concentrations, contracting effect of vanadate was greater in vein than artery. Pretreatment with methylene blue ( ), soluble guanylate cyclase inhibitor and verapamil ( ), L-type channel blocker, did not affect vanadate-induced contractions of umbilical vessels. After chemical denudation with saponin (0.03㎎/ml, 45min), the contractile response to vanadate was not changed. To test whether prostanoid is related to this contraction, vascular preparations were pretreated with indomethacin ( ), cyclooxygenase inhibitor. Indomethacin suppressed the contracile response by 97.6±0.02% in the umbilical vein and by 97.3±0.01% in the umbilical artery. In both types of preparations, vanadate-induced contractions were not altered by OKY046( ), TXA₂(thromboxan A₂) inhibitor.
These results suggest that vanadate produces contracions both in the isolated HUV and HUA, and that the vanadate-induced contractions are mediated, at least in part, through prostanoids other than TXA₂.