Abstract:Exogenous glucocorticoids act within the hindbrain to enhance the arterial pressure response to acute novel stress. Here we tested the hypothesis that endogenous glucocorticoids act at hindbrain glucocorticoid receptors (GR) to augment cardiovascular responses to restraint stress in a model of stress hyperreactivity, the borderline hypertensive rat (BHR). A 3-to 4-mg pellet of the GR antagonist mifepristone (Mif) was implanted over the dorsal hindbrain (DHB) in WistarKyoto (WKY) and BHRs. Control pellets consi… Show more
“…Consistent with previous reports (4,5,22,23), repeated exposure to restraint stress resulted in an adaptation of the HPA axis that was manifested as a habituation to stress-induced corticosterone secretion, as well as a mild but reliable hypersecretion of basal corticosterone (24,25). Our data demonstrate that AEA and 2-AG are divergently regulated by repeated stress, and independently contribute to distinct forms of HPA axis adaptation.…”
Secretion of glucocorticoid hormones during stress produces an array of physiological changes that are adaptive and beneficial in the short term. In the face of repeated stress exposure, however, habituation of the glucocorticoid response is essential as prolonged glucocorticoid secretion can produce deleterious effects on metabolic, immune, cardiovascular, and neurobiological function. Endocannabinoid signaling responds to and regulates the activity of the hypothalamic-pituitary-adrenal (HPA) axis that governs the secretion of glucocorticoids; however, the role this system plays in adaptation of the neuroendocrine response to repeated stress is not well characterized. Herein, we demonstrate a divergent regulation of the two endocannabinoid ligands, N-arachidonylethanolamine (anandamide; AEA) and 2-arachidonoylglycerol (2-AG), following repeated stress such that AEA content is persistently decreased throughout the corticolimbic stress circuit, whereas 2-AG is exclusively elevated within the amygdala in a stress-dependent manner. Pharmacological studies demonstrate that this divergent regulation of AEA and 2-AG contribute to distinct forms of HPA axis habituation. Inhibition of AEA hydrolysis prevented the development of basal hypersecretion of corticosterone following repeated stress. In contrast, systemic or intra-amygdalar administration of a CB 1 receptor antagonist before the final stress exposure prevented the repeated stress-induced decline in corticosterone responses. The present findings demonstrate an important role for endocannabinoid signaling in the process of stress HPA habituation, and suggest that AEA and 2-AG modulate different components of the adrenocortical response to repeated stressor exposure.corticosterone | endocannabinoid | habituation | hypothalamic-pituitaryadrenal axis | amygdala
“…Consistent with previous reports (4,5,22,23), repeated exposure to restraint stress resulted in an adaptation of the HPA axis that was manifested as a habituation to stress-induced corticosterone secretion, as well as a mild but reliable hypersecretion of basal corticosterone (24,25). Our data demonstrate that AEA and 2-AG are divergently regulated by repeated stress, and independently contribute to distinct forms of HPA axis adaptation.…”
Secretion of glucocorticoid hormones during stress produces an array of physiological changes that are adaptive and beneficial in the short term. In the face of repeated stress exposure, however, habituation of the glucocorticoid response is essential as prolonged glucocorticoid secretion can produce deleterious effects on metabolic, immune, cardiovascular, and neurobiological function. Endocannabinoid signaling responds to and regulates the activity of the hypothalamic-pituitary-adrenal (HPA) axis that governs the secretion of glucocorticoids; however, the role this system plays in adaptation of the neuroendocrine response to repeated stress is not well characterized. Herein, we demonstrate a divergent regulation of the two endocannabinoid ligands, N-arachidonylethanolamine (anandamide; AEA) and 2-arachidonoylglycerol (2-AG), following repeated stress such that AEA content is persistently decreased throughout the corticolimbic stress circuit, whereas 2-AG is exclusively elevated within the amygdala in a stress-dependent manner. Pharmacological studies demonstrate that this divergent regulation of AEA and 2-AG contribute to distinct forms of HPA axis habituation. Inhibition of AEA hydrolysis prevented the development of basal hypersecretion of corticosterone following repeated stress. In contrast, systemic or intra-amygdalar administration of a CB 1 receptor antagonist before the final stress exposure prevented the repeated stress-induced decline in corticosterone responses. The present findings demonstrate an important role for endocannabinoid signaling in the process of stress HPA habituation, and suggest that AEA and 2-AG modulate different components of the adrenocortical response to repeated stressor exposure.corticosterone | endocannabinoid | habituation | hypothalamic-pituitaryadrenal axis | amygdala
