Effects of high potassium on the release of [3H]dopamine from the cat carotid body in vitro.

Almaraz, L.; González, C.; Obeso, Ana

doi:10.1113/jphysiol.1986.sp016254

Cited by 54 publications

(41 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, in these studies the cells were most probably damaged by the microelectrode since, as was shown in the preceding article (Urefia et al, 1989), type I cells subjected to voltage and current clamp have an appreciable density of Na, Ca, and K channels and they can generate large action potentials. These results explain previous experiments indicating that transmitter release in type I cells induced by hypoxia and high external potassium was blocked by Ca channel antagonists (Almaraz et al, 1986;Obeso et al, 1987). The electrophysiological properties of these cells are further documented in this article; it is shown that a K conductance is selectively and reversibly inhibited by a decrease in pO2.…”

Section: Introductionsupporting

confidence: 91%

Low pO2 selectively inhibits K channel activity in chemoreceptor cells of the mammalian carotid body.

López‐López

González

Ureña

et al. 1989

The Journal of General Physiology

191

View full text Add to dashboard Cite

The hypothesis that changes in environmental 02 tension (pOi) could affect the ionic conductances of dissociated type I cells of the carotid body was tested. Cells were subjected to whole-cell patch clamp and ionic currents were recorded in a control solution with normal pO 2 (pO~ = 150 mmHg) and 3-5 min after exposure to the same solution with a lower pO,. Na and Ca currents were unaffected by lowering pO, to 10 mmHg, however, in all cells studied (n = 42) exposure to hypoxia produced a reversible reduction of the K current. In 14 cells exposed to a pO 2 of 10 mmHg peak K current amplitude decreased to 35 +_ 8% of the control value. The effect of low pO2 was independent of the internal Ca 2+ concentration and was observed in the absence of internal exogenous nucleotides. Inhibition of K channel activity by hypoxia is a graded phenomenon and in the range between 70 and 120 mmHg, which includes normal pO, values in arterial blood, it is directly correlated with pO 2 levels. Low pO2 appeared to slow down the activation time course of the K current but deactivation kinetics seemed to be unaltered. Type I cells subjected to current clamp generate large Na-and Cadependent action potentials repetitively. Exposure to low pO~ produces a 4-10 mV increase in the action potential amplitude and a faster depolarization rate of pacemaker potentials, which leads to an increase in the firing frequency. Repolarization rate of individual action potentials is, however, unaffected, or slightly increased. The selective inhibition of K channel activity by low pO, is a phenomenon without precedents in the literature that explains the chemoreceptive properties of type I cells. The nature of the interaction of molecular O, with the K channel protein is unknown, however, it is argued that a hemoglobin-like O, sensor, perhaps coupled to a G protein, could be involved.

show abstract

Section: Introductionsupporting

confidence: 91%

Low pO2 selectively inhibits K channel activity in chemoreceptor cells of the mammalian carotid body.

López‐López

González

Ureña

et al. 1989

The Journal of General Physiology

191

View full text Add to dashboard Cite

show abstract

“…These findings fit quite well with biochemical studies in explanted carotid bodies (25,26) or dispersed rat glomus cells (27), indicating that dopamine is a major substance released by the carotid body in response to hypoxia and that secretion requires extracellular Ca2+. We have also shown, in excellent agreement with recent work in chromaffin cells (19), that in dialyzed glomus cells, Ca2+ influx through voltage-gated channels can trigger quantal transmitter release.…”

supporting

confidence: 83%

Hypoxia induces voltage-dependent Ca2+ entry and quantal dopamine secretion in carotid body glomus cells.

