Voderholzer W A, Allescher H D, Müller-Lissner S A
Medizinische Klinik, Klinikum Innenstadt, University of Munich, Germany.
Neurogastroenterol Motil. 1995 Mar;7(1):15-21. doi: 10.1111/j.1365-2982.1995.tb00204.x.
We have previously shown that restriction of water intake decreased stool frequency and stool weight in volunteers. The aim of this study was to investigate whether these effects of thirst could be mediated by an action of systematically released hormones on colonic smooth muscle. Using isolated colonic smooth muscle strips the effect of arginine-vasopressin (AVP), angiotensin II (ANG II) and aldosterone on rat colonic motility in vitro was investigated. AVP (10(-12)-10(-10) mol/l) and aldosterone (3 x 10(-10)-3 x 10(-8) mol/l) and physiological hormonal concentrations of ANG II (10(-13)-10(-10) mol/l) had no effect on either basal activity, direct stimulation of colonic smooth muscle or neurally stimulated contractions using carbachol 10(-7)-3 x 10(-5) mol/l or neurally stimulated contractions using electrical field stimulation at various stimulation frequencies (1-10 pps, 1 ms, 40 V). ANG II in higher concentrations (10(-7)-10(-6) mol/l) increased basal activity and neurally mediated contractions. Accordingly, ANG II (10(-6) mol/l) caused a prestimulation but did not increase the maximum contractile effect of carbachol. The response to ANG II was not affected by atropine (10(-6) mol/l). TTX (10(-6) mol/l) and N-nitro-L8-arginine (L-NNA) (3 x 10(-4) mol/l) stimulated basal muscular activity but did not affect the maximum contractile effect of ANG II. Systemic serum concentrations of AVP, aldosterone and ANG II are presumably not involved in thirst-induced colonic motility changes. The ANG II effect in higher concentrations is mediated by a direct stimulatory smooth muscle effect and/or by facilitating neuronal liberation of acetylcholine.(ABSTRACT TRUNCATED AT 250 WORDS)
我们之前已经表明,限制志愿者的水摄入量会降低其排便频率和粪便重量。本研究的目的是调查口渴的这些影响是否可由系统性释放的激素对结肠平滑肌的作用介导。使用离体结肠平滑肌条,研究了精氨酸加压素(AVP)、血管紧张素II(ANG II)和醛固酮对大鼠结肠体外运动的影响。AVP(10⁻¹² - 10⁻¹⁰ mol/L)、醛固酮(3×10⁻¹⁰ - 3×10⁻⁸ mol/L)以及生理激素浓度的ANG II(10⁻¹³ - 10⁻¹⁰ mol/L)对基础活性、直接刺激结肠平滑肌或使用10⁻⁷ - 3×10⁻⁵ mol/L卡巴胆碱进行神经刺激的收缩或在各种刺激频率(1 - 10次/秒、1毫秒、40伏)下使用电场刺激进行神经刺激的收缩均无影响。较高浓度(10⁻⁷ - 10⁻⁶ mol/L)的ANG II会增加基础活性和神经介导的收缩。因此,ANG II(10⁻⁶ mol/L)会引起预刺激,但不会增加卡巴胆碱的最大收缩效应。对ANG II的反应不受阿托品(10⁻⁶ mol/L)影响。河豚毒素(10⁻⁶ mol/L)和N - 硝基 - L - 精氨酸(L - NNA)(3×10⁻⁴ mol/L)刺激基础肌肉活性,但不影响ANG II的最大收缩效应。AVP、醛固酮和ANG II的全身血清浓度可能与口渴诱导的结肠运动变化无关。较高浓度的ANG II的作用是由直接刺激平滑肌效应和/或促进乙酰胆碱的神经元释放介导的。(摘要截短于250字)