Role of central angiotensinergic mechanism in shaking stress-induced ACTH and catecholamine secretion

Hirasawa, Ryuto; Hashimoto, Kozo; Ota, Zensuke

doi:10.1016/0006-8993(90)91787-h

Cited by 18 publications

(15 citation statements)

References 17 publications

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“…Accordingly, forebrain AT 1 receptors have been implicated in physiological arousal caused by various emotional stressors in rats (17,20,29,42). It seems unlikely that the decrease in the stress response in our study was due to a nonspecific inhibitory action of candesartan, associated with microinjecting the highly concentrated solution of this substance.…”

Section: Discussionmentioning

confidence: 67%

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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Section: Discussionmentioning

confidence: 67%

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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“…3 and 4), a finding that is in line with various studies showing 1) that candesartan reduces the corticosterone release stimulated by ANG in rats (17), 2) that captopril after icv administration attenuates the ACTH release in response to hemorrhage (38), and 3) that losartan reduces ACTH responses to hypoglycemia in volunteers (39). On the other hand, there is evidence that central ANG is not required for the secretory response of the hypothalamus and pituitary gland to stress because ACTH responses to ether, shaking, or immobilization stress in rats are unchanged by central AT 1 antagonists or ACE inhibitors (13,40,41).…”

Section: Discussionmentioning

confidence: 93%

“…It is conspicuous that studies showing no influence of AT 1 or ACE inhibition on HPA axis reactivity were performed in normotensive rats (13,40,41). Because hypertensive patients exhibit larger cortisol elevations during stress compared with normotensive patients (19,34) and because the increase in endocrine stress response was paralleled by an increase of AT 1A receptors in pituitary glands of SHR (18), hypertension may be a prerequisite for an effective attenuation of the HPA axis reactivity after AT 1 blockade.…”

Section: Discussionmentioning

confidence: 98%

Angiotensin II Inhibition Reduces Stress Sensitivity of Hypothalamo-Pituitary-Adrenal Axis in Spontaneously Hypertensive Rats

et al. 2006

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Angiotensin II type 1 (AT(1)) receptors are expressed within organs of the hypothalamo-pituitary-adrenal (HPA) axis and seem to be important for its stress responsiveness. Secretion of CRH, ACTH, and corticosterone (CORT) is increased by stimulation of AT(1) receptors. In the present study, we tested whether a blockade of the angiotensin II system attenuates the HPA axis reactivity in spontaneously hypertensive rats. Spontaneously hypertensive rats were treated with candesartan (2 mg/kg), ramipril (1 mg/kg), or mibefradil (12 mg/kg) for 5 wk. In addition to baseline levels, CORT and ACTH responses to injection of CRH (100 microg/kg) were monitored over 4 h. mRNA of CRH, proopiomelanocortin, AT(1A), AT(1B), and AT(2) receptors was quantified by real-time PCR. All treatments induced equivalent reductions of blood pressure and had no effect on baseline levels of CORT and ACTH. However, both candesartan and ramipril significantly reduced CRH-stimulated plasma levels of ACTH (-26 and -15%) and CORT (-36 and -18%) and lowered hypothalamic CRH mRNA (-25 and -29%). Mibefradil did not affect any of these parameters. Gene expression of AT(1A), AT(1B), and AT(2) receptors within the HPA axis was not altered by any drug. We show for the first time that antihypertensive treatment by inhibition of AT(1) receptors or angiotensin-converting enzyme attenuates HPA axis reactivity independently of blood pressure reduction. This action is solely evident after CRH stimulation but not under baseline conditions. Both a reduced pituitary sensitivity to CRH and a down-regulation of hypothalamic CRH expression have the potential to reduce HPA axis activity during chronic AT(1) blockade or angiotensin-converting enzyme inhibition.

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“…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%

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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Role of central angiotensinergic mechanism in shaking stress-induced ACTH and catecholamine secretion

Cited by 18 publications

References 17 publications

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

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

Angiotensin II Inhibition Reduces Stress Sensitivity of Hypothalamo-Pituitary-Adrenal Axis in Spontaneously Hypertensive Rats

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

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