Nitric oxide at the CVLM is involved in the attenuation of the reflex bradycardia in renovascular hypertensive rats
| Autor: | Marcelo Eustáquio Silva, Luiz Eduardo Sousa, Mauro César Isoldi, Uberdan Guilherme Mendes de Castro, Graziele Galdino de Sousa, Andréia Carvalho Alzamora, Raquel do Pilar Machado, Robson A.S. Santos, Ana Paula Nadu, Maria José Campagnole-Santos |
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| Jazyk: | angličtina |
| Předmět: |
Male
Cancer Research Mean arterial pressure medicine.medical_specialty Nitric Oxide Synthase Type III Physiology Clinical Biochemistry Blood Pressure Ascorbic Acid Nitric Oxide Synthase Type I Baroreflex Arginine Biochemistry Nitric oxide Phenylephrine chemistry.chemical_compound Heart Rate Superoxides Internal medicine Bradycardia medicine Animals Renovascular hypertension-Goldblatt-2K1C Superoxide anion Microinjection Analysis of Variance Medulla Oblongata Rostral ventrolateral medulla Ascorbic acid Rats Inbred F344 Rats Caudal ventrolateral medulla Hypertension Renovascular NG-Nitroarginine Methyl Ester Blood pressure Endocrinology chemistry Reflex bradycardia Regression Analysis |
| Zdroj: | Repositório Institucional da UFOP Universidade Federal de Ouro Preto (UFOP) instacron:UFOP |
| ISSN: | 1089-8603 |
| DOI: | 10.1016/j.niox.2012.01.002 |
| Popis: | Hypertension is associated to an increase in central oxidative stress and an attenuation of the baroreflex control of arterial pressure. The present study evaluated the effect of alterations in the levels of nitric oxide (NO) and superoxide anion in the caudal ventrolateral medulla (CVLM), a key area of the brainstem for the baroreflex control of arterial pressure, in renovascular hypertensive rats (2K1C). Baseline mean arterial pressure (MAP), heart rate (HR), and reflex bradycardia were evaluated 30 days after renal artery occlusion in anesthetized (urethane, 1.2 g/kg, i.p.) 2K1C or normotensive (SHAM) rats. The MAP, HR, and baroreflex control of HR were evaluated before and after CVLM microinjections of the non-selective NOS inhibitor l -NAME (10 nmol), the NO precursor l -ARG (50 nmol), or the antioxidant ascorbic acid, Vit C (10 nmol). In both 2K1C and SHAM animals, CVLM microinjection of l -NAME produced a decrease in MAP, whereas l -ARG induced a significant increase in MAP. However, microinjection of Vit C into the CVLM produced a decrease in MAP and HR only in 2K1C and not in SHAM rats. Cardiovascular effects produced by microinjection of l -ARG into the CVLM were abolished by prior microinjection of l -NAME in the CVLM of 2K1C and SHAM rats. Microinjection of l -NAME into the CVLM increased the sensitivity of reflex bradycardia in 2K1C animals. In contrast, the CVLM microinjection of l -ARG reduced reflex bradycardia only in SHAM rats. Vit C in the CVLM did not change reflex bradycardia in either 2K1C or in SHAM rats. These results suggest that increased oxidative stress in the CVLM during hypertension contributes to the reduced baroreflex sensitivity and to maintain hypertension in the 2K1C model. |
| Databáze: | OpenAIRE |
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