Browsing by Autor "Joseph, Vincent"

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    Dopaminergic metabolism in carotid bodies and high altitude acclimatization in female rats
    (Facultad de Medicina, Enfermería, Nutrición y Tecnología Médica, 2002) Joseph, Vincent
    We tested the hypothesis that ovarian steroids stimulate breathing through a dopaminergic mechanism in the carotid bodies (CB). In ovariectomized female rats raised at sea level, domperidone, a peripheral D2 receptor antagonist, increased ventilation in normoxia (Ve : + 55%) and acute hypoxia (+ 32%). This effect disappeared after 10 daily injections of ovarian steroids (progesterone + estradiol). At high altitude (HA--3,600 m, IBBA, La Paz, Bolivia), neutered females had higher CB tyrosine hydroxylase activity (the rate-limiting enzyme for catecholamine synthesis: + 129%) and dopamine utilization (+ 150%), lower Ve (- 30%) and hypoxic ventilatory response (- 57%), and higher hematocrit (+ 18%) and hemoglobin concentration (+ 21%) than intact female rats. Consistent signs of arterial pulmonary hypertension (right ventricular hypertrophy) also appeared in ovariectomized females. None of these parameters was affected by gonadectomy in males. Our results show that ovarian steroids stimulate breathing by lowering a peripheral dopaminergic inhibitory drive. This process may partially explain the deacclimatization of postmenopausal women at high altitude.
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    Erythropoietin Produces a Dual Effect on Carotid Body Chemoreception in Male Rats.
    (2021) Arias-Reyes, Christian; Laouafa, Sofien; Zubieta-DeUrioste, Natalia; Joseph, Vincent; Bairam, Aida; Schneider Gasser, Edith M; Soliz, Jorge
    Erythropoietin (EPO) regulates respiration under conditions of normoxia and hypoxia through interaction with the respiratory centers of the brainstem. Here we investigate the dose-dependent impact of EPO in the CB response to hypoxia and hypercapnia. We show, in isolated "en bloc" carotid body (CB) preparations containing the carotid sinus nerve (CSN) from adult male Sprague Dawley rats, that EPO acts as a stimulator of CSN activity in response to hypoxia at concentrations below 0.5 IU/ml. Under hypercapnic conditions, EPO did not influence the CSN response. EPO concentrations above 0.5 IU/ml decreased the response of the CSN to both hypoxia and hypercapnia, reaching complete inhibition at 2 IU/ml. The inhibitory action of high-dose EPO on the CSN activity might result from an increase in nitric oxide (NO) production. Accordingly, CB preparations were incubated with 2 IU/ml EPO and the unspecific NO synthase inhibitor (L-NAME), or the neuronal-specific NO synthase inhibitor (7NI). Both NO inhibitors fully restored the CSN activity in response to hypoxia and hypercapnia in presence of EPO. Our results show that EPO activates the CB response to hypoxia when its concentration does not exceed the threshold at which NO inhibitors masks EPO's action.