Antagonism of adenosine A1 receptors in the NTS does not affect the chemoreflex in awake rats

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Abstract
The possible involvement of adenosine A1 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 (ED50) 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 A1 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 before and 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 A1 receptors and that blockade of these receptors produced no changes in cardiovascular responses to chemoreflex activation. We conclude that adenosine A1 receptors are not involved in processing of the chemoreflex afferents at the NTS level.