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P Sánchez-García

Publications and source records attributed to P Sánchez-García.

At least 19 recordsLinked to original sources
PubMed2000

Ba(2+)-induced chromaffin cell death: cytoprotection by Ca(2+) channel antagonists.

Exposure of bovine adrenal medullary chromaffin cells to Ba(2+) ions (in the absence of Ca(2+) ions) caused their death, measured as lactate dehydrogenase (LDH) release. The concentration of Ba(2+) required to damage the cells by about 65% ranged between 1 and 10 mM (no Ca(2+) added); the required exposure time was rather brief (15 min-4 h). The simultaneous presence of Ca(2+), Mg(2+) or Zn(2+) together with Ba(2+) (2 mM, 4 h) afforded cyprotection (60-80%). Individual selective blockers of Ca(2+) channel subtypes afforded no protection. However, combined nifedipine (3 microM) plus omega-conotoxin MVIIC (3 microM) offered full protection. Substantial protection was also seen with the "wide-spectrum" Ca(2+) channel blockers penfluridol (0.3 microM), lubeluzole (3 microM), dotarizine (3 microM), flunarizine (3 microM), and mibefradil (3 microM). This protection was due to blockade of Ba(2+) entry through Ca(2+) channels because dotarizine (10 microM) inhibited the increase in cytosolic [Ba(2+)] seen in fura-2-loaded chromaffin cells. Once Ba(2+) accumulated in the cytosol, it was not extruded by the Na(+)/Ca(2+) exchanger, as shown by the prolonged and sustained elevation of the fura-2 signal. This contrasts with the fast dissipation of the fura-2 signal generated by [Ca(2+)](i) elevation. Thus, Ba(2+) overload can cause cell death by mechanisms similar to those reported for Ca(2+) overload and might be used as a novel and convenient tool to search for new cytoprotective compounds.

Animals↗
PubMed1999

Effects of dotarizine and flunarizine on chromaffin cell viability and cytosolic Ca2+.

Dotarizine (a novel piperazine derivative with antimigraine properties) and flunarizine (a Ca2+ channel antagonist) were compared concerning: first, their ability to cause chromaffin cell damage in vitro; second, the possible correlation of their octanol/water partition coefficients and those of another 28 compounds (i.e., Ca2+ channel antagonists, blockers of histamine H1 receptors, antimycotics, beta-adrenoceptor antagonists, neuroleptics), with their ability to cause cell damage; third, their capacity to protect the cells against the damaging effects of veratridine; and fourth, their capabilities to enhance the basal cytosolic Ca2+ concentration in fura-2-loaded single chromaffin cells, or to modify the pattern of [Ca2+]i oscillations elicited by veratridine. After 24-h exposure to 1-30 microM dotarizine, the viability of bovine adrenal chromaffin cells (measured under phase contrast or as lactate dehydrogenase, released into the medium) was similar to that of control, untreated cells; at 100 microM, 80% lactate dehydrogenase release was produced. At 1-3 microM flunarizine caused no cell damage; however 10 microM caused 20% lactate dehydrogenase release and 30 and 100 microM over 90% lactate dehydrogenase release. The time course of cell damage was considerably faster for flunarizine, in comparison to dotarizine. Out of 30 molecules tested (at 10 microM), having different octanol/water partition coefficients (log P), dotarizine was among the molecules causing no cell damage; flunarizine caused 20% cell loss, lidoflazine and verapamil over 50% cell loss, and penfluridol, draflazine, astemizole or nifedipine over 80% cell loss. No correlation was found between log P and cytotoxicity. Both dotarizine (10-30 microM) and flunarizine (3-10 microM) provided protection against veratridine-induced cell death; however, at 30 microM dotarizine afforded a pronounced protection while flunarizine enhanced the cytotoxic effects of veratridine. Dotarizine (30 microM) (but not flunarizine) caused a prompt transient elevation of the basal [Ca2+]i. Both compounds abolished the K+-induced increases of [Ca2+]i as well as the oscillations of [Ca2+]i induced by veratridine. The blocking effects of dotarizine were readily reversed after washout, while those of flunarizine were long-lasting. These differences might be relevant to the clinical use of dotarizine as an antimigraine drug.

Animals↗
PubMed1998

Effects of the neuroprotectant lubeluzole on the cytotoxic actions of veratridine, barium, ouabain and 6-hydroxydopamine in chromaffin cells.

