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Biomedical subjects

K T Kim

Publications and source records attributed to K T Kim.

At least 37 records · Page 2Linked to original sources
PubMed2001

Effects of polychlorinated biphenyl 19 (2,2',6-trichlorobiphenyl) on contraction, Ca2+ transient, and Ca2+ current of cardiac myocytes.

Polychlorinated biphenyls (PCBs) have been known as serious environmental pollutants, causing developmental delays, motor dysfunction, and decrease in brain dopamine level in humans and animals. We have investigated the effects of a PCB congener, 2,2',6-trichlorobiphenyl (PCB 19) on contractile force, Ca2+ transient, and L-type Ca2+ current (I(Ca,L)) in guinea pig ventricular myocytes stimulated at a rate of 0.25-0.33 Hz. PCB 19 decreased contractile force in a concentration-dependent manner. During the negative inotropic response, the action potential duration at 20% (APD20), 90% of repolarization (APD90), and the action potential amplitude (APA) were decreased concentration dependently: 30 microM PCB 19 reduced APD20, APD90 and APA by 36.7 +/- 3.5%, 22.6 +/- 3.9%, and 2.4 +/- 0.6%, respectively (n = 11, p < 0.01). PCB 19 30 microM decreased the Ca2+ transient and the I(Ca,L) by 46.8 +/- 1.8% (n = 9, p < 0.01) and 47.1 +/- 3.1% (n = 9, p < 0.01), respectively. The results suggest that PCB 19 decreased the Ca2+ transient through inhibition of L-type Ca2+ channels and that the decreased Ca2+ transient consequently caused a negative inotropic effect in cardiac myocytes.

Animals↗
PubMed2001

Coupling of L-type voltage-sensitive calcium channels to P2X(2) purinoceptors in PC-12 cells.

Extracellular ATP elevates cytosolic Ca(2+) by activating P2X and P2Y purinoceptors and voltage-sensitive Ca(2+) channels (VCCCs) in PC-12 cells, thereby facilitating catecholamine secretion. We investigated the mechanism by which ATP activates VSCCs. 2-Methylthioadenosine 5'-triphosphate (2-MeS-ATP) and UTP were used as preferential activators of P2X and P2Y, respectively. Nifedipine inhibited the ATP- and 2-MeS-ATP-evoked cytosolic Ca(2+) concentration increase and [(3)H]norepinephrine secretion, but not the UTP-evoked responses. Studies with Ca(2+) channel blockers indicated that L-type VSCCs were activated after the P2X activation. Mn(2+) entry profiles and studies with thapsigargin revealed that Ca(2+) entry, rather than Ca(2+) release, was sensitive to nifedipine. Although P2X(2) and P2X(4) receptor mRNAs were detected, studies with pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid revealed that P2X(2) was mainly coupled to the L-type VSCCs. The inhibitory effect of nifedipine did not occur in the absence of extracellular Na(+), suggesting that Na(+) influx, which induces depolarization, was essential for the P2X(2)-mediated activation of VSCCs. We report that depolarization induced by Na(+) entry through the P2X(2) purinoceptors effectively activates L-type VSCCs in PC-12 cells.

Adenosine Triphosphate↗
PubMed2001

Characteristics of body heat balance of paraplegics during exercise in a hot environment.

The purpose of this investigation was to clarify the characteristics of body temperature regulation in paraplegics due to spinal cord injury (SCI) during an arm cranking exercise in a hot environment. Twelve paraplegics with lesions located between Th3 and L1,2 and seven able-bodied subjects (AB) participated in this study. The subjects were exposed to a hot (33 degrees C) or a moderate temperature (25 degrees C) environment for one hour and during the last 10 min of the exposure, the subjects performed arm cranking exercises at an exercise intensity of 40 W. The skin temperatures at the chest, the upper arm, the thigh and the calf, the tympanic membrane temperature (Tty), and the skin blood flow of the thigh (SBFT) were continuously monitored during the experiment. Although no systematical variation was found in the Tty at 25 degrees C, the Tty at 33 degrees C in paraplegics during exercise was significantly greater than that at rest (P < 0.01), which indicated a pronounced heat stress for paraplegics at 33 degrees C. SBFT of paraplegics with high lesions of the SCI remained unchanged during the experiment at 25 degrees C and 33 degrees C, while paraplegics with low lesions in this study showed consecutive increases in SBFT during exercise in both environmental conditions similar to AB. The increased core temperature in paraplegics with high lesions was considered to be due to a lack of sweat response and vasomotor activity in the paralyzed area. On the basis of the findings in this study, it can be suggested that high core temperature without any increment of SBFT may be characterized as body heat balance of paraplegics with high lesions during exercise in a hot environment.

