Browsing by Author "Alcayaga, J"

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    Dopamine modulates carotid nerve responses induced by acetylcholine on the cat petrosal ganglion in vitro
    (1999) Alcayaga, J; Varas, R; Arroyo, J; Iturriaga, R; Zapata, P
    We have recently reponed that application of acetylcholine (ACh) or nicotine to the petrosal ganglion-the sensory ganglion of the glossopharyngeal nerve-elicits a burst of discharges in the carotid nerve branch, innervating the carotid body and sinus, but not in the glossopharyngeal branch, innervating the tongue and pharynx, Thus, the perikarya of sensory neurons for the carotid bifurcation exhibit selective cholinosensitivity. Since dopamine (DA) modulates carotid nerve chemosensory activity, we searched for the presence of DA sensitivity at the perikarya of these neurons in the cat petrosal ganglion superfused in vitro. Applications of DA in doses of up to 5 mg to the ganglion did not modify the rate of spontaneous discharges in the carotid nerve, However, if DA was applied 30 s before ACh injections, ACh-evoked reactions were modified: low doses of DA enhanced the subsequent responses to ACh, while high doses of DA depressed the responses to ACh. This depressant effect of DA on ACh responses was partially antagonized by adding spiroperone to the superfusate. Our results show that the response to ACh of petrosal ganglion neurons projecting through the carotid nerve is modulated by DA acting on D-2 receptors located in the somata of these neurons. Thus, dopaminergic modulation of cholinosensitivity could be shared also by the membranes of peripheral endings and perikarya of primary sensory neurons involved in arterial chemoreception. (C) 1999 Elsevier Science B.V. All rights reserved.
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    Effects of CO2-HCO3- on catecholamine efflux from cat carotid body
    (1998) Iturriaga, R; Alcayaga, J
    Using a chronoamperometric technique with carbon-fiber microelectrodes and neural recordings, we simultaneously measured the effects of the following procedures on catecholamine efflux (Delta CA) and frequency of chemosensory discharges (f(x)) from superfused cat carotid body: 1) the addition of CO2-HCO3- to Tyrode solution previously buffered with N-2-hydroxyethylpiperazine-N'-2-ethane-sulfonic acid, maintaining pH at 7.40; 2) hypercapnia (10% CO2, pH 7.10); 3) hypoxia (Po-2 h approximate to 40 Torr) with and without CO2-HCO3-; and 4) the impact of several boluses of dopamine (DA; 10-100 mu g) on hypoxic and hypercapnic challenges. With CO2-HCO3-, hypoxia increased f(x) which preceded Delta CA increases, whereas hypercapnia raised f(x) but did not consistently increase Delta CA. Repeated stimuli induced similar f(x) increases, but attenuated Delta CA. After DA, hypoxia produced larger Delta CA, which preceded chemosensory responses. Without CO2-HCO3-, hypoxia produced a similar pattern of Delta CA and f(x) responses. Switching to Tyrode solution with CO2-HCO3- at pH 7.40 raised f(x) but did not increase Delta CA. With CO2-HCO3- and after DA, hypoxic-induced Delta CAs were larger than in its absence. Results suggest that DA release is not essential for chemosensory excitation.
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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.