“…To this point, it has been indicated that chronic stress does not have an effect on BP (Scheuer et al 2007;Bechtold et al 2009;Scheuer 2010) and nesfatin-1 increases BP Samson 2009, 2010;García-Galiano et al 2010). Yosten and his colleagues have showed that intracerebroventricular nesfatin-1 administration increases BP (Yosten and Samson 2009) and this effect of nesfatin-1 occurs via sympathetic system activation (Yosten and Samson 2010).…”
Section: Discussionmentioning
confidence: 99%
“…Cardiovascular responses occur after acute and chronic stress, which can increase the risk of hypertension and cardiovascular diseases (Bechtold et al 2009). Nesfatin-1 can control appetite in a different pathway than leptin and increases insulin secretion by activation of L-type Ca 2+ channels in pancreatic islet beta cells (Cowley and Grove 2006;Nakata et al 2011).…”
Section: Discussionmentioning
confidence: 99%
“…It is very well known that stress response correlates with increased basal blood level of mineralocorticoids and glucocorticoids (McEwen 2007;Ulrich-Lai and Herman 2009;Bechtold et al 2009). On the other hand, desensitization to repeated stress exposure has been explained linked with recovery of plasma level of corticosterones and adrenocorticotropic hormone (ACTH).…”
Abstract. Nesfatin is a peptide secreted by peripheral tissues, central and peripheral nervous system. It is involved in the regulation of homeostasis. Although the effects of nesfatin-1 on nutrition have been studied widely in the literature, the mechanisms of nesfatin-1 action and also relations with other physiological parameters are still not clarified well. We aimed to investigate the effect of peripheral chronic nesfatin-1 application on blood pressure regulation in normal and in rats exposed to restraint immobilization stress. In our study, three month-old male Wistar rats were used. Rats were divided into 4 groups as Control, Stress, Control+Nesfatin-1, Nesfatin-1+Stress. Angiotensinogen, angiotensin converting enzyme 2, angiotensin II, endothelin-1, endothelial nitric oxide synthase, aldosterone, cortisol, nesfatin-1 levels were determined in plasma samples by ELISA. Our results have shown that chronic peripheral nesfatin-1 administration increases blood pressure in normal and in rats exposed to chronic restraint stress. Effect of nesfatin-1 on circulating level of angiotensinogen, angiotensin converting enzyme 2, angiotensin II, endothelin-1, endothelial nitric oxide synthase, aldosterone and cortisol has been identified. We can conclude that elevated high blood pressure after chronic peripheral nesfatin-1 administration in rats exposed to chronic restraint stress may be related to decreased plasma level of endothelial nitric oxide synthase concentration.
“…Different types of stress have been applied, such as emotional stimuli, psychosocial stress, immobilization stress, food deprivation and electric stimuli, air jet noise, flashing lights, cold, and interaction of members of a social group as they compete for food and water (Henry 1975;Friedman and Dahl 1975;Papanek et al 1991;Henry et al 1993;Tucker and Hunt 1993;Bechtold et al 2009). …”
Section: Psychosocial and Environment-induced Hypertensionmentioning
Hypertension is one of the leading causes of disability or death due to stroke, heart attack and kidney failure. Because the etiology of essential hypertension is not known and may be multifactorial, the use of experimental animal models has provided valuable information regarding many aspects of the disease, which include etiology, pathophysiology, complications and treatment. The models of hypertension are various, and in this review, we provide a brief overview of the most widely used animal models, their features and their importance.
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