1. Incubation of bovine adrenal chromaffin cells with veratridine (10-100 microM) during 24 h, caused a concentration-dependent release of the cytosolic lactate dehydrogenase (LDH) into the bathing medium, an indicator of cell death. Lubeluzole or its R(-) enantiomer, R91154, did not enhance LDH release. Both lubeluzole and R91154 (0.3-10 microM) decreased the veratridine-induced LDH release. 2. Penfluridol did not increase LDH release at concentrations 0.003-1 microM; 3-10 microM increased LDH release to 50-60%, after 24 h exposure. Penfluridol (0.03-0.3 microM) did not protect against the cytotoxic effects of veratridine; at 1 microM, 15% protection was produced. Higher concentrations (3-10 microM) enhanced the cytotoxic effects of veratridine. 3. Ba2+ ions caused a concentration-dependent increase of LDH release. This cytotoxic effect was partially prevented by 3 microM lubeluzole and fully counteracted by 1 microM penfluridol. R91154 was less potent than lubeluzole and only protected against the lesion induced by 0.5 mM Ba2+. 4. Ouabain (10 microM during 24 h) increased LDH release to about 30%. Both lubeluzole (0.3-10 microM) and the lower concentrations of penfluridol (0.003-0.3 microM) prevented the ouabain cytotoxic effects. At higher concentrations (3 microM), penfluridol increased drastically the ouabain cytotoxic effects. 5. 6-Hydroxydopamine (6-OHDA) caused significant cytotoxic effects at 30 and 100 microM. Lubeluzole (3-10 microM) or penfluridol (0.03-0.3 microM) had no cytoprotective effects against 6-OHDA. 6. Lubeluzole (3 microM), R91154 (3 microM) and penfluridol (1 microM) blocked the current through Na+ channels in voltage-clamped chromaffin cells (I(Na)) by around 20-30%. Ca2+ current through Ca2+ channels (I(Ca)) was inhibited 57% by lubeluzole and R91154 and 50% by penfluridol. The effects of penfluridol were not washed out, but those of lubeluzole and R91154 were readily reversible. 7. Lubeluzole (3 microM) induced reversible blockade of the oscillations of the cytosolic Ca2+, [Ca2+]i, in fura-2-loaded cells exposed to 30 or 100 microM veratridine. Penfluridol (1 microM) inhibited those oscillations in an irreversible manner. 8. The results suggest that lubeluzole and its R-isomer caused cytoprotection against veratridine cell damage, by blocking the veratridine stimulated Na+ and Ca2+ entry, as well as the [Ca2+]i oscillations. The Ba2+ and ouabain cytotoxic effects were prevented more efficiently by penfluridol, likely by blocking the plasmalemmal Na+/Ca2+ exchanger. It remains dubious whether these findings are relevant to the reported neuroprotective action of lubeluzole in stroke; the doubt rests in the stereoselective protecting effects of lubeluzole in in vivo stroke models, as opposed to its lack of stereoselectivity in the in vitro model reported here.

Adrenal Glands↗
PubMed1997

Pharmacokinetic study of ebrotidine administered in multiple doses to healthy volunteers for 4 days.

The safety of ebrotidine (N-[(E)-[[2-[[[2-[(diaminomethylene)amino]-4- thiazolyl]methyl]thio]ethyl]amino] methylene]-4-bromo-benzenesulfonamide, CAS 100981-43-9, FI-3542), a new H2-receptor antagonist with gastroprotective activity, was assessed and its main pharmacokinetic parameters were determined in order to establish the dose linearity after the repeated administration of three different dose levels. The study was carried out in a group of 8 healthy volunteers of either sex, aged between 20 to 29 years. Oral doses of ebrotidine were administered in a randomized, single-blind design. Volunteers remained in the Unit for two days at each of the three study phases with washout intervals of 2 weeks and received seven doses of ebrotidine (150, 300 and 500 mg b.i.d). Pharmacological evaluation included vital signs, laboratory tests, adverse events and blood and urine samplings for pharmacokinetic analysis. Ebrotidine was determined by high performance liquid chromatography (HPLC) with UV detection. The results showed a good tolerability of ebrotidine after the administration of seven doses for 4 days, with no changes in the vital signs or laboratory parameters. No clinically significant dose-related adverse events were reported during the study. The absorption of ebrotidine was relatively rapid (tmax approximately 2 h) and linear within the dose range from 150 to 500 mg. Drug biotransformation was linear with doses tested, and no metabolic saturation occurred. The terminal elimination half-life of ebrotidine was between 7 and 11 h or even longer. There was no accumulation of ebrotidine and the steady state was reached, regardless of the dose administered, within the first 24-48 h.

