Selective antagonism of hormone-induced vasoconstriction by synthetic atrial natriuretic factor in the rat microcirculation.

Selective antagonism of hormone-induced vasoconstriction by synthetic atrial natriuretic factor in the rat microcirculation.
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合成心房钠尿因子在大鼠微循环中选择性拮抗激素诱导的血管收缩。

DOI:
10.1161/01.res.61.1.42
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发表时间:
1987
影响因子:
20.1
通讯作者:
Bealer,SL
Bealer,SL
中科院分区:
医学1区
文献类型:
--
作者:
Proctor,KG;Bealer,SL

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将合成的心钠素(ANF)加入到麻醉大鼠的灌注液(30 nM)中或注入麻醉大鼠的颈静脉(0.1纳摩尔/分钟/100 g)。稳态血流量计算从微动脉直径和红细胞速度测量使用视频显微镜在肠道或骨骼肌微循环。通过局部腺苷扩张,小动脉表现出自发的血管舒缩张力,但局部或静脉注射ANF不会引起血管扩张。在存在或不存在环氧合酶抑制剂(30 μ M,甲氨蝶呤或吲哚美辛)的情况下,将血管紧张素、去甲肾上腺素或加压素加入到灌注液中,因为已知每种激动剂都能刺激血管活性前列腺素类合成。在肠道中,血管紧张素(500 nM)在静脉注射生理盐水期间引起40 +/- 2%的血流量减少,但在静脉注射ANF期间仅引起23 +/- 6%的血流量减少。血管紧张素(162 nM)和环氧合酶抑制剂导致19 +/- 4%的血流量减少,但环氧合酶抑制剂和局部ANF仅减少8 +/- 5%。相反,去甲肾上腺素(2-5 μ M)引起的血管收缩不被局部或静脉内ANF改变,无论是单独使用还是与环氧合酶抑制剂联合使用。在脊髓背角肌中,血管紧张素(1-2 nM)加环氧合酶抑制剂导致40-60%的血流量减少,但在静脉内或局部ANF期间仅减少20-30%。局部或静脉注射ANF不会改变精氨酸加压素(0.5-1.0 nM)或去甲肾上腺素(40-230 nM)引起的血管收缩。因此,超生理浓度的ANF在肠道或骨骼肌微循环中不产生直接的血管舒张。(250字处删节)
Synthetic atrial natriuretic factor (ANF) was either added to suffusate solutions (30 nM) or infused into the jugular vein (0.1 nanomol/min/100 g) of anesthetized rats. Steady-state blood flow was calculated from arteriolar diameter and red blood cell velocity measurements using video microscopy in the intestinal or skeletal muscle microcirculation. Arterioles demonstrated spontaneous vasomotor tone by dilating to topical adenosine, but topical or intravenous ANF did not cause vasodilation. Either angiotensin, norepinephrine, or vasopressin was added to the suffusates in the presence or absence of a cyclooxygenase inhibitor (30 microM, meclofenamate or indomethacin) because each agonist is known to stimulate vasoactive prostanoid synthesis. In the intestine, angiotensin (500 nM) caused 40 +/- 2% blood flow decreases during intravenous saline but only 23 +/- 6% during intravenous ANF. Angiotensin (162 nM) and a cyclooxygenase inhibitor caused 19 +/- 4% blood flow decreases but only 8 +/- 5% decreases with cyclooxygenase inhibitor and topical ANF. In contrast, norepinephrine (2-5 microM) caused vasoconstriction that was not altered by topical or intravenous ANF, either alone or in combination with cyclooxygenase inhibitors. In the spinotrapezius muscle, angiotensin (1-2 nM) plus a cyclooxygenase inhibitor caused 40-60% blood flow decreases but only 20-30% decreases during intravenous or topical ANF. Topical or intravenous ANF did not alter the vasoconstriction evoked by arginine vasopressin (0.5-1.0 nM) or by norepinephrine (40-230 nM). Thus, supraphysiologic concentrations of ANF produced no direct vasodilation in the intestinal or skeletal muscle microcirculation.(ABSTRACT TRUNCATED AT 250 WORDS)
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影响因子: 5
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影响因子: 20.1
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