Stress and Brain Angiotensin II Receptors

Watanabe, Tatsuo; Fujioka, Takashi; Hashimoto, Makoto; Nakamura, Shôji

doi:10.1615/critrevneurobiol.v12.i4.20

Cited by 43 publications

(28 citation statements)

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“…5,6 In particular, it has been shown that central or systemic administration of AT 1 receptor antagonists attenuated the increase in blood pressure and plasma catecholamine levels caused by several psycho-and physico-emotional stressors in rats and rabbits. 12,[24][25][26] Our data extend these findings by showing that targeted deletion of the AT 1A receptor gene selectively attenuates the pressor response to stress in mice.…”

Section: Stress Responsementioning

confidence: 99%

“…Recent pharmacological studies, however, indicate that the activation of angiotensin II type 1 (AT 1 ) receptors, and specifically those in the dorsomedial hypothalamus (DMH) and rostral ventrolateral medulla (RVLM), is required for full expression of sympathetic cardiovascular responses to various psychoemotional stressors in rats and rabbits. [3][4][5][6][7] Nonetheless, the effect of genetic deficiency of AT 1 receptors on cardiovascular reactivity to stress is yet to be determined.…”

Section: Introductionmentioning

confidence: 99%

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Blood pressure reactivity to emotional stress is reduced in AT1A-receptor knockout mice on normal, but not high salt intake

et al. 2009

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Pharmacological evidence suggests that angiotenisn II type 1 (AT 1 ) receptors are involved in the regulation of cardiovascular response to emotional stress and reinforcing effect of dietary salt on this response. In this study, we examined the effect of genetic deletion of AT 1A receptors on the cardiovascular effects of stress and salt in mice. AT 1A receptor knockout (AT 1A À/À ) and wild-type (AT 1A +/+ ) mice were implanted with telemetry devices and placed on a normal (0.4%) or high (3.1%) salt diet (HSD). Resting blood pressure (BP) in AT 1AÀ/À mice (84 ± 3 mm Hg) was lower than in AT 1A +/+ mice (107 ± 2 mm Hg). Negative emotional (restraint) stress increased BP by 33±3 mm Hg in AT 1A +/+ mice. This response was attenuated by 40% in AT 1AÀ/À mice (18 ± 3 mm Hg). Conversely, the BP increase caused by food presentation and feeding was similar in AT 1AÀ/À (25 ± 3 mm Hg) and AT 1A +/+ mice (26 ± 3 mm Hg). HSD increased resting BP by 14 ± 4 mm Hg in AT 1A À/À mice without affecting it significantly in AT 1A +/+ mice. Under these conditions, the pressor response to restraint stress in AT 1A À/À mice (30±3 mm Hg) was no longer different from that in wild-type animals (28 ± 3 mm Hg). The BP response to feeding was not altered by HSD in either AT 1A À/À or AT 1A +/+ mice (25 ± 2 and 27 ± 3 mm Hg, respectively). These results indicate that AT 1A receptor deficiency leads to a reduction in BP reactivity to negative emotional stress, but not feeding. HSD can selectively reinforce the cardiovascular response to negative stress in AT 1A À/À mice. However, there is little interaction between AT 1A receptors, excess dietary sodium and feeding-induced cardiovascular arousal.

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Section: Stress Responsementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Blood pressure reactivity to emotional stress is reduced in AT1A-receptor knockout mice on normal, but not high salt intake

et al. 2009

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“…The change of ACTH and Cor adapt to the adverse environment, which is the evaluated index for the degree of stress and plays an extremely important role in the body (5). The weight of the organs change under the state of stress (6), including the pituitary, adrenal and hypothalamus. In the present study, by testing the organ coefficient of the pituitary and adrenal glands, and by testing the levels of ACTH and Cor in serum, whether the high temperature environment (32˚C) caused the heat-stress response in rats was explored.…”

Section: Introductionmentioning

confidence: 99%

Effect of acute heat stress on adrenocorticotropic hormone, cortisol, interleukin-2, interleukin-12 and apoptosis gene expression in rats

et al. 2015

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Abstract. The aim of the present study was to investigate the effect of acute heat stress on the neuroendocrine and immunological function in rats. Male Sprague-Dawley rats were randomly divided into two groups and respectively exposed to heat (32˚C) or to room temperature (24˚C). After 7 days of heat exposure, the heat-stress rat model was established. The organ coefficients of the pituitary and adrenal glands were determined. The body temperature was measured by telemetry. The average contents of adrenocorticotropic hormone (ACTH), cortisol (Cor), interleukin-2 (IL-2) and IL-12 in serum were detected. The expression of apoptotic genes in the spleen was measured. The results showed that acute heat stress did not evidently affect the body temperature and body weight (P>0.05), but the exposure increased the organ coefficients of the pituitary and adrenal glands (P<0.05). Heat exposure significantly elevated the level of ACTH, Cor, IL-2 and IL-12 (P<0.05). The expression of caspase-3 and Bax were not changed significantly (P>0.05), while Bcl2 was reduced (P<0.05).