Adult↗
PubMed1996

The actions of ouabain and lithium chloride on cytosolic Ca2+ in single chromaffin cells.

The effects of ouabain, Li+ and veratridine on the concentration of cytosolic free Ca2+ ([Ca2+]i) were studied in single fura-2-loaded bovine adrenal chromaffin cells. Superfusion of cells with ouabain (10 microM for 60 min) caused only a delayed mild increase of the Ca2+]i, from around 0.1 microM to 0.2-0.3 microM; this increase was Nao(+)-dependent. Replacement of all NaCl of the Krebs-Hepes solution by LiCl (144 mM) produced a gradual increase of [Ca2+]i, which remained elevated at a stable plateau of 0.4-0.5 microM for 40-50 min. When ouabain (in the presence of normal Nao+) or Li+ (in the absence of Nao+) was given in Krebs-Hepes solution containing no Ca2+, the reintroduction of 2.5 mM Ca2+ produced a fast elevation of the [Ca2+]i. In the case of ouabain-treated cells, the [Ca2+]i curve exhibited an initial phasic component which inactivated to a tonic component. omega-Conotoxin MVIIC (3 microM) and R56865 (10 microM) inhibited the phasic but not the tonic component. Veratridine (30 microM) induced large [Ca2+]i oscillations. Both ouabain or Li+ abolished such oscillations. These results are compatible with ouabain causing elevation of [Ca2+]i in bovine chromaffin cells through a dual mechanism, i.e. cell depolarisation and slowing down of the Na(+)-Ca2+ exchanger of their plasmalemma. Through its binding to the Na+ site on the Na(+)-Ca2+ exchanger, Li+ ions generate powerful Cai2+ signals that might be relevant to its known effects on neurosecretory mechanisms.

Adrenal Glands↗
PubMed1995

Contribution of SK and BK channels in the control of catecholamine release by electrical stimulation of the cat adrenal gland.

1. Transmural electrical stimulation (10 Hz, 1 ms, 40 V for 10 s) of cat adrenal glands perfused at room temperature with Krebs-Hepes solution produced catecholamine secretory responses which were reproducible when stimulations were applied at 5 min intervals. Such responses were inhibited about 20% by atropine (1 microM) and 80% by hexamethonium (30 microM). Apamin (100 nM) increased the secretory response 2.5-fold in the presence of atropine and 8-fold in the presence of hexamethonium. 2. Potentiation by apamin of secretory responses evoked by 100-pulse trains was similar at 5, 10 and 20 Hz (about 2-fold). When glands were continuously stimulated at 3 Hz, apamin increased 4-fold the initial secretion plateau. Continuous stimulation at a higher frequency (20 Hz) produced a sharp secretory peak followed by a small, sustained plateau; apamin did not alter this plateau. Apamin also enhanced the secretory responses obtained with sustained stimulation with acetylcholine (10 or 200 microM). 3. Secretion peaks induced by brief acetylcholine pulses (10 microM for 10 s) applied to isolated and superfused cat adrenal chromaffin cells were enhanced more than 3-fold by 100 nM apamin. Charybdotoxin (10 nM) did not enhance these secretory peaks. 4. In perfused cat adrenal glands, charybdotoxin (10 nM) affected neither the secretion evoked by trains of electrical stimulation applied at different frequencies nor the secretion evoked by acetylcholine pulses. 5. In 0.5 mM [Ca2+]o, apamin enhanced 3-fold the secretion evoked by electrical stimulation trains of 100 pulses (10 Hz, 10 s) and almost 6-fold the acetylcholine (10 microM for 10 s)-induced secretion. In 5 mM Ca2+, apamin enhanced the secretory responses to electrical stimulation and acetylcholine 2- and 10-fold, respectively. Charybdotoxin enhanced 2.5-fold the secretory response to electrical stimulation in 0.5 mM Ca2+, although this effect was not statistically significant. A synergistic interaction between the two toxins on catecholamine release induced by electrical stimulation was observed at low but not at high [Ca2+]o. 6. Simultaneous release of acetylcholine and catecholamines upon electrical stimulation was achieved in glands in which the endogenous acetylcholine stores in the splanchnic nerve terminals had been prelabelled by perfusion with [3H]choline. While apamin enhanced more than 2-fold the postsynaptic release of catecholamines, the presynaptic release of acetylcholine remained unaffected. 7. The results are compatible with the hypothesis that, under physiological conditions, Ca(2+)-activated SK channels present in chromaffin cells control the firing patterns of action potentials induced by the acetylcholine released from splanchnic nerves during stress.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1995

