Lateral septal area α₁‐ and α₂‐adrenoceptors differently modulate baroreflex activity in unanaesthetized rats

Abstract

2012Lateral septal area alpha(1)-and alpha(2)-adrenoceptors differently modulate baroreflex activity in unanaesthetized rats EXPERIMENTAL PHYSIOLOGY, HOBOKEN, v. 97, n. 9, pp. 1018-1029, SEP, 2012 http://www.producao.usp.br/handle/BDPI/42780 The lateral septal area (LSA) is a limbic structure involved in autonomic, neuroendocrine and behavioural responses. An inhibitory influence of the LSA on baroreflex activity has been reported; however, the local neurotransmitter involved in this modulation is still unclear.In the present study, we verified the involvement of local LSA adrenoceptors in modulating cardiac baroreflex activity in unanaesthetized rats. Bilateral microinjection of the selective α 1 -adrenoceptor antagonist WB4101 (10 nmol in a volume of 100 nl) into the LSA decreased baroreflex bradycardia evoked by blood pressure increases, but had no effect on reflex tachycardia evoked by blood pressure decreases. Nevertheless, bilateral administration of the selective α 2 -adrenoceptor antagonist RX821002 (10 nmol in 100 nl) increased baroreflex tachycardia without affecting reflex bradycardia. Treatment of the LSA with a cocktail containing WB4101 and RX821002 decreased baroreflex bradycardia and increased reflex tachycardia. The nonselective β-adrenoceptor antagonist propranolol (10 nmol in 100 nl) did not affect either reflex bradycardia or tachycardia. Microinjection of noradrenaline into the LSA increased reflex bradycardia and decreased the baroreflex tachycardic response, an opposite effect compared with those observed after double blockade of α 1 -and α 2 -adrenoceptors, and this effect of noradrenaline was blocked by local LSA pretreatment with the cocktail containing WB4101 and RX821002. The present results provide advances in our understanding of the baroreflex neural circuitry. Taken together, data suggest that local LSA α 1 -and α 2 -adrenoceptors modulate baroreflex control of heart rate differently. Data indicate that LSA α 1 -adrenoceptors exert a facilitatory modulation on baroreflex bradycardia, whereas local α 2 -adrenoceptors exert an inhibitory modulation on reflex tachycardia.

Influence of Apnea-induced Hypoxia on Catecholamine Release and Cardiovascular Dynamics

“…Norepinephrine seems to play an important role influencing bradycardia via α1-adrenoceptors in the lateral septal area of the limbic structure. This was further substantiated by Scopinho et al, who were able to decrease baroreflex dependent bradycardia by a selective α1-adrenoceptor antagonist in the situation of high blood pressure [39]. This finding is supported by our result of an inverse correlation between HR and norepinephrine concentration.…”

Cardiovascular and autonomic alterations in rats with Parkinsonism induced by 6-OHDA and treated with L-DOPA

“…The direct recording of BP and HR was conducted using the implanted arterial cannula in the femoral artery in accordance with previous work ( [23,50,51,10]). The recording was done while the animals were awake and freely moving.…”

The medial amygdaloid nucleus modulates the baroreflex activity in conscious rats

“…Therefore, we suggest that the MeA could be modulating the baroreflex parasympathetic component during defensive situations. Baroreflex inhibition was also reported to involve other areas of the limbic system, such as the dorsolateral periaqueductal gray matter (Nosaka et al, 1993;Pelosi et al, 2007), the medial prefrontal cortex Resstel et al, 2004), lateral septal area (Scopinho et al, 2007(Scopinho et al, , 2012 and the diagonal band of Broca (Crestani et al, 2008b). These areas are connected to the MeA (Bienkowski et al, 2013;Canteras et al, 1995), suggesting the existence of an interrelation between them in baroreflex modulation under aversive conditions.…”

“…However, the observation that the magnitude of the bradycardic response evoked by noradrenaline in this area significantly correlates with the magnitude of the pressor response favors the idea of a reflex mechanism. The involvement of the noradrenergic neurotransmission from several brain regions of the central nervous system in the control of baroreflex response has been well documented (Alves et al, 2009b;Crestani et al, 2008a;Hwang et al, 1998;Scopinho et al, 2012). This modulation could either be due to inhibition of baroreceptor input to vagal neurons or to facilitation of an inhibitory drive to these neurons, thus enhancing parasympathetic response to blood pressure increase.…”

“…Moreover, it sends projections to several limbic structures that are involved in baroreflex modulation, such as the medial prefrontal cortex Sevoz-Couche et al, 2006), the bed nucleus of the stria terminalis (Crestani et al, 2006), the periaqueductal grey area (Pelosi et al, 2007), the hypothalamus (Crestani et al, 2010a;Sevoz-Couche et al, 2006), lateral septal area (Scopinho et al, 2007(Scopinho et al, , 2012 and the diagonal band of Broca (Crestani et al, 2008b).…”