Reflex pressor response to arterial phenylbiguanide: role of abdominal sympathetic visceral afferents.

Reflex pressor response to arterial phenylbiguanide: role of abdominal sympathetic visceral afferents.
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对动脉苯双胍的反射升压反应:腹部交感内脏传入的作用。

DOI:
10.1152/ajpheart.1998.275.6.h2025
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发表时间:
1998
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Longhurst,JC
Longhurst,JC
中科院分区:
--
文献类型:
--
作者:
Fu,LW;Longhurst,JC

文献摘要

被引文献

相似文献

苯基双胍(Phenylbiguanide,PBG)是一种5-HT 3(5-serotonin)受体激动剂,在许多研究中被用作“选择性”激动剂,通过激活心脏和肺迷走神经传入引起反射性心动过缓和低血压。由于我们已经证明内源性5-HT通过5-HT 3受体刺激缺血敏感的腹部交感神经传入,我们研究了左心室(LV)和动脉内给予PBG可能通过增加麻醉猫交感内脏传入的活性而引起竞争性反射反应的可能性。监测平均动脉压(MAP)和心率(HR)。在迷走神经和交感神经传入均完整的情况下,PBG(40 μg/kg,左室注射)使8只猫的MAP和HR显著降低,而使2只猫的MAP显著升高。双侧颈迷走神经切断后,左室PBG显著增加MAP。PBG(40 μg/kg,ia)显著增加MAP和HR,而静脉注射PBG显著降低MAP和HR(n= 10只猫)。此外,腹腔和肠系膜神经节切除可使PBG(40 μg /kgia)引起的升压反应降低68%(P< 0.05;n= 4)。在单一单位腹部交感神经传入的研究中,动脉内而不是静脉内PBG(40 μg/kg)显著增加10个缺血敏感传入的活性,但不增加缺血不敏感传入的活性。iv托烷司琼(200 μg/kg)阻断5-HT_3受体可消除PBG引起的传入反应和升压反应。这些数据表明,PBG给药到LV通常,但不总是,引起降压反应,转换为升压反应后,颈部迷走神经切断术。此外,动脉内PBG通过刺激主要与缺血敏感的腹部交感神经传入相关的5-HT 3受体诱导升压反应。
Phenylbiguanide (PBG), a 5-HT3(serotonin) receptor agonist, has been used in many studies as a “selective” agonist to elicit reflex bradycardia and hypotension through activation of cardiac and pulmonary vagal afferents. Because we have shown that endogenous 5-HT stimulates ischemically sensitive abdominal sympathetic afferents through 5-HT3receptors, we investigated the possibility that left ventricular (LV) and intra-arterial administration of PBG may evoke a competing reflex response by increasing the activity of sympathetic visceral afferents in anesthetized cats. Mean arterial pressure (MAP) and heart rate (HR) were monitored. When both vagal and sympathetic afferents were intact, PBG (40 μg/kg, injected into the LV) significantly decreased MAP and HR in 8 of 10 cats but increased MAP in the remaining 2 cats. After bilateral cervical vagotomy, LV PBG significantly increased MAP. PBG (40 μg/kg ia) significantly increased MAP and HR, whereas intravenous PBG significantly decreased MAP and HR (n= 10 cats). Furthermore, the pressor response to PBG (40 μg /kg ia) was reduced by 68% (P< 0.05;n= 4 cats) by celiac and mesenteric ganglionectomies. In studies of single-unit abdominal sympathetic afferents, intra-arterial but not intravenous PBG (40 μg/kg) significantly increased activity of 10 ischemically sensitive afferents but not ischemically insensitive afferents. Blockade of 5-HT3receptors with tropisetron (200 μg/kg iv) eliminated the response of the afferents and the pressor response to PBG. These data indicate that PBG administered into the LV usually, but not always, evokes a depressor response that is converted to a pressor response following cervical vagotomy. Also, intra-arterial PBG induces a pressor response by stimulating 5-HT3receptors largely associated with ischemically sensitive abdominal sympathetic afferents.