Adult↗
PubMed2001

Modulation of H2 histamine receptor-mediated cAMP generation and granulocytic differentiation by extracellular nucleotides via activation of protein kinase C.

Extracellular ATP exerts a variety of biological actions through several kinds of P2 receptor in HL-60 promyelocytes. We show that stimulation of P2Y2 receptors with ATP and analogs resulted in the inhibition of a subsequently histamine-induced cAMP production and functional differentiation. Treatment of the cells with phorbol 12-myristate 13-acetate also blocked the histamine-mediated cAMP generation just as ATP did. Incubation of the cells with the protein kinase C inhibitor bisindolylmaleimide (GF109203X) abolished the inhibitory effects of extracellular nucleotides, suggesting that protein kinase C may act as an inter-regulator between two receptors. However, ATP did not affect the binding affinity or total binding of [3H]histamine to membrane receptors; it also did not heterologously desensitize H2 receptors. The ATP treatment synergistically elevated the cAMP levels induced directly by forskolin or indirectly by G protein activation after cholera toxin treatment. This indicates that the site of the protein kinase C action is not the G protein or effector enzyme. Co-stimulation of the cells with nucleotides and histamine inhibited histamine-mediated granulocytic differentiation, which was evaluated by looking at the extent of N-formyl-methionyl-leucyl-phenylalanine responses. Taken together, the results demonstrate that extracellular nucleotides are negatively involved in the modulation of histamine signaling via activation of protein kinase C, probably by inhibiting coupling between receptor and G protein.

Adenosine Triphosphate↗
PubMed2000

Loading of oxidizable transmitters into secretory vesicles permits carbon-fiber amperometry.

Carbon-fiber amperometry detects oxidizable molecules released by exocytosis. We extended this electrochemical technique to cells that do not normally secrete oxidizable transmitters. We incubated AtT-20 cells, pituitary gonadotropes, cultured cerebellar granule cells, and yeast with high concentrations of dopamine (DA) and observed spontaneous and evoked quantal release of DA by amperometry. The rate of detectable spontaneous amperometric events was used as a measure of loading in AtT-20 cells. With 70 mm DA in the bath, loading was complete within 40 min. Cytoplasmic accumulation preceded vesicular loading. Loading decreased proportionally as the bath DA concentration was lowered. Loading rates were similar at 37 and 25 degrees C and much slower at 15 degrees C. Loading was blocked by bafilomycin A(1), a proton pump inhibitor, but not by bupropion, an inhibitor of the plasma membrane DA transporter. Other cells were tested. Spontaneous quantal events became more frequent and evoked events became larger and more frequent when PC12 cells were loaded with DA. Fluid-phase loading of neurons by short stimulation in DA solutions seemed selective for the synaptic vesicles. Thus, many cell types can be loaded with DA to study spontaneous and evoked exocytosis. The amine molecules enter these cells passively and may become concentrated in acidic vesicles by protonation.

Action Potentials↗
PubMed2000

Capsaicin inhibits platelet-activating factor-induced cytosolic Ca2+ rise and superoxide production.