Pharmacological protection against the cytotoxicity induced by 6-hydroxydopamine and H2O2 in chromaffin cells.

We present in this report the characteristics of the damage induced by 6-hydroxydopamine and H2O2 on bovine chromaffin cells in primary culture. Cytotoxicity was quantified using catecholamine cell contents, lactate dehydrogenase (LDH) release, trypan blue exclusion and morphological appearance. An excellent correlation between these four parameters was found. The cytotoxic effects of 6-hydroxydopamine were Ca(2+)-independent. In spite of this, the Ca2+ channel antagonists R56865 (N-[1-(4-(fluorophenoxy)butyl)]-4-piperidinyl-N-methyl-2-benzo-thiazo lamine) lidoflazine exhibited marked cytoprotective effects against both 6-hydroxydopamine and H2O2. The selective dopamine uptake blocker, bupropion, increased the viability of 6-hydroxydopamine and H2O2-treated cells from 20% to around 80%. Catalase drastically protected against the cytotoxic effects of 6-hydroxydopamine and H2O2. In contrast, desferrioxamine gave better protection against H2O2 cytotoxicity; glutathione and N-acetylcysteine only afforded substantial protection against 6-hydroxydopamine. Three main conclusions emerge from this study. (1st) 6-Hydroxydopamine causes chromaffin cell damage via a mechanism probably related to the production of free radicals, but unrelated to Ca2+ ions. Cytoprotection afforded by R56865 and lidoflazine must be unrelated to their Ca2+ antagonist properties. This suggests a novel component in the cytoprotective mechanism of action of these drugs. (2nd) The strong cytoprotective effects of bupropion seem to be unrelated to its ability to block the plasmalemmal dopamine carrier. (3rd) Bovine adrenal chromaffin cells in primary cultures are a suitable model for adult neurons to study the basic mechanism of cell damage, and to screen new drugs with putative neuroprotective properties.

Acetylcysteine↗
PubMed1994

Endothelium-independent relaxation by 17-alpha-estradiol of pig coronary arteries.

We have studied the effects of 17-alpha-estradiol, a non-estrogenic steroid, on pig coronary arteries contracted by K+, Ca2+ or serotonin. Experiments were performed on helicoidal strips and rings of left circumflex coronary arteries from freshly slaughtered white pigs and on helicoidal strips of rat thoracic aorta. The strips and rings were suspended inside a water-jacketed muscle chamber in an oxygenated Krebs solution at 37 degrees C. From the initial K(+)-evoked contraction, 17-alpha-estradiol caused a relaxation with an IC50 (15 microM) which was in the range of the IC50s obtained for nitroglycerin (1.3 microM) and nicorandil (50 microM). Contractions evoked by Ca2+ were inhibited by 17-alpha-estradiol, but full blockade could not be achieved. Serotonin-evoked contractions were also blocked by 17-alpha-estradiol with an IC50 of 2.1 microM; 17-beta-estradiol also inhibited the serotonin-evoked contractions. In the presence of 100 microM of the nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester, the relaxing properties of 17-alpha-estradiol in pig coronary arteries and rat thoracic aorta were unaffected, suggesting that endothelial NO release was unrelated to these effects. 17-alpha-Estradiol also relaxed denuded pig coronary artery strips, suggesting that other endothelial-derived relaxing factors were not involved in its vascular effects. The results are compatible with the idea that 17-alpha-estradiol causes relaxation of coronary vessels by acting directly on the cell membrane of smooth muscle cells; these effects seem to be unrelated to the genomic physiological effects of estrogens.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Activation of adrenal medullary L-arginine: nitric oxide pathway by stimuli which induce the release of catecholamines.

