Role of pulmonary stretch receptors and sympathetic system in the inhibition of reflex bradycardia produced by chemical stimulation of the periaqueductal gray matter of the rat

• Published in: Neuroscience Vol. 210; pp. 222 - 233
• Main Authors: Sampaio, K.N, Mauad, H, Vasquez, E.C, Schenberg, L.C
• Format: Journal Article
• Language: English
• Published: 2012
• Subjects: Neurology; nucleus retroambiguous; VLPAG or VL; MPBA; DgL; pulsatile arterial pressure; HR; Mean arterial pressure; Bötzinger complex; DR; lateral parabrachial area; ANCOVA; GLU; sol; supraoculomotor periaqueductal gray matter; DPAG; caudal ventrolateral medulla; IC; trochlear nucleus; Cun; glutamate; nucleus ambiguous; cpm; scp; chemical stimulation; deep mesencephalic nucleus; LPGi; nucleus cuneiformis; oculomotor nucleus, parvocellular; nucleus tractus solitarius; CVLM; RA; dorsal raphe nucleus; Kölliker-Fuse nucleus; InCo; NA; 3; RF; 4; DeMe; analysis of covariance; MAP; oculomotor nucleus; deep white layer of superior colliculus; NTS; PHE; ventrolateral periaqueductal gray matter; LPAG or LT; deep gray layer of superior colliculus; dorsal periaqueductal gray matter; DLPAG or DL; dorsolateral periaqueductal gray matter; dorsomedial periaqueductal gray matter; BÖ; phenylephrine; inferior colliculus; respiratory frequency; KF; LPBA; heart rate; lateral periaqueductal gray matter; rostral ventrolateral medulla; intercollicular nucleus; RVLM; baroreceptor reflex; superior cerebellar peduncle; 3pc; cycles per minute; lateral paragigantocellular nucleus; pulmonary stretch receptors; Su3; solitary tract; PAG; respiratory amplitude; DMPAG or DM; DwL; periaqueductal gray matter; medial parabrachial area; NRA; PAP
• ISSN: 0306-4522
• DOI: 10.1016/j.neuroscience.2012.02.041

Abstract The present study examined the role of the sympathetic system and pulmonary afferent feedback in the baroreflex inhibition by chemical stimulation of the dorsal periaqueductal gray matter (DPAG) of the anesthetized rat. The baroreflex bradycardia was induced by phenylephrine infusions (PHE, 50 μg/ml/min, i.v.) given either alone or combined with glutamate microinjections (GLU, 10 nmol/100 nl) into the DPAG. GLU microinjections alone produced marked increases in respiratory amplitude (67±19%), but barely changed the respiratory frequency (15±3 cpm) and blood pressure (14±2 mm Hg), and did not affect the heart rate. In contrast, the same injections produced a 92% inhibition of PHE-induced bradycardia (from −62 to −5 bpm). Because GLU microinjections per se had little effects on blood pressure, the baroreflex inhibition should be credited to the deactivation of both the vagal and sympathetic reflex pathways at the medulla. Indeed, the baroreflex was inhibited in only 47% following the DPAG stimulation of atenolol-treated rats. The GLU-evoked inhibition of baroreflex was also correlated with concomitant increases in respiratory amplitude. The role of pulmonary feedback in baroreflex inhibition was thus examined before and after the neuromuscular blockade of atenolol-treated rats. In spontaneously breathing rats, GLU microinjections reversed PHE-induced bradycardia to tachycardia, thereby producing a 153% inhibition of reflex bradycardia (from −38 bpm to +20 bpm). In contrast, the baroreflex inhibition was attenuated in only 53% after neuromuscular blockade (from −34 to −16 bpm). Data are the first evidence of the contribution of pulmonary stretch receptor feedback in DPAG-evoked inhibition of reflex bradycardia.