Ureña

Fernández‐Chacón

Benot

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

195

148

View full text Add to dashboard Cite

We desired 02 concentrations. Po2 in the chamber was monitored with an O2-sensing electrode (9). Macroscopic calcium currents were studied using the whole-cell configuration of the patch-clamp technique (3,13) and recorded in isolation after blockade of the voltage-dependent Na+ and K+ channels. Cytosolic [Ca2W] was estimated in unclamped cells loaded with fura-2 by incubation for 10 min at 37°C with saline containing 1 AM fura-2 acetoxymethyl ester. Experiments were performed on an inverted microscope with standard optical components and equipped for epifluorescence and photometry (14). For the two excitation wavelengths, we used the filters shortwave-pass SWP 357 (excitation at =360 nm) and band-pass BP 380 (excitation at 380 nm; bandwidth, 10 nm). Fluorescence from the cells was measured by a dual wavelength photometer. The two output voltage signals from the photometer were digitized and displayed on-line on the screen of a computer in parallel with the estimated [Ca2+] concentration (15). Calibration of the fluorescence signals in terms of [Ca2+] was performed in vitro as described (16). Secretion was monitored in amperometric mode with a glass-sealed 8-,um diameter carbon electrode fabricated as described (17)(18)(19)(20). In most experiments, we used an amplifier built in our laboratory that has in the headstage a Burr-Brown OPA 111 wired as a current-to-voltage converter with a feedback resistor of 500 MQ1. The high-resolution recordings (see below) were obtained with a standard List EPC-7 patch-clamp amplifier. The single events of high resolution, similar to those shown in Fig. 2C, were recorded with a carbon electrode covered with polyethylene, which, as shown before (19), decreases noise and permits the acquisition of signals at a broader bandwidth. We held the carbon fiber at a constant voltage of +950 mV, a potential more positive than the oxidation potential of dopamine, thus assuring the oxidation of dopamine released by the cells (see below). Cyclic voltammograms were obtained by applying voltage ramps from -600 to + 1000 mV (at a rate of 170 V/s) to the carbon-fiber electrode. The signals are characterized by typical reduction (at approximately -400 mV) and oxi-*To whom reprint requests should be addressed. 10208The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

show abstract

“…Elevated concentrations of K+ have previously been shown to stimulate the carotid body in vivo (Band & Linton, 1986;Burger, Estavillo, Kumar, Nye & Patterson, 1988) and to evoke the Ca2+-dependent release of catecholamines in vitro (Almarez, Gonzalez & Obeso, 1986); but in the absence of Ca2+, the release of neurotransmitters from type I cells is depressed by over 90% Almarez et al 1986). Thus, the failure of APIII to inhibit CSN activity elicited by elevated K+ (in zero Ca2+) suggests that depolarized chemoreceptive nerve terminals remain capable of generating propagated action potentials in the presence of the drug.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms underlying chemoreceptor inhibition induced by atrial natriuretic peptide in rabbit carotid body.

Wang

Chen

et al. 1993

The Journal of Physiology

View full text Add to dashboard Cite

SUMMARY1. Previous studies in our laboratory revealed the presence of atrial natriuretic peptide (ANP) in preneural chemosensory type I cells of the cat carotid body, and demonstrated that submicromolar concentrations of the peptide inhibited carotid sinus nerve (CSN) activity evoked by hypoxia. In the present study, we have evaluated the role of the cyclic nucleotide second messenger, cyclic G-MP (cGMP), and the involvement of type I cells in rabbit chemosensory inhibition.2. Submicromolar concentrations of the potent ANP analogue, APIII, greatly elevated both the content and release of cGMP from the carotid body. Denervation experiments confirmed earlier immunocytochemical studies which suggested that APIII-induced cGMP production occurs almost exclusively in type I cells; these experiments also indicate that both the sympathetic and sensory innervation to the carotid body exert a trophic influence on the metabolism of this second messenger.3. Submicromolar concentrations of APIII inhibited the CSN activity evoked by hypoxia (79-8 + 3-2 % (mean + S.E.M.) inhibition with 100 nM APIII) and nicotine (74-5 + 3-6 % inhibition with 100 nM APIII), but did not affect basal CSN activity established in 100% 02-equilibrated superfusion solutions.4. The biologically inactive analogue of ANP, C-ANP, failed to produce CSN inhibition; however, the inhibitory effects of APIII were mimicked by cell-permeant analogues of cGMP (dibutyryl-cGMP and 8-bromo-cGMP, 2 mM), which likewise did not alter basal CSN activity. Because we found that unmodified cGMP was an ineffective inhibitor of CSN activity, our data suggest that APIII inhibition is mediated intracellularly by cGMP produced within the type I cells.5. APIII does not inhibit the CSN activity produced by 20 mm K+ (in zero Ca2+ media), which very probably results from direct depolarization of the sensory nerve terminals.6. Catecholamine release from the carotid body evoked by hypoxia is likewise not altered by APIII (100 nM).7. The data are consistent with the notion that APIII and analogues of cGMP alter the release of excitatory and/or inhibitory transmitters from chemosensory type I cells in the carotid body. MS 9953W.-J. WANG AND OTHERS

show abstract

Effects of high potassium on the release of [3H]dopamine from the cat carotid body in vitro.

Cited by 54 publications

References 41 publications

Low pO2 selectively inhibits K channel activity in chemoreceptor cells of the mammalian carotid body.

Low pO2 selectively inhibits K channel activity in chemoreceptor cells of the mammalian carotid body.

Hypoxia induces voltage-dependent Ca2+ entry and quantal dopamine secretion in carotid body glomus cells.

Mechanisms underlying chemoreceptor inhibition induced by atrial natriuretic peptide in rabbit carotid body.

Contact Info

Product

Resources

About