Browsing by Author "Rey, S"

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    Cardiovascular and ventilatory acclimatization induced by chronic intermittent hypoxia
    (2005) Iturriaga, R; Rey, S; Del Río, R
    Patients with obstructive sleep apnea (OSA) show augmentes ventilatory, sympathetic and cardiovascular responses to hypoxia. The facilitatory effect of chronic intermittent hypoxia (CIH) on the hypoxic ventilatory response has been attributed to a potentiation of the carotid body (CB) chemosensory response to hypoxia. However. it is a matter of debate whether the effects induced by CIH oil ventilatory responses to hypoxia are due to all enhanced CB activity. Recently, we studied the effects of short cyclic hypoxic episodes oil cat cardiorespiratory reflexes, heart rate variability, and CB chemosensory activity. Cats were exposed to cyclic hypoxic episodes repealed during 8 hours for 4 days. Our results showed that CIH selcectively enhanced ventilatory and carotid chemosensory responses to acute hypoxia. Exposure to CIH did not increase basal arterial pressure, heart-rate. or-the changes induced by acute hypoxia. However. the spectral analysis of heart rate variability of CIH cats showed a marked increase of the low/high frequency ratio and an increased variability in the low frequency band of heart rate variability, similar to what is observed ill OSA patients. Thus, it is likely that the enhanced CB reactivity to hypoxia may contribute to the augmented ventilatory response to hypoxia.
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    Inhibitory effects of NO on carotid body
    (2003) Valdés, V; Mosqueira, M; Rey, S; Del Rio, R; Iturriaga, R
    We tested the hypothesis that nitric oxide (NO) produced within the carotid body is a tonic inhibitor of chemoreception and determined the contribution of neuronal and endothelial nitric oxide synthase (eNOS) isoforms to the inhibitory NO effect. Accordingly, we studied the effect of NO generated from S-nitroso-N-acetylpenicillamide (SNAP) and compared the effects of the nonselective inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME) and the selective nNOS inhibitor 1-(2-trifluoromethylphenyl)- imidazole (TRIM) on chemosensory dose-response curves induced by nicotine and NaCN and responses to hypoxia (P-O2 approximate to 30 Torr). CBs excised from pentobarbitone-anesthetized cats were perfused in vitro with Tyrode at 38degreesC and pH 7.40, and chemosensory discharges were recorded from the carotid sinus nerve. SNAP (100 muM) reduced the responses to nicotine and NaCN. L-NAME (1 mM) enhanced the responses to nicotine and NaCN by increasing their duration, but TRIM (100 muM) only enhanced the responses to high doses of NaCN. The amplitude of the response to hypoxia was enhanced by L-NAME but not by TRIM. Our results suggest that both isoforms contribute to the NO action, but eNOS being the main source for NO in the cat CB and exerting a tonic effect upon chemoreceptor activity.
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    Sodium nitroprusside blocks the cat carotid chemosensory inhibition induced by dopamine, but not that by hyperoxia
    (1998) Iturriaga, R; Alcayaga, J; Rey, S
    We studied the effects of the nitric oxide (NO) synthase inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME), and the NO donor, sodium nitroprusside (SNP) on cat chemosensory responses to intravenous injections of NaCN (0.1-100 mu g/kg) and dopamine (0.1-20 mu g/kg), and to hyperoxic ventilation (100% O-2, 60-120 s). Cats were anesthetized with sodium pentobarbitone, paralyzed and artificially ventilated to prevent secondary ventilatory effects. The frequency of chemosensory discharges (f(x)) was recorded from one sectioned carotid sinus nerve. L-NAME (50 mg/kg i.v.) increased basal f(x) and slightly potentiated the responses to NaCN and dopamine. SNP (1-2 mg/kg i.v.) increased basal f(x), but reduced the NaCN-induced increases of f(x) over baseline and the transient f(x) inhibitions induced by dopamine, but not those produced by hyperoxia. Present results indicate that besides the known inhibitory effect of NO on chemosensory responses to low PO2, NO also blocks the chemosensory response to dopamine, leaving hyperoxic responses largely unchanged. (C) 1998 Elsevier Science B.V. All rights reserved.