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首页> 外文期刊>American Journal of Physiology >Antagonism of adenosine A(1) receptors in the NTS does not affect the chemoreflex in awake rats.
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Antagonism of adenosine A(1) receptors in the NTS does not affect the chemoreflex in awake rats.

机译：NTS中的腺苷A（1）受体拮抗作用不会影响清醒大鼠的化学反射。

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摘要

The possible involvement of adenosine A(1) receptors in neurotransmission of the sympathoexcitatory component of the chemoreflex in the nucleus tractus solitarii (NTS) of awake rats was evaluated. Unilateral microinjection of increasing doses of adenosine (0.01, 0.06, 0.12, 1.25, 2.5, and 5.0 nmol/50 nl) into the lateral aspect of the commissural NTS produced a long-lasting increase in baseline mean arterial pressure (MAP) and no changes in baseline heart rate (HR). Microinjection of adenosine at 1.25 nmol/50 nl (ED(50)) into the NTS (n = 9) produced a significant increase in baseline MAP (119 +/- 3, 122 +/- 4, and 117 +/- 4 mmHg at 30 s, 1 min, and 2 min, respectively) compared with control (102 +/- 3 mmHg) but no significant changes after previous microinjection of 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), an adenosine A(1) receptor antagonist (107 +/- 3, 107 +/- 3, and 106 +/- 3 mmHg at 30 s, 1 min, and 2 min, respectively) compared with control (102 +/- 3 mmHg). Microinjection of adenosine beforeand after DPCPX into the same site of the lateral commissural NTS produced no changes in baseline HR. In another group of rats (n = 8), microinjection of DPCPX (0.285 nmol/50 nl) into lateral and midline aspects of the commissural NTS produced no significant changes in pressor (+46 +/- 4 vs. +47 +/- 2 mmHg) or bradycardic responses (-216 +/- 9 vs. -226 +/- 12 beats/min) to chemoreflex activation with intravenous potassium cyanide compared with control responses. These data show that microinjection of adenosine into the NTS produced a small and long-lasting pressor response by activating A(1) receptors and that blockade of these receptors produced no changes in cardiovascular responses to chemoreflex activation. We conclude that adenosine A(1) receptors are not involved in processing of the chemoreflex afferents at the NTS level.
机译：评估可能的腺苷A（1）受体参与清醒大鼠孤束核（NTS）化学反射的交感兴奋成分的神经传递。向连合NTS侧面单侧显微注射剂量不断增加的腺苷（0.01、0.06、0.12、1.25、2.5和5.0 nmol / 50 nl）可使基线平均动脉压（MAP）长期持续增加，且无变化基线心率（HR）。在1.25 nmol / 50 nl（ED（50））处向NTS（n = 9）微注射腺苷可显着提高基线MAP（119 +/- 3、122 +/- 4和117 +/- 4 mmHg与对照组（102 +/- 3 mmHg）相比，分别在30 s，1 min和2 min时），但在先前微量注射8-环戊基-1,3-二丙基黄嘌呤（DPCPX）后，腺苷A（1 ）受体拮抗剂（分别在30 s，1分钟和2分钟时分别为107 +/- 3、107 +/- 3和106 +/- 3 mmHg）与对照组（102 +/- 3 mmHg）相比。在DPCPX之前和之后向侧连合NTS的同一部位微量注射腺苷不会导致基线HR的变化。在另一组大鼠（n = 8）中，将DPCPX（0.285 nmol / 50 nl）微量注射到连合NTS的外侧和中线部位不会产生明显的升压变化（+46 +/- 4与+47 +/-与对照组相比，静脉内氰化钾对化学反射激活的心动过缓反应（-2毫米汞柱）或心动过缓反应（-216 +/- 9 vs -226 +/- 12次/分钟）。这些数据表明，通过激活A（1）受体，将腺苷微量注射到NTS中会产生小的持久的升压反应，而这些受体的阻滞不会对化学反射激活产生心血管反应的改变。我们得出结论，腺苷A（1）受体不参与NTS级别的化学反射传入的处理。

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