Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study assessed the effect of non-peptide angiotensin II receptor subtype antagonists on the cardiovascular response to footshock. Effects of electric stimulation (1, 2 or 5 Hz) on mean arterial pressure (MAP) and heart rate (HR) were determined. Peripheral or central administration of losartan, an angiotensin AT1 receptor antagonist (1 or 10 mg/kg s.c., or at 10, 30 or 100 micrograms/5 microliters i.c.v.), inhibited the mean arterial pressure response but not the heart rate response to footshock. In contrast, the MAP response to exogenous administration of norepinephrine was not inhibited by subcutaneous administration of losartan (10 mg/kg). Given at 100 micrograms/5 microliters i.c.v., the angiotensin AT2-selective receptor antagonist, PD 123319, did not reduce hemodynamic responses to electric stimulation. These results suggest that, in acute stress, endogenous angiotensin II facilitation of noradrenergic transmission is mediated through the angiotensin AT1 receptor.
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PMID:Role of angiotensin AT1 receptor in the cardiovascular response to footshock. 813 66

A change from group housing to isolation in unfamiliar metabolic cages represents, for rodents, a significant emotional stress. We studied the effect of candesartan, a peripheral and central angiotensin II AT1-receptor antagonist, on the hormonal and sympathetic response to acute isolation. We pretreated rats with 1 mg/kg/day candesartan for 13 days via subcutaneously implanted osmotic minipumps, followed by 24-hour isolation in individual metabolic cages. We measured brain, pituitary and adrenal angiotensin II (Ang II) receptor binding by quantitative autoradiography and adrenal hormones and catecholamines by RIA and HPLC. Isolation increased adrenal catecholamines, aldosterone and corticosterone, AT1-receptor binding in the zona glomerulosa and AT2-receptor binding in the adrenal medulla. Candesartan pretreatment decreased adrenal catecholamines, aldosterone and corticosterone, AT1-receptor binding in adrenal zona glomerulosa and medulla, pituitary gland and the hypothalamic paraventricular nucleus, and AT2-receptor binding in adrenal medulla, but increased AT2-receptor binding in zona glomerulosa. We conclude that peripheral and central AT1-receptor blockade with candesartan decreases the sympatho-adrenal and hormonal response to acute stress. Our results indicate that Ang II is an important stress hormone and suggest that blockade of the physiologically active AT 1-receptors could influence stress-related disorders.
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PMID:Candesartan decreases the sympatho-adrenal and hormonal response to isolation stress. 2809 44