Sunano S, Shimada T, Shimamura K
Research Institute of Hypertension, Kinki University, Osaka, Japan.
Jpn Heart J. 1987 Sep;28(5):765-81. doi: 10.1536/ihj.28.765.
The effects of vanadate on the vascular smooth muscle of Wistar Kyoto rats (WKY) and stroke prone spontaneously hypertensive rats (SHRSP) were examined. It was shown that sodium vanadate caused contraction of the aortae, mesenteric and basilar arteries of both strains, and that the reactivity was higher in SHRSP in the aorta and mesenteric artery. The vanadate-induced contractions were not blocked by 6-hydroxydopamine, adrenergic blocking agents, indomethacin or ouabain, while 4,4'-diisothiocyano-2,2'-disulfonic acid stilbene did. An increase in K+-concentration potentiated the vanadate-induced contractions of the mesenteric arteries and minimized the difference between preparations from WKY and SHRSP. In depolarized preparations incubated in K-Tyrode's solution (140 mM KCl), vanadate induced phasic contractions followed by marked relaxation in the aortae of both species, the relaxation being more prominent in SHRSP aorta, while depolarized mesenteric arteries showed sustained contractions. It was revealed that vanadate caused contractions by acting inside the cell, and membrane permeability to vanadate might be higher in the vascular smooth muscle of SHRSP. The findings also suggested that vanadium, an inorganic element, can be involved in the initiation of hypertension in SHRSP when it acts on vascular smooth muscle.
研究了钒酸盐对Wistar Kyoto大鼠（WKY）和易中风自发性高血压大鼠（SHRSP）血管平滑肌的影响。结果表明，钒酸钠可引起两种品系大鼠的主动脉、肠系膜动脉和基底动脉收缩，且SHRSP大鼠主动脉和肠系膜动脉的反应性更高。钒酸盐诱导的收缩不受6-羟基多巴胺、肾上腺素能阻滞剂、吲哚美辛或哇巴因的阻断，而4,4'-二异硫氰基-2,2'-二磺酸芪则可阻断。钾离子浓度升高可增强钒酸盐诱导的肠系膜动脉收缩，并使WKY和SHRSP大鼠的标本之间的差异最小化。在含140 mM氯化钾的K-台氏液中孵育的去极化标本中，钒酸盐可诱导两种大鼠主动脉出现相性收缩，随后出现明显舒张，SHRSP大鼠主动脉的舒张更为显著，而去极化的肠系膜动脉则表现为持续性收缩。研究发现，钒酸盐通过作用于细胞内引起收缩，且SHRSP大鼠血管平滑肌对钒酸盐的膜通透性可能更高。这些发现还表明，无机元素钒作用于血管平滑肌时，可能参与了SHRSP大鼠高血压的发生。
