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KMID : 0811720000040000016
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Korean Journal of Physiology & Pharmacology
2000 Volume.4 No. 0 p.16 ~ p.0
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Effects of ATP on the Contractility of Small Mesenteric Artery from 2K1C and DOCA Hypertensive Rats
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Kang Seong-Su
Nam Sang-Chae
Kim Won-Jae
Lee Jong-Un
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Abstract
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There is considerable evidence that adenosine triphosphate (ATP) is co-localized and co-released with norepinephrine (NE) in the perivascular sympathetic nerve terminals. However, the precise role of ATP and the interaction between NE and ATP on the vascular contractility in hypertension are unclear. The aim of the present study was to elucidate the effects of ATP on the contractility of the small artery with or without precontraction generated by NE in hypertension animal models. Two-kidney, one clip (2K1C) and deoxycorticosterone acetate (DOCA)/salt hypertensive rats and sham-operated normotensive rats were used. Four weeks after surgery, blood pressure was measured using the Rat Tail Indirect Blood Pressure System. Small segments of the third branch of the mesenteric arteries were threaded onto two tungsten wires and suspended in a myograph. The effects of NE and ATP on their wall tension were investigated.
ATP caused the small mesenteric artery from all groups contract in a dose-dependent manner. The vascular contraction induced by ATP displayed longer duration in 2K1C and DOCA hypertension. Magnitude of the ATP-induced tension increase was significantly larger in 2K1C and DOCA/salt hypertension than in control. In the presence of NE, the ATP-induced contractility of the vessel from all groups was significantly increased compared with that in the absence of NE. In contrast, the NE-induced contractility of the vessel in the presence of ATP was decreased in control and DOCA/salt hypertension, whereas it was not altered in 2K1C. In addition to the ATP-induced vascular contraction, the precontracted vessel by either NE or high KCl was relaxed by ATP after transient contraction. These results suggest that ATP might contribute to 2K1C and DOCA hypertension via both direct and indirect modulation of the contractility of the small artery.
Source: Korean Journal of Physiology & Pharmacology.2000 Oct;4(Suppl):S12-S12
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