Abstract
The insular cortex (IC) is a limbic structure involved in cardiovascular responses observed during aversive threats. However, the specific neurotransmitter mediating IC control of cardiovascular adjustments to stress is yet unknown. Therefore, in the present study we investigated the role of local IC adrenoceptors in the cardiovascular responses elicited by acute restraint stress in rats. Bilateral microinjection of different doses (0.3, 5, 10 and 15 nmol/100 nl) of the selective α1-adrenoceptor antagonist WB4101 into the IC reduced both the arterial pressure and heart rate increases elicited by restraint stress. However, local IC treatment with different doses (0.3, 5, 10 and 15 nmol/100 nl) of the selective α2-adrenoceptor antagonist RX821002 reduced restraint-evoked tachycardia without affecting the pressor response. The present findings are the first direct evidence showing the involvement of IC adrenoceptors in cardiovascular adjustments observed during aversive threats. Our findings indicate that IC noradrenergic neurotransmission acting through activation of both α1- and α2-adrenoceptors has a facilitatory influence on pressor response to acute restraint stress. Moreover, IC α1-adrenoceptors also play a facilitatory role on restraint-evoked tachycardiac response.
Highlights
Stress situations happen during real or perceived threat to homeostasis or well-being
Time-course analysis of restraint-evoked cardiovascular responses indicated that insular cortex (IC) treatment with WB4101 reduced both Mean arterial pressure (MAP) (F(4,660) = 336, P,0.0001) and heart rate (HR) (F(4,660) = 50, P,0.0001) responses, when compared with artificial cerebrospinal fluid (ACSF)-treated animals (n = 7)
The results of the present work provide the first direct evidence for the involvement of IC adrenoceptors in cardiovascular responses observed during aversive threats
Summary
Stress situations happen during real or perceived threat to homeostasis or well-being. Stressors include either interoceptive changes (e.g., blood volume or osmolality changes) or environmental threat that may be physical (e.g., hypoxia) or psychological (e.g., presence of a predator). During stress a spectrum of physiological responses are evoked to maintain the physiologic integrity of the organism [1]. The physiological responses to stress are mainly characterized by autonomic nervous system alterations, increase in plasma catecholamine levels and activation of the hypothalamus-pituitary-adrenal (HPA) axis [1,2]. Autonomic responses include increase on both blood pressure and heart rate (HR) [3,4]. Cardiovascular changes during stress are accompanied by a resetting of baroreflex toward higher arterial pressure values, allowing simultaneous blood pressure and HR increases [5,6,7,8]
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