title: Importance of angiotensinergic mechanisms for the pressor response to l-glutamate into the rostral ventrolateral medulla.
abstract: Pressor responses to l-glutamate into the rostroventrolateral medulla (RVLM) are reduced by lesions of the anteroventral third ventricle (AV3V) region, a main site related to central angiotensinergic pressor mechanisms. Therefore, similar to AV3V lesions, in the present study we investigated if the blockade of central angiotensinergic mechanisms with losartan or ZD 7155 might affect pressor responses to l-glutamate into the RVLM. Male Holtzman rats (280-320g, n=4-8/group) with cannulas implanted into the RVLM and lateral ventricle (LV) were used. Injections of l-glutamate (5nmol/100nl) or angiotensin II (200ng/100nl) into the RVLM increased MAP (54+/-5 and 26+/-3mm Hg, respectively). Losartan (100 microg/1 microl) or ZD 7155 (50 microg/1 microl) injected into the LV reduced the pressor responses to l-glutamate into the RVLM (22+/-5 and 26+/-7mm Hg, respectively), without changing the pressor responses to angiotensin II into the RVLM. Losartan (10 microg/100 nl) or ZD 7155 (5 microg/100 nl) into the RVLM reduced the pressor response to l-glutamate (5+/-3 and 33+/-4mm Hg, respectively) or angiotensin II (5+/-3 and 6+/-2mm Hg, respectively) into the RVLM. Previous injection of angiotensin II (50ng/100nl) into the RVLM increased the pressor response to l-glutamate into the RVLM (from 44+/-5 to 68+/-7mm Hg). The results suggest that angiotensinergic mechanisms directly in the RVLM and outside the RVLM (probably forebrain) are important for the pressor responses to l-glutamate into the RVLM.
authors.affiliation: Department of Physiology and Pathology, School of Dentistry, São Paulo State University (UNESP), Araraquara, SP 14801-903, Brazil.
authors.forename: Alexandre Antonio
authors.initials: AA
authors.lastname: Vieira
authors.forename: Eduardo
authors.initials: E
authors.lastname: Colombari
authors.forename: Laurival A
authors.initials: LA
authors.lastname: De Luca
authors.forename: Débora S A
authors.initials: DS
authors.lastname: Colombari
authors.forename: Patrícia M
authors.initials: PM
authors.lastname: De Paula
authors.forename: José V
authors.initials: JV
authors.lastname: Menani
mesh_terms: D000804:Angiotensin II / Q000378:metabolism / Q000494:pharmacology; D000809:Angiotensins / Q000378:metabolism* / Q000494:pharmacology; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology; D017776:Autonomic Pathways / Q000033:anatomy & histology / Q000187:drug effects / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D002320:Cardiovascular Physiological Phenomena; D018698:Glutamic Acid / Q000378:metabolism* / Q000494:pharmacology; D019808:Losartan / Q000494:pharmacology; D008297:Male; D008526:Medulla Oblongata / Q000033:anatomy & histology / Q000187:drug effects / Q000378:metabolism*; D009287:Naphthyridines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012154:Reticular Formation / Q000033:anatomy & histology / Q000187:drug effects / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000033:anatomy & histology / Q000187:drug effects / Q000378:metabolism; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*
chemical_list: D000809:Angiotensins; D000889:Anti-Arrhythmia Agents; D009287:Naphthyridines; C095905:ZD 7155; D000804:Angiotensin II; D018698:Glutamic Acid; D019808:Losartan