Baro‐ and chemoreflex function during transient increase in arterial pressure caused by bilateral carotid occlusion in conscious mice.

The involvement of either baro‐ or chemoreflex in the hypertensive response to BCO was previously demonstrated in rats and in anesthetized mice. The goal of this study was to develop an assay of baro‐ and chemoreceptor reflex function in conscious mice that will enable future analysis of these sensitive pathways using genetically manipulated mice. Under tribromoethanol (2.5 μg/g, ip) anesthesia, carotid sinus of C57Bl mice were isolated and the carotid sinus artery was identified and disrupted (n=5). Sham operated mice (n=7) had the carotid sinus artery left intact. Pneumatic cuffs were placed around the common carotid arteries and catheters were indwelled into femoral artery and vein. On the following day, after basal recording of arterial pressure (AP), mice were submitted to BCO during 30 s. Basal AP was found similar in sham operated (110±2 mmHg) in and in chemoreflex denervated mice (113±2 mmHg). BCO elicited a prompt rise in AP that lasted until the end of occlusion. In sham operated mice the hypertensive response was greater (43±4 and 40±5 mmHg at 15 and 30 s after the onset of BCO) as compared to chemoreceptor denervated mice (22±4 mmHg at 15 and 30 s after the onset of BCO, P<0.01). We conclude that the hypertensive response to BCO is mediated by both baro‐ and chemoreflex in conscious mice, and this approach promises to be useful in future studies. Support: FAPESP, CNPq, CAPES, FAEPA.