title: Involvement of brain ANG II in acute sodium depletion induced salty taste changes.
abstract: Many investigations have been devoted to determining the role of angiotensin II (ANG II) and aldosterone (ALD) in sodium-depletion-induced sodium appetite, but few were focused on the mechanisms mediating the salty taste changes accompanied with sodium depletion. To further elucidate the mechanism of renin-angiotensin-aldosterone system (RAAS) action in mediating sodium intake behavior and accompanied salty taste changes, the present study examined the salty taste function changes accompanied with sodium depletion induced by furosemide (Furo) combined with different doses of angiotensin converting enzyme (ACE) inhibitor, captopril (Cap). Both the peripheral and central RAAS activity and the nuclei Fos immunoreactivity (Fos-ir) expression in the forebrain area were investigated. Results showed that sodium depletion induced by Furo+low-Cap increased taste preference for hypertonic NaCl solution with amplified brain action of ANG II but without peripheral action, while Furosemide combined with a high dose of captopril can partially inhibit the formation of brain ANG II, with parallel decreased effects on salty taste changes. And the resulting elevating forebrain ANG II may activate a variety of brain areas including SFO, PVN, SON and OVLT in sodium depleted rats injected with Furo+low-Cap, which underlines salty taste function and sodium intake behavioral changes. Neurons in SFO and OVLT may be activated mainly by brain ANG II, while PVN and SON activation may not be completely ANG II dependent. These findings suggested that forebrain derived ANG II may play a critical role in the salty taste function changes accompanied with acute sodium depletion.
authors: Department of Physiology and Pathophysiology, Xi'an Jiaotong University School of Medicine, Xi'an, Shaanxi, 710061, P R China.
authors: Bo
authors: B
authors: Lu
authors: Jianqun
authors: J
authors: Yan
authors: Xuejuan
authors: X
authors: Yang
authors: Jinrong
authors: J
authors: Li
authors: Ke
authors: K
authors: Chen
mesh_terms: D000450:Aldosterone / Q000378:metabolism; D000803:Angiotensin I / Q000378:metabolism; D000804:Angiotensin II / Q000378:metabolism*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D001066:Appetite / Q000187:drug effects; D001070:Appetitive Behavior / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002216:Captopril / Q000008:administration & dosage / Q000494:pharmacology; D004338:Drug Combinations; D004353:Drug Evaluation, Preclinical; D005665:Furosemide / Q000494:pharmacology; D007150:Immunohistochemistry; D008297:Male; D010286:Paraventricular Hypothalamic Nucleus / Q000187:drug effects* / Q000473:pathology; D011863:Radioimmunoassay; D051381:Rats; D017207:Rats, Sprague-Dawley; D012084:Renin-Angiotensin System; D012964:Sodium / Q000378:metabolism*; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage / Q000494:pharmacology; D013356:Subfornical Organ / Q000187:drug effects / Q000473:pathology; D013495:Supraoptic Nucleus / Q000187:drug effects* / Q000473:pathology; D013649:Taste / Q000187:drug effects*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D004338:Drug Combinations; D017673:Sodium Chloride, Dietary; D000804:Angiotensin II; D000450:Aldosterone; D005665:Furosemide; D000803:Angiotensin I; D002216:Captopril; D012964:Sodium