Increased expression of macrophage migration inhibitory factor in the nucleus of solitary tract attenuates the renovascular hypertension
| Autor: | D.S.A. Colombari, Eduardo Colombari, André Henrique Freiria-Oliveira, Hongwei Li, JoséVanderlei Menani, Guilherme Fleury Fina Speretta, Colin Sumners, Rafaela Moreira Barbosa |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
medicine.medical_specialty
Endocrine and Autonomic Systems business.industry Solitary tract medicine.disease Adenosine Renovascular hypertension Cellular and Molecular Neuroscience chemistry.chemical_compound Endocrinology Blood pressure chemistry Capsaicin Internal medicine Reflex Medicine Neurology (clinical) medicine.symptom business Acidosis Phenylbiguanide medicine.drug |
| Zdroj: | Autonomic Neuroscience. 192:94 |
| ISSN: | 1566-0702 |
| DOI: | 10.1016/j.autneu.2015.07.130 |
| Popis: | We investigatedwhether hemorrhagic hypotension (HH) altered the sensitivity of vagal pulmonary C-fibers in this study. The fiber activity (FA) of single vagal pulmonary C-fiber was continuously recorded in anesthetized rats before, during, and after HH was induced by bleeding from the femoral arterial catheter into a blood reservoir and lowering the mean systemic arterial blood pressure (MSAP) to ~40 mmHg for 20 min. Our results showed: 1)AfterMSAP reached a steady state of HH, the peak FA response to intravenous injection of capsaicin was elevated by ~5 folds. The enhanced C-fiber sensitivity continued to increase during HH and sustained even after MSAP returned to baseline during the recovery, but slowly returned to control ~20 min later. 2) Responses of FA to intravenous injections of other chemical stimulants of pulmonary Cfibers (phenylbiguanide, lactic acid and adenosine) and a constantpressure lung hyperinflation were all significantly potentiated by HH. 3) Infusion of sodium bicarbonate alleviated the systemic acidosis during HH, and it also attenuated, but did not completely prevent the HHinduced C-fiber hypersensitivity. In conclusion, the pulmonary C-fiber sensitivity was elevated during HH, probably caused by the endogenous release of chemical substances (e.g., lactic acid) that were produced by tissue ischemia during HH. This enhanced C-fiber sensitivity may heighten the pulmonary protective reflexes mediated through these afferents (e.g., J reflex) during hemorrhage when the body is more susceptible to other hazardous insults and pathophysiological stresses. (Supported in part by NHLBI and DoD grants) |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect