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Aims: This study aims to identify the contribution of myelinated (A-fiber) and unmyelinated (C-fiber) baroreceptor central pathways to the baroreflex control of sympathetic nerve activity and arterial pressure. Main methods: Two binary white noise stimulation protocols were used to electrically stimulate the aortic depressor nerve and activate reflex responses from either A-fiber (3V, 20–100Hz) or C-fiber (20V, 0–10Hz) baroreceptor in anesthetized Sprague-Dawley rats (n =10). Transfer function analysis was performed between stimulation and sympathetic nerve activity (central arc), sympathetic nerve activity and arterial pressure (peripheral arc), and stimulation and arterial pressure (Stim-AP arc). Key findings: The central arc transfer function from nerve stimulation to splanchnic sympathetic nerve activity displayed derivative characteristics for both stimulation protocols. However, the modeled steady-state gain (0.28±0.04 vs. 4.01±0.2%·Hz−1, P <0.001) and coherence at 0.01Hz (0.44±0.05 vs. 0.81±0.03, P <0.05) were significantly lower for A-fiber stimulation compared with C-fiber stimulation. The slope of the dynamic gain was higher for A-fiber stimulation (14.82±1.02 vs. 7.21±0.79dB·decade−1, P <0.001). The steady-state gain of the Stim-AP arc was also significantly lower for A-fiber stimulation compared with C-fiber stimulation (0.23±0.05 vs. 3.05±0.31mmHg·Hz−1, P <0.001). Significance: These data indicate that the A-fiber central pathway contributes to high frequency arterial pressure regulation and the C-fiber central pathway provides more sustained changes in sympathetic nerve activity and arterial pressure. A sustained reduction in arterial pressure from electrical stimulation of arterial baroreceptor afferents is likely mediated through the C-fiber central pathway. [ABSTRACT FROM AUTHOR]

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]

Aims To assess the acute effects of intravenous azelnidipine, a third-generation L-type calcium channel blocker, on sympathetic outflow from the central nervous system and to compare the effects of intravenous azelnidipine with those of intravenous nifedipine. Main methods In anesthetized Wistar Kyoto rats, carotid sinus baroreceptor regions were isolated. Changes in sympathetic nerve activity (SNA) and arterial pressure (AP) in response to a stepwise baroreceptor pressure input were examined before and during intravenous nifedipine or azelnidipine (for each: 100 μg/kg bolus followed by 300 μg/kg/h infusion, n = 6). Key findings Nifedipine significantly reduced the range of the AP response from 76.8 ± 7.4 to 45.4 ± 7.0 mm Hg (P < 0.01) but did not affect the range of the SNA response (from 84.4 ± 5.1 to 85.9 ± 10.2%) or the SNA maximum gain (from 2.26 ± 0.28 to 2.35 ± 0.55%/mm Hg). Similarly, azelnidipine significantly reduced the range of the AP response from 62.4 ± 3.9 to 31.4 ± 4.1 mm Hg (P < 0.01) but did not affect the range of the SNA response (from 71.2 ± 5.5 to 74.9 ± 7.2%) or the SNA maximum gain (from 1.64 ± 0.17 to 2.08 ± 0.26%/mm Hg). Significance A depressor dose of nifedipine or azelnidipine does not have an acute sympathoinhibitory effect in normotensive Wistar Kyoto rats even when the level of SNA was varied over the entire operating range of the carotid sinus baroreflex. [ABSTRACT FROM AUTHOR]