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一氧化氮作为肾上腺血流的调节因子。

Nitric oxide as a regulator of adrenal blood flow.

作者信息

Breslow M J, Tobin J R, Bredt D S, Ferris C D, Snyder S H, Traystman R J

机构信息

Department of Anesthesiology/Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287.

出版信息

Am J Physiol. 1993 Feb;264(2 Pt 2):H464-9. doi: 10.1152/ajpheart.1993.264.2.H464.

DOI:10.1152/ajpheart.1993.264.2.H464
PMID:7680537
Abstract

To determine whether nitric oxide (NO) is involved in adrenal medullary vasodilation during splanchnic nerve stimulation (NS)-induced catecholamine secretion, blood flow (Q) and secretory responses were measured in pentobarbital-anesthetized dogs before and after administration of the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME). L-NAME (40 mg/kg iv over 5 min, followed by 40 mg.kg-1.h-1) reduced NO synthase activity of medullary and cortical homogenates from 5.2 +/- 0.3 to 0.7 +/- 0.1 pmol.min-1.mg protein-1 and from 1.2 +/- 0.2 pmol.min-1.mg protein-1 to undetectable levels, respectively. L-NAME reduced resting medullary and cortical Q by 42 and 60%, respectively. NS before L-NAME increased medullary Q from 181 +/- 16 to 937 +/- 159 ml.min-1.100 g-1 and epinephrine secretion from 1.9 +/- 0.8 to 781 +/- 331 ng/min. NS after L-NAME had no effect on medullary Q (103 +/- 14 vs. 188 +/- 34 ml.min-1.100 g-1), while epinephrine secretion increased to the same extent as in control animals (1.9 +/- 0.7 vs. 576 +/- 250 ng/min). L-NAME also unmasked NS-induced cortical vasoconstriction; cortical Q decreased from 96 +/- 8 to 50 +/- 5 ml.min-1.100 g-1. Administration of hexamethonium (30 mg/kg iv), a nicotinic receptor antagonist, reduced NS-induced epinephrine secretion by 90%. These data suggest independent neural control of medullary Q and catecholamine secretion, the former by NO and the latter by acetylcholine.

摘要

为了确定一氧化氮(NO)是否参与内脏神经刺激(NS)诱导的儿茶酚胺分泌过程中的肾上腺髓质血管舒张,在给予NO合酶抑制剂NG-硝基-L-精氨酸甲酯(L-NAME)之前和之后,对戊巴比妥麻醉的犬的血流量(Q)和分泌反应进行了测量。L-NAME(40mg/kg静脉注射,持续5分钟,随后以40mg·kg⁻¹·h⁻¹给药)使髓质和皮质匀浆的NO合酶活性分别从5.2±0.3降至0.7±0.1pmol·min⁻¹·mg蛋白⁻¹以及从1.2±0.2pmol·min⁻¹·mg蛋白⁻¹降至无法检测的水平。L-NAME分别使静息时的髓质和皮质Q降低了42%和60%。在给予L-NAME之前,NS使髓质Q从181±16增加至937±159ml·min⁻¹·100g⁻¹,肾上腺素分泌从1.9±0.8增加至781±331ng/min。给予L-NAME之后,NS对髓质Q没有影响(103±14 vs. 188±34ml·min⁻¹·100g⁻¹),而肾上腺素分泌增加到与对照动物相同的程度(1.9±0.7 vs. 576±250ng/min)。L-NAME还揭示了NS诱导的皮质血管收缩;皮质Q从96±8降至50±5ml·min⁻¹·100g⁻¹。给予烟碱受体拮抗剂六甲铵(30mg/kg静脉注射)使NS诱导的肾上腺素分泌减少了90%。这些数据表明,髓质Q和儿茶酚胺分泌受独立的神经控制,前者受NO控制,后者受乙酰胆碱控制。

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