Role of the pons in the carotid sympathetic chemoreflex.

The mass discharges of the splanchnic sympathetic (SND) and phrenic nerves (PND) were recorded in urethananesthetized rats with resected vagal and aortic nerves. Carotid chemoreceptor (CC) stimulation with N2 inhalation (4-12 s) or cyanide (50-100 micrograms/kg iv) activated SND in bursts synchronized with the postinspiratory phase (mean SND increase: 105 +/- 8%), raised AP, and increased PND rate and amplitude (n = 40). Brain transection at superior collicular level produced no effect. The sympathetic (SChR) and respiratory chemoreflexes (RChR) were reduced after transections through the pons. Lesions of the dorsolateral pons (dl-pons) produced CO2-dependent apneusis and/or tachypnea at rest. After such lesions, CC stimulation produced expiratory apnea and a 30% increase in SChR due to tonic activation of SND. In contrast, bilateral lesions of the ventrolateral pons (vl-pons) reduced the SChR by 54-76%. Muscimol (Mus) injections (bilateral, 175 pmol/side) into vl-pons did not change resting SND, MAP, baroreflex, and RChR but reduced the SChR (54-82%). In conclusion, under anesthesia: 1) the pathway of the carotid chemoreflex is confined to the pons and medulla, 2) the dl-pons exerts indirect control over the SChR via its role in respiratory rhythmogenesis, and 3) neurons in the vl-pons contribute selectively to the SChR but not to PND activation during CC activation.