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“…Forebrain angiotensin II (ANG II) has been implicated in controlling cardiovascular and neuroendocrine responses to various psychological and physical stressors (42). In particular, blockade of AT 1 receptors in the anterior and paraventricular hypothalamic nuclei has been shown to attenuate increases in blood pressure and plasma catecholamines caused by immobilization stress in rats (18,21).…”

mentioning

confidence: 99%

Angiotensin II in dorsomedial hypothalamus modulates cardiovascular arousal caused by stress but not feeding in rabbits

Matteo¹,

Head²,

Mayorov³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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The dorsomedial hypothalamus (DMH) is critically implicated in the cardiovascular response to emotional stress. This study aimed to determine whether the DMH is also important in cardiovascular arousal associated with appetitive feeding behavior and, if so, whether locally released angiotensin II and glutamate are important in this arousal. Emotional (air-jet) stress and feeding elicited similar tachycardic (ϩ51 and ϩ45 beats/min, respectively) and pressor (ϩ16 and ϩ9 mmHg, respectively) responses in conscious rabbits. Bilateral microinjection of GABAA agonist muscimol (500 pmol) into the DMH, but not nearby hypothalamic regions, attenuated pressor and tachycardic responses to air-jet by 56 -63% and evoked anorexia. Conversely, stimulation of the DMH with the glutamate analog kainic acid (250 pmol) elicited hypertension (ϩ25 mmHg) and tachycardia (ϩ114 beats/min) and activated feeding behavior. Local microinjection of a glutamate receptor antagonist, kynurenic acid (10 nmol), decreased pressor responses to stress and eating by 46 and 72%, respectively, without affecting feeding behavior. Bilateral microinjection of a selective AT1-receptor antagonist, candesartan (500 pmol), into the DMH, but not nearby sites, attenuated pressor and tachycardic stress responses by 31 and 33%, respectively. Candesartan did not alter feeding behavior or circulatory response to feeding. These results indicate that, in addition to its role in mediating stress responses, the DMH may be important in regulating cardiovascular arousal associated with feeding. Local glutamatergic inputs appear to regulate cardiovascular response to both stress and feeding. Conversely, angiotensin II, acting via AT1 receptors, may selectively modulate, in the DMH, cardiovascular response to stress, but not feeding. cardiovascular response; tachycardia; glutamate GROWING EVIDENCE INDICATES that the dorsomedial hypothalamus (DMH) plays a key role in modulating autonomic, neuroendocrine, and behavioral arousal caused by threatening stimuli (12). Activation of inhibitory GABA A receptors or blockade of excitatory amino acid (EAA) receptors in the DMH, but not nearby hypothalamus regions, markedly decreases the cardiovascular response to emotional stress in rats (38). Conversely, chemical stimulation of the DMH or blockade of local GABA A receptors elicits increases in blood pressure, heart rate (HR), and behavioral measures of anxiety in rats (32, 33). Moreover, excitotoxic lesions of the DMH cause hypophagia (3) and dramatically reduce circadian rhythms of wakefulness, feeding, and locomotor activity in rats (2, 6), indicating that, apart from the defense response, this region is critically involved in controlling a wide range of other behavioral activities. Although these activities, and particularly feeding, are normally associated in animals with distinct, central nervous systemmediated sympathetic activation (10,11,23), the functional role of the DMH in the regulation of the cardiovascular response to nonthreatening, arousing stimuli remains untested.For...

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Stress and Brain Angiotensin II Receptors

Cited by 43 publications

References 0 publications

Blood pressure reactivity to emotional stress is reduced in AT1A-receptor knockout mice on normal, but not high salt intake

Blood pressure reactivity to emotional stress is reduced in AT1A-receptor knockout mice on normal, but not high salt intake

Effect of acute heat stress on adrenocorticotropic hormone, cortisol, interleukin-2, interleukin-12 and apoptosis gene expression in rats

Angiotensin II in dorsomedial hypothalamus modulates cardiovascular arousal caused by stress but not feeding in rabbits

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