Cardiovascular changes following acute and chronic chemical lesions of the dorsal periaqueductal gray in conscious rats.
This study was carried out to investigate the effects of chemical lesions of dorsal periaqueductal gray (DPAG) on resting arterial pressure (AP) and heart rate (HR) as well as on cardiac baroreflex of conscious normotensive rats. Lesions were performed by bilateral microinjections of 150 mM NMDA into the DPAG (DPAG-lesion group). Controls were similarly injected with 165 mM NaCl (DPAG-sham group). Animals with chronic lesions confined only to the superior colliculus (SC-lesion group) were also used as controls of DPAG-lesion. Cardiovascular parameters were recorded 1 or 7 days after the microinjections of NMDA in acute and chronic groups, respectively. Cardiac baroreflex was assessed by measuring the HR responses to the intravenous injection of phenylephrine or sodium nitroprusside. Baroreflex was estimated by sigmoidal curve fitting of HR responses. An increased baroreflex gain was observed in chronic DPAG-lesion rats compared to both DPAG-sham (p < 0.01) and SC-lesion (p < 0.05) chronic groups. The chronic DPAG-lesion group showed also an elevation of both the tachycardia (p < 0.05) and bradycardia (p < 0.01) plateaus compared to chronic DPAG-sham rats, while the SC-lesion group showed an elevation of the bradycardia plateau only (p < 0.01). Similar results on baroreflex function were observed following acute lesion of the DPAG, i.e. an increase in baroreflex gain (p < 0.01) and the elevation of both tachycardia (p < 0.05) and bradycardia plateaus (p < 0.01) compared to the acute DPAG-sham group. Resting AP and HR did not differ among the chronic groups. In contrast, the acute lesion of the DPAG produced a reduction in AP (p < 0.01) accompanied by an increase in HR (p < 0.01). The present data suggest that the DPAG is involved in the tonic and reflex control of AP and HR in conscious rats. In addition, the SC seems to contribute to the baroreflex cardioinhibition.
Department of Physiological Sciences, Biomedical Center, Federal University of Espirito Santo, Vitoria, Brazil.
K N
KN
Sampaio
H
H
Mauad
V C
VC
Biancardi
J L
JL
Barros
F T
FT
Amaral
L C
LC
Schenberg
E C
EC
Vasquez
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000465:Algorithms; D000818:Animals; D017704:Baroreflex / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D003714:Denervation; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology*; D008297:Male; D008845:Microinjections; D016202:N-Methylaspartate / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D010487:Periaqueductal Gray / Q000033:anatomy & histology / Q000502:physiology*; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D014665:Vasodilator Agents / Q000494:pharmacology
D000316:Adrenergic alpha-Agonists; D018690:Excitatory Amino Acid Agonists; D014665:Vasodilator Agents; D009599:Nitroprusside; D010656:Phenylephrine; D016202:N-Methylaspartate