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Pressor Component of the Chemoreflex Response Is Not Mediated by P2 Purinergic Receptors in the A5 Area

Previous studies have shown that the noradrenergic neurons of the A5 area have an important role in the regulation of the pressor component of the chemoreflex. The aim of the present study was to evaluate the role of ATP and P2 purinergic receptors in the A5 area in the cardiovascular regulation as well as in the pressor component of the chemoreflex response in conscious rats. Unilateral microinjection of α,β‐methylene ATP (1.25 nmol/100 nl, n = 7), a selective P2 purinergic agonist, into the A5 area produced pressor (+33 ± 7 mmHg) and tachycardic responses (+66 ± 10 bpm). Ipsilateral microinjection of PPADS (0.5 nmol/100 nl), a P2 receptors antagonist, reduced the cardiovascular responses produced by α,β‐methylene ATP (+14 ± 4 mmHg and +29 ± 12 bpm) microinjected into the A5 area. Bilateral microinjection of PPADS (0.5 nmol/100 nl, n = 5) into the A5 area produced no changes in the pressor (+38 ± 6 vs +39 ± 5 mmHg) and bradycardic responses (‐253 ± 8 vs ‐237 ± 25 bpm, n = 5) induced by chemoreflex stimulation (KCN, 40 µg, i.v.). Baseline mean arterial pressure and heart rate (111 ± 5 vs 116 ± 4 mmHg and 347 ± 16 vs 335 ± 22 bpm) were also not changed by bilateral microinjection of PPADS into the A5 area. These results suggest that the P2 purinergic receptors in the A5 area participate in the modulation of the cardiovascular control, but are not involved in the integration of cardiovascular responses of the chemoreflex. Supported by Capes, INCT/CNPq, Fapemig.