The activation of the L-arginine: nitric oxide (NO) pathway in the cat adrenal medulla by different stimuli which induce the release of catecholamines was studied. Stimuli that evoke catecholamine release, such as electrical stimulation of splanchnic nerves (50 V, 5 Hz, 1 ms), methacholine (100 microM), dimethyl-4-phenylpiperazinium iodide (DMPP; 10 microM), high K+ (35 mM) and alamethicin (15 micrograms ml-1) also caused a rise in cyclic GMP in the perfused cat adrenal medulla. NG-nitro-L-arginine methyl ester (L-NAME; 1 mM) abolished the rise in cyclic GMP induced by these stimuli without affecting the catecholamine release. Bovine adrenal medulla cytosol contained an NO synthase which was L-arginine- and Ca(2+)-dependent. In conclusion cat and bovine adrenal medulla stimulated with a variety of secretagogues synthesize NO from L-arginine to activate the soluble guanylate cyclase. The present data do not rule out a role for cyclic GMP in the regulation of catecholamine secretion; however, it seems more plausible that cyclic GMP may play a role in controlling local blood flow and thus the access of the released catecholamines to the systemic circulation during stressful conflicts.

Adrenal Medulla↗
PubMed1993

Two components in the adrenal nicotinic secretory response revealed by cobalt ramps.

Prolonged stimulation with nicotine (50 microM) enhanced the secretion of catecholamines from perfused cat adrenal glands. The profile of secretion consisted of a quick activation phase to a peak of 7.68 micrograms/min followed by a second inactivation phase which exhibited a t1/2 of 3.75 min. Sustained stimulation with a solution enriched in K+ (59 mM) also evoked a transient secretory response, with a peak release of 8.62 micrograms/2 min and a t1/2 for inactivation of 4.8 min. Co2+ (10 mM) blocked the nicotinic response by 58% and the K(+)-evoked secretory response by over 96%. In the presence of Co2+ (5 mM), continuous perfusion with nicotine produced a transient but large initial secretory response; the gradual decrease of the extracellular Co2+ concentration, [Co2+]0, as a continuous ramp allowed the development of a second component of secretion which inactivated later on. When the glands were continuously stimulated with 59 mM K+ in the presence of Co2+, the first component of secretion was missing; the second component appeared as [Co2+]0 decreases as a ramp. In similar experiments performed in low-Na+ solution (10 mM Na+), only the first secretion component evoked by nicotine was observed. This finding suggests that the second component of secretion depends on Na+ entry through the nicotinic receptor, on the ensuing cell depolarization and on Ca2+ entry through voltage-dependent Ca2+ channels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1992

Effects of several calcium channels modulators on the [3H]noradrenaline release and 45Ca influx in the rat vas deferens.

1. The effects of nifedipine (1 microM), CdCl2 (0.1 mM) and the Bay K 8644 enantiomers (1 microM) on [3H]noradrenaline release and 45Ca uptake in epididymal and prostatic rat vas deferens were investigated. 2. Nifedipine, CdCl2 and Bay K 8644 optical isomers did not affect the basal tritium release. However, the [3H]noradrenaline release evoked by high potassium (50 mM) from both portions of rat vas deferens was markedly inhibited by CdCl2, scarcely affected by nifedipine and not modified by Bay K 8644 enantiomers. 3. (-)-Bay K 8644 increased the basal and potassium (50 mM) induced 45Ca uptake whereas (+)-Bay K 8644, nifedipine and CdCl2 did not alter the basal 45Ca uptake. However, they strongly inhibited the uptake induced by potassium in both portions of rat vas deferens. 4. These results suggest that the calcium channels (mainly L type) are involved on the contractions in rat vas deferens epididymal and prostatic halves; these channels differ from those present in sympathetic nerve terminals (likely of N Type) which modulates the NA release. 5. This study also shows that Bay K 8644 optical isomers possess opposite effects on the L channels of bisected rat vas deferens smooth muscle.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1991

Mechanism of blockade by (+)isradipine of adrenal catecholamine release.

