title: Cardiovascular responses produced by central injection of hydrogen peroxide in conscious rats.
abstract: Reactive oxygen species (ROS) have been shown to modulate neuronal synaptic transmission and may play a role on the autonomic control of the cardiovascular system. In this study we investigated the effects produced by hydrogen peroxide (H(2)O(2)) injected alone or combined with the anti-oxidant agent N-acetil-l-cysteine (NAC) or catalase into the fourth brain ventricle (4th V) on mean arterial pressure and heart rate of conscious rats. Moreover the involvement of the autonomic nervous system on the cardiovascular responses to H(2)O(2) into the 4th V was also investigated. Male Holtzman rats (280-320 g) with a stainless steel cannula implanted into the 4th V and polyethylene cannulas inserted into the femoral artery and vein were used. Injections of H(2)O(2) (0.5, 1.0 and 1.5 micromol/0.2 microL, n=6) into the 4th V produced transient (for 10 min) dose-dependent pressor responses. The 1.0 and 1.5 micromol doses of H(2)O(2) also produced a long lasting bradycardia (at least 24 h with the high dose of H(2)O(2)). Prior injection of N-acetyl-l-cysteine (250 nmol/1 microL/rat) into the 4th V blockade the pressor response and attenuated the bradycardic response to H(2)O(2) (1 micromol/0.5 microL/rat, n=7) into the 4th V. Intravenous (i.v.) atropine methyl bromide (1.0 mg/kg, n=11) abolished the bradycardia but did not affect the pressor response to H(2)O(2). Prazosin hydrochloride (1.0 mg/kg, n=6) i.v. abolished the pressor response but did not affect the bradycardia. The increase in the catalase activity (500 UEA/1 microL/rat injected into the 4th V) also abolished both, pressor and bradycardic responses to H(2)O(2). The results suggest that increased ROS availability into 4th V simultaneously activate sympathetic and parasympathetic outflow inducing pressor and bradycardic responses.
authors.affiliation: Department of Physiology, Federal University of São Paulo (UNIFESP), Rua Botucatu, 862, 04023-060 São Paulo, SP, Brazil.
authors.forename: Leonardo
authors.initials: L
authors.lastname: Máximo Cardoso
authors.forename: Débora Simões
authors.initials: DS
authors.lastname: de Almeida Colombari
authors.forename: José
authors.initials: J
authors.lastname: Vanderlei Menani
authors.forename: Deoclécio
authors.initials: D
authors.lastname: Alves Chianca
authors.forename: Eduardo
authors.initials: E
authors.lastname: Colombari
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D000975:Antioxidants / Q000494:pharmacology; D001342:Autonomic Nervous System Diseases / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001919:Bradycardia / Q000139:chemically induced / Q000503:physiopathology; D002320:Cardiovascular Physiological Phenomena / Q000187:drug effects*; D002374:Catalase / Q000378:metabolism / Q000494:pharmacology; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions / Q000502:physiology; D006861:Hydrogen Peroxide / Q000378:metabolism / Q000494:pharmacology*; D006973:Hypertension / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D016877:Oxidants / Q000378:metabolism / Q000494:pharmacology; D010275:Parasympathetic Nervous System / Q000187:drug effects* / Q000502:physiology; D010276:Parasympatholytics / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000502:physiology
chemical_list: D000959:Antihypertensive Agents; D000975:Antioxidants; D016877:Oxidants; D010276:Parasympatholytics; D017382:Reactive Oxygen Species; D006861:Hydrogen Peroxide; D002374:Catalase