7 results on '"López-López, J."'
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2. Properties of ionic currents from isolated adult rat carotid body chemoreceptor cells: effect of hypoxia.
- Author
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López-López, J R, González, C, and Pérez-García, M T
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- 1997
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3. Local control of excitation‐contraction coupling in rat heart cells.
- Author
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Wier, W G, Egan, T M, López‐López, J R, and Balke, C W
- Abstract
1. Cytosolic free calcium ion concentration ([Ca2+]i) and whole‐cell L‐type Ca2+ channel currents were measured during excitation‐contraction (E‐C) coupling in single voltage‐clamped rat cardiac ventricular cells. The measurements were used to compute the total cellular efflux of calcium ions through sarcoplasmic reticulum (SR) Ca2+ release channels (FSR,rel) and the influx of Ca2+ via L‐type Ca2+ channels (FICa). 2. FSR,rel was elicited by depolarizing voltage‐clamp pulses 200 ms in duration to membrane potentials from ‐30 to +80 mV. Over this range, peak FSR,rel had a bell‐shaped dependence on clamp pulse potential. In all cells, the ‘gain’ of the system, measured as the ratio, FSR,rel(max)/FICa(max), declined from about 16, at 0 mV, to much lower values as clamp pulse voltage was made progressively more positive. We named this phenomenon of change in gain as a function of membrane potential, ‘variable gain’. At clamp pulse potentials in the range ‐30 to 0 mV, the gain differed from cell to cell, being constant at about 16 in some cells, but decreasing from high values (approximately 65) at ‐20 mV in others. 3. At clamp pulse potentials at which Ca2+ influx (FICa) was maintained, FSR,rel also had a small maintained component. When macroscopic Ca2+ influx was brief (1‐2 ms, during ‘tails’ of FICa), FSR,rel rose rapidly to a peak after repolarization and then declined with a half‐time of about 9 ms (typically). 4. The rising phase of [Ca2+]i transients could be interrupted by stopping Ca2+ influx rapidly (by voltage clamp). We therefore termed this phenomenon ‘interrupted SR Ca2+ release’.(ABSTRACT TRUNCATED AT 250 WORDS) more...
- Published
- 1994
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4. Release of dopamine and chemoreceptor discharge induced by low pH and high PCO2 stimulation of the cat carotid body.
- Author
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Rigual, R, López-López, J R, and Gonzalez, C
- Abstract
1. Cat carotid bodies were incubated with the precursor [3H]tyrosine to label the catecholamine deposits and then mounted in a superfusion chamber which allowed simultaneous collection of the released [3H]dopamine (DA) and recording of action potentials from the carotid sinus nerve. 2. Low pH (7.2‐6.6) superfusion of the carotid bodies for periods of 10 min produced a parallel increase in the release of [3H]DA and chemoreceptor discharge. 3. Carotid sinus nerve denervation of the carotid body 12‐15 days prior to the experiments did not modify the release of [3H]DA elicited by low pH. 4. Superfusion of the carotid bodies with Ca(2+)‐free, high‐Mg2+ (1.6 mM) media reduced basal release of [3H]DA and chemoreceptor discharge by about 30%. Release evoked by low pH was reduced by 82%. Peak and average chemoreceptor discharge recorded in response to low pH were reduced by 28%. 5. Solutions containing weak acids (sodium acetate, 10 mM), adjusted at pH 7.4, elicited release of [3H]DA and increased chemoreceptor discharge. 6. With HCO3‐CO2‐buffered superfusion media, a reduction of bicarbonate to 5.6 mM (pH 6.8), an increase in CO2 to 20% (pH 6.8), or a simultaneous increase in CO2 to 20% and bicarbonate to 90 mM (pH 7.4), resulted in all cases in a corresponding increase in [3H]DA release and chemoreceptor discharge. The most effective stimulus was 20% CO2‐pH 6.8 and the least effective 5% CO2‐5.6 mM‐HCO3‐pH 6.8. 7. Inhibition of carbonic anhydrase with acetazolamide while perfusing the carotid bodies with a 20% CO2‐equilibrated (pH 7.4) solution resulted in comparable reductions in the release of [3H]DA and chemoreceptor discharge. 8. It is concluded that the effective acidic stimulus at the carotid body chemoreceptors is an increase in hydrogen ion concentration in type I cells. It is also concluded that DA plays a critical role in the genesis of carotid sinus nerve discharges. more...
- Published
- 1991
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5. Properties of a transient K+ current in chemoreceptor cells of rabbit carotid body.