Cat adrenal glands were perfused at a high rate with various modified Krebs solutions containing different concentrations of K+ but no Ca2+. Catecholamine release was tested by applying brief Ca2+ pulses (10 s of a solution containing 120 mM K+ and 2.5 mM Ca2+). Under polarizing conditions (10 min perfusion with 1.4 mM K+ with no Ca2+), the total catecholamines released by the Ca2+ pulse amounted to 5 micrograms; in depolarizing conditions (10 min perfusion with a solution containing 70 mM K+ but no Ca2+), secretion was somewhat less (4-4.5 micrograms). (+)Isradipine, a 1,4-dihydropyridine Ca2+ channel blocker, did not affect the secretory response under polarizing conditions at 10(-8) M; at 10(-6) M, the secretory response was halved. When present under depolarizing conditions (70 mM K+ in 0 Ca2+), (+)isradipine (10(-8) M) blocked catecholamine release by 90%. In contrast, the inorganic Ca2+ channel blocker, Co2+, inhibited secretion equally well under polarizing or depolarizing conditions. Since 45Ca2+ uptake into adrenal medullary chromaffin cells was also inhibited by (+)isradipine (10(-8) M) in a voltage-dependent manner, it seems likely that blocking effects of the drug on catecholamine release are associated with inhibition of Ca2+ entry into cells through L-type Ca2+ channels. The association of (+)isradipine to its receptor is very rapid under polarizing conditions; dissociation is very slow in depolarized cells and very rapid upon polarization of such cells. Since chromaffin cells are being depolarized during stressful situations to secrete catecholamines into the circulation, (+)isradipine is likely to bind better to dihydropyridine receptors in this state; in this manner, the ensuing blockade of adrenal secretion could serve as a protective mechanism of cardiovascular tissues against massive increases in circulating catecholamines. If this suggestion is correct this mechanism could have additional therapeutic value in the treatment of hypertensive patients with (+)isradipine.

Adrenal Glands↗
PubMed1990

Alamethicin-evoked catecholamine release from cat adrenal glands.

Alamethicin enhances the rate of catecholamine output from perfused cat adrenal glands in a concentration-dependent manner. At 37 degrees C, catecholamine released went from 4.29 +/- 0.25 to 20.51 +/- 0.63 micrograms/stimulus at ionophore concentrations ranging from 20 to 100 micrograms/ml. Secretion was abolished at 22 degrees C or in the absence of extracellular Ca. The time-course of secretion (quick activation followed by a decline) evoked by alamethicin considerably differs from the catecholamine release pattern seen with A23187, X537A or ionomycin, which evoke a slowly developing, non-inactivating secretory response. In fact, its transient secretion pattern resembles that of nicotinic or high-K stimulation of cat adrenal glands, thus suggesting that alamethicin might form Ca permeable artificial channels in chromaffin cell plasma membranes.

Adrenal Medulla↗
PubMed1989

The key role of sodium in the ouabain-mediated potentiation of potassium-evoked catecholamine release in cat adrenal glands.

1. The effect of [Na]o on the catecholamine release evoked by K in ouabain pretreated, isolated adrenal glands of the cat, was investigated. 2. Reduction of [Na]o to 70, 50 and 25 mM, with sucrose as a substitute, did not modify the spontaneous catecholamine release but progressively increased the K (17.7 mM)-evoked secretory response. 3. Ouabain pretreatment (100 microM; 10 min) greatly increased the K (17.7 mM)-evoked catecholamine secretory response in glands perfused with normal Krebs. Such an increase was still seen in glands perfused with 70 mM Na-containing solution but disappeared when [Na]o was reduced to 25 and 10 mM. 4. Preperfusion of non-ouabain treated glands with Li-enriched Krebs, for a 40 min period, caused an increase in the K (17.7 mM)-evoked secretory response which was dependent on [Li]o and essentially similar to that induced by ouabain pretreatment. 5. Ouabain treatment (100 microM; 10 min) of glands perfused with normal Krebs evoked a long lasting catecholamine release, which reached a plateau at about 36 min and amounted to 0.68 +/- 0.25 microgram 2 min-1 (n = 9). Such a secretory response was dramatically increased, and its shape modified, when glands were preperfused with K (17.7 mM)-Krebs: a peak of 3.77 +/- 0.42 micrograms 2 min-1 (n = 7) was reached at 18 min. This response was drastically reduced in the presence of nitrendipine (1 microM). 6. In summary, our results indicate that both [Na]0 reduction or Na accumulation into the chromaffin cell by inhibition of the Na pump with ouabain, greatly enhance the secretory efficacy of small increments of [K]0, and suggest that sodium may play a role in the regulation of catecholamine release mediated by voltage-dependent Ca channels in adrenal glands.

Adrenal Glands↗
PubMed1988

"Doctor" in Spain.

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Education, Medical↗