Systematic understanding of acute effects of intravenous guanfacine on rat carotid sinus baroreflex-mediated sympathetic arterial pressure regulation.

Aims To assess the acute effects of intravenous guanfacine, an α 2A -adrenergic agonist, on sympathetic outflow from the central nervous system and on sympathetic arterial pressure (AP) response. Main methods In anesthetized Wistar Kyoto rats, carotid sinus baroreceptor regions were isolated. Changes in electrical sympathetic nerve activity (SNA) and AP in response to a baroreceptor pressure input were examined before and after an intravenous administration of a high dose (100 μg/kg, n = 7) or a low dose (20 μg/kg, n = 5) of guanfacine. Key findings The higher dose of guanfacine significantly narrowed the range of the AP response (86.8 ± 6.4 to 38.4 ± 12.9 mm Hg, P < 0.01) but increased the minimum AP (79.3 ± 7.5 to 93.2 ± 8.7 mm Hg, P < 0.05). In the neural arc, guanfacine reduced both the response range (90.4 ± 2.3 to 33.4 ± 10.7%, P < 0.01) and the minimum SNA (11.4 ± 1.9 to 2.6 ± 1.5%, P < 0.01). In the peripheral arc, guanfacine increased the intercept (67.6 ± 7.1 to 92.8 ± 8.5 mm Hg, P < 0.01) without a significant effect on the slope. The lower dose of guanfacine weakened the effects on both the neural and peripheral arcs. Significance Guanfacine suppressed SNA without a significant reduction of AP, which may be attributable to the peripheral vasoconstrictive effect. Reducing the dose of acutely administered intravenous guanfacine does not aid in separating the central sympathoinhibitory effect from the peripheral vasoconstrictive effect on AP in anesthetized rats in vivo. [ABSTRACT FROM AUTHOR]