Alpha2 but not alpha1 and beta adrenoceptors in the lateral septal area modulates cardiovascular responses evoked by restraint stress in rats

Abstract

s / Autonomic Neuroscience: Basic and Clinical 163 (2011) 1–133 57 P.042 Alpha2 but not alpha1 and beta adrenoceptors in the lateral septal area modulates cardiovascular responses evoked by restraint stress in rats A.A. Scopinho, D.G. Reis, L.B.M. Resstel, F.M.A. Correa (Faculdade de Medicina de Ribeirao Preto, USP Farmacologia, Brazil) Background/aims: The lateral septal area (LSA) is involved in cardiovascular responses connected with emotional behavior. Restraint stress (RS) causes hypertension and tachycardia, and these responses are significantly reduced by microinjection of cobalt chloride (inhibitor synaptic) in LSA. RS also causes increased expression of c-fos in ASL, suggesting that this structure is involved in the modulation of cardiovascular responses evoked by the RS. Microdialysis studies showed that the levels of noradrenaline (NA) are increased during RS in several limbic regions involved in behavioral and autonomic responses, including LSA. Then, the aim of our study was to investigate the involvement of the noradrenergic system of ASL on the cardiovascular responses caused by the RS. Methods: Wistar rats were used (240-280 g). Guide-cannulae were implanted bilaterally in the LSA for microinjection of alpha2-receptor antagonist RX821002 (10 nmol/100 nL), alpha1-receptor antagonist WB4101 (10 nmol/100 nL), beta receptor antagonist propranolol (10 nmol/100 nL) or vehicle artificial cerebrospinal fluid (aCSF). A catheter was implanted in the femoral artery to record arterial pressure and heart rate. Ten minutes after the microinjection of drugs, the animals were submitted to the RS for an hour. Results: Acute restraint caused significant increases in both MAP (F35,360=5.2; P<0.001) and HR (F35,360=7.56; P<0.001). RX821002 treatment significantly reduced the MAP increase (F1,360=32.66, P<0.0001) and tachycardiac response (F1,350=84.96, P<0.0001) evoked by RS. In contrast, WB4101 did not change the MAP increase (F1,280=2.1; P=0,1452) and tachycardia (F1,280=0.68; P=0,4091) evoked by RS. Also, propranolol did not change the MAP increase (F1,315=3.5; P=0,0589) and tachycardia (F1,315=2.9; P=0,0853) evoked by RS. Conclusion: These results suggest that noradrenergic alpha2adrenoceptors in the LSA has facilitatory role in controlling cardiovascular responses to RS. Moreover, alpha1 and beta adrenoceptors do not seem to be involved in these responses.