Kwang-lae Hoe - Academia.edu (original) (raw)

Papers by Kwang-lae Hoe

Research paper thumbnail of Peripheral Administration of an Angiotensin II AT 1 Receptor Antagonist Decreases the Hypothalamic-Pituitary-Adrenal Response to Isolation Stress

Endocrinology, 2001

Angiotensin II, which stimulates AT 1 receptors, is a brain and peripheral stress hormone. We pre... more Angiotensin II, which stimulates AT 1 receptors, is a brain and peripheral stress hormone. We pretreated rats with the AT 1 receptor antagonist candesartan for 13 d via sc-implanted osmotic minipumps, followed by 24-h isolation in individual metabolic cages. We measured angiotensin II receptor-type binding and mRNAs and tyrosine hydroxylase mRNA by quantitative autoradiography and in situ hybridization, catecholamines by HPLC, and hormones by RIA. Isolation increased AT 1 receptor binding in hypothalamic paraventricular nucleus as well as anterior pituitary ACTH, and decreased posterior pituitary AVP. Isolation stress also increased AT 1 receptor binding and AT 1B mRNA in zona glomerulosa and AT 2 binding in adrenal medulla, adrenal catecholamines, tyrosine hydroxylase mRNA, aldosterone, and corticosterone. Candesartan blocked AT 1 binding in paraventricular nucleus and adrenal gland; prevented the isolation-induced alterations in pituitary ACTH and AVP and in adrenal corticosterone, aldosterone, and catecholamines; abolished the increase in AT 2 binding in adrenal medulla; and substantially decreased urinary AVP, corticosterone, aldosterone, and catecholamines during isolation. Peripheral pretreatment with an AT 1 receptor antagonist blocks brain and peripheral AT 1 receptors and inhibits the hypothalamicpituitary-adrenal response to stress, suggesting a physiological role for peripheral and brain AT 1 receptors during stress and a possible beneficial effect of AT 1 antagonism in stressrelated disorders.

Research paper thumbnail of Peripheral Administration of an Angiotensin II AT 1 Receptor Antagonist Decreases the Hypothalamic-Pituitary-Adrenal Response to Isolation Stress

Endocrinology, 2001

Angiotensin II, which stimulates AT 1 receptors, is a brain and peripheral stress hormone. We pre... more Angiotensin II, which stimulates AT 1 receptors, is a brain and peripheral stress hormone. We pretreated rats with the AT 1 receptor antagonist candesartan for 13 d via sc-implanted osmotic minipumps, followed by 24-h isolation in individual metabolic cages. We measured angiotensin II receptor-type binding and mRNAs and tyrosine hydroxylase mRNA by quantitative autoradiography and in situ hybridization, catecholamines by HPLC, and hormones by RIA. Isolation increased AT 1 receptor binding in hypothalamic paraventricular nucleus as well as anterior pituitary ACTH, and decreased posterior pituitary AVP. Isolation stress also increased AT 1 receptor binding and AT 1B mRNA in zona glomerulosa and AT 2 binding in adrenal medulla, adrenal catecholamines, tyrosine hydroxylase mRNA, aldosterone, and corticosterone. Candesartan blocked AT 1 binding in paraventricular nucleus and adrenal gland; prevented the isolation-induced alterations in pituitary ACTH and AVP and in adrenal corticosterone, aldosterone, and catecholamines; abolished the increase in AT 2 binding in adrenal medulla; and substantially decreased urinary AVP, corticosterone, aldosterone, and catecholamines during isolation. Peripheral pretreatment with an AT 1 receptor antagonist blocks brain and peripheral AT 1 receptors and inhibits the hypothalamicpituitary-adrenal response to stress, suggesting a physiological role for peripheral and brain AT 1 receptors during stress and a possible beneficial effect of AT 1 antagonism in stressrelated disorders.