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López‐López, J R, De Luis, D A, and Gonzalez, C
- Abstract
1. Adult rabbit carotid body chemoreceptor cells, enzymatically dispersed and short‐term cultured, exhibit an inactivating outward K+ current that is reversibly inhibited by low PO2. In the present work we have characterized the biophysical and pharmacological properties of this current using the whole‐cell voltage clamp recording technique. 2. Inactivating current was recorded after blockage of Ca2+ currents with extracellular Co2+, Cd2+, or after complete washing out of Ca2+ channels. 3. The threshold of activation of this inactivating current was about ‐40 mV. Current activated very quickly (mean rise time 4.8 +/‐ 0.42 ms at +60 mV) but inactivated more slowly. Inactivation was well fitted by two exponentials with time constants of 79.7 +/‐ 6.6 and 824 +/‐ 42.8 ms (at +40 mV). The inactivation process showed a little voltage dependence. 4. The steady‐state inactivation was well fitted by a Boltzman function. Inactivation was fully removed at potentials negative to ‐80 mV and was complete at voltages near ‐10 mV; 50% inactivation occurred at ‐41 mV. 5. Recovery from inactivation had several components and was voltage dependent. Initial recovery was fast, but full recovery, even at ‐100 mV, required more than 30 s. 6. Inactivating current was selectively blocked by 4‐aminopyridine (4‐AP), in a dose‐dependent manner (IC50, 0.2 mM). The duration of chemoreceptor cells action potentials was augmented by 1 mM 4‐AP from 2.3 +/‐ 0.36 to 7.0 +/‐ 0.25 ms at 0 mV. Tetraethylamonium (TEA), at concentrations above 5 mM, blocked inactivating and non‐inactivating components of the whole K+ current. 7. Inactivating current was modulated by cyclic AMP (cAMP). Bath application of 2 mM dibutyryl cAMP reduced peak amplitude by 18.7 +/‐ 2.9% (at +30 mV) and slowed down the rise time of the current. The effect was not voltage dependent. Forskolin (10‐20 microM) also affected inactivating current, by accelerating the inactivation process. In the same preparations neither dibutyryl cAMP nor forskolin affected Ca2+ currents. 8. It is concluded that modulation of K+ channels by cAMP might play a physiological role potentiating the low PO2 inhibition of K+ channels. more...
- Published
- 1993
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6. Inhibition of [3H]catecholamine release and Ca2+ currents by prostaglandin E2 in rabbit carotid body chemoreceptor cells.
- Author
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Gómez‐Niño, A, López‐López, J R, Almaraz, L, and González, C
- Abstract
Basal release of [3H]catecholamine ([3H]CA) from rabbit carotid bodies (CBs), previously incubated in the presence of [3H]tyrosine, was not significantly modified by prostaglandin E2 (PGE2). On the contrary, PGE2 (3‐300 nM) produced a dose‐dependent inhibition of the low PO2‐evoked release of [3H]CA. The inhibition was greatest (55%) at a low intensity of hypoxic stimulation (incubating solution PO2 approximately 66 mmHg) and decreased with increasing intensities of hypoxia. Chronic denervation of the CB did not modify the response to PGE2. The release of [3H]CA induced by incubating the CBs in a hypercapnic‐acidic solution (PCO2 approximately 132 mmHg; pH = 6.60) and by dinitrophenol (100 microM) was not significantly modified by 300 nM PGE2. PGE2 (300 nM) inhibited the release of [3H]CA elicited by incubating the CBs in a high K+ (35 mM)‐containing solution. The release response elicited by high K+ (25 mM) was strongly augmented by a dihydropyridine agonist of Ca2+ channels, Bay K 8644, at a concentration of 1 microM. The Bay K 8644 effect was partly inhibited by PGE2 (300 nM). Using whole‐cell recordings in freshly dispersed or short‐term cultured chemoreceptor cells from adult rabbits it was found that Ca2+ currents (ICa) were reversibly inhibited by bath application of PGE2. A good parallelism exits between the dose‐response curves for PGE2 inhibition of ICa in isolated chemoreceptor cells and high extracellular [K+]‐ or hypoxia‐evoked release of [3H]CA from the whole CB.(ABSTRACT TRUNCATED AT 250 WORDS) more...
- Published
- 1994
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7. Local, stochastic release of Ca2+ in voltage‐clamped rat heart cells: visualization with confocal microscopy.
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López-López, J R, Shacklock, P S, Balke, C W, and Wier, W G
- Abstract
1. Confocal microscopy and the fluorescent Ca2+ indicator fluo‐3 (K+ salt) were used to measure cytosolic free calcium ion concentration ([Ca2+]) during excitation‐contraction (E‐C) coupling in single, voltage‐clamped, rat cardiac ventricular cells. 2. Local [Ca2+]i transients were measured nearly simultaneously in different, separate, subcellular volumes of approximately 2.0 microns 3. During depolarization, local [Ca2+]i transients were distinctly different from each other and from whole‐cell [Ca2+]i transients. These differences were particularly apparent during small depolarizations, and were substantially reduced by ryanodine. 3. Components of the local [Ca2+]i transients, particularly those evoked by small depolarizations, were closely similar, in time course and amplitude, to spontaneous local [Ca2+]i transients, or ‘sparks’ (which have been shown previously to be Ca2+ released from sarcoplasmic reticulum). 4. Analysis of local [Ca2+]i transients in the spatial frequency domain (power spectrum) revealed that high power at spatial frequencies of 0.05‐0.2 microns‐1 was always associated with spontaneous calcium ‘sparks’ and with local [Ca2+]i transients evoked by small depolarizing pulses (e.g. to ‐31 mV). Evoked local [Ca2+]o transients in the presence of ryanodine, and those evoked by depolarization to very positive clamp‐pulse potentials (+45 mV), were associated with considerably lower power at this frequency. 5. The results suggest that whole‐cell [Ca2+]i transients evoked by voltage‐clamp depolarization, and thus by L‐type Ca2+ current, are comprised of local [Ca2+]i transients that are similar to the spontaneous calcium ‘sparks’. At very positive clamp‐pulse potentials, however, the electrically evoked local [Ca2+]i transients may be smaller, perhaps as a result of smaller unitary L‐type Ca2+ current. more...
- Published
- 1994
- Full Text
- View/download PDF
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