Platelet-activating factor (PAF) is an important participant in the inflammatory process. We studied the regulation of PAF activity by capsaicin in human promyelocytic leukemia HL-60 cells. Capsaicin inhibited PAF-induced superoxide production in a concentration-dependent manner. In addition to PAF, the fMLP- and extracellular ATP-induced superoxide productions were inhibited by capsaicin, whereas PMA-induced superoxide production was not affected. In the PAF-stimulated cytosolic Ca2+ increase, capsaicin inhibited in particular the sustained portion of the raised Ca2+ level without attenuation of the peak height. In the absence of extracellular Ca2+, the PAF-induced Ca2+ elevation was not inhibited by capsaicin because capsaicin only inhibited the Ca2+ influx from the extracellular space. In addition, capsaicin did not affect PAF-induced inositol 1,4,5-trisphosphate production, suggesting that phospholipase C activation by PAF is not affected by capsaicin. Store-operated Ca2+ entry (SOCE) induced by thapsigargin was inhibited by capsaicin in a concentration-dependent manner. This capsaicin effect was also observed on thapsigargin-induced Ba2+ and Mn2+ influx. Furthermore, capsaicin's inhibitory effect on the thapsigargin-induced Ca2+ rise overlapped with that of SK&F96365, an inhibitor of SOCE. Both capsaicin and SK&F96365 also inhibited PAF-induced cytosolic superoxide generation in HL-60 cells differentiated by all-trans-retinoic acid. Our data suggest that capsaicin exerts its anti-inflammatory effect by inhibiting SOCE elicited via PLC activation, which occurs upon PAF activation and results in the subsequent superoxide production.

Apoptosis↗
PubMed2000

Torsional rigidity of scoliosis constructs.

STUDY DESIGN: A biomechanical study of the rigidity of various scoliosis constructs instrumented with and without caudal pedicle screw anchors and with none, one, or two cross-link devices. OBJECTIVES: To determine whether the increased torsional rigidity provided by distal pedicle screw fixation might make cross-linking unnecessary. SUMMARY OF BACKGROUND DATA: Pedicle screws and cross-linking devices have been shown to increase the structural rigidity of spinal constructs. Their relative contributions to scoliosis construct rigidity has not been determined. METHODS: "Short" (T2-T11) and "long" (T2-L3) scoliosis constructs were mounted on an industrially fabricated spine model and tested in a hydraulic testing machine. Four different short and four different long constructs were tested: hooks only, hooks with concave side thoracic sublaminar wires, hooks with distal pedicle screw anchors, and hooks, distal pedicle screw anchors, and concave thoracic sublaminar wires. There were four iterations for each construct tested: no cross-links, one superior cross-link at T4-T5, one inferior cross-link at T9-T10, and two cross-links. Torsional rigidity was tested by applying a rotational torque at T2. Vertebral body motion was recorded with a three-dimensional video analysis system. RESULTS: Constructs with distal pedicle screws were statistically more rigid in torsion than those with hooks as distal anchors. The additional torsional rigidity from one or more cross-links was negligible compared with that provided by pedicle screws. CONCLUSIONS: With pedicle screws as distal anchors in scoliosis constructs, cross-linking with one or two devices adds very little additional rotational stiffness and may be unnecessary in many cases.

Bone Screws↗
PubMed2000

Inhibition of nicotinic receptor-mediated catecholamine secretion by Dryobalanops aromatica in bovine adrenal chromaffin cells.

Effect of the aqueous extract from a medicinal plant Dryobalanops aromatica(Dipterocarpaceae) on catecholamine secretion was investigated in bovine adrenal chromaffin cells. The aqueous extract inhibited [(3)H]norepinephrine ([(3)H]NE) secretion induced by 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP), a nicotinic acetylcholine receptor (nAChR) agonist, with a half-maximal inhibitory concentration (IC(50)) of 8.4 +/- 1.7 microgml(-1). Increases in cytosolic calcium ([Ca(2+)](i)) and sodium ([Na(+)](i)) induced by DMPP were also inhibited by the extract. However, the binding of [(3)H]nicotine to nAChRs was not affected by the addition of the extract in receptor binding competition analysis, suggesting that active components in the extract and nicotine do not share the binding site in the nAChR. On the other hand, [Ca(2+)](i)increases induced by high K(+), ionomycin, bradykinin, angiotensin II, and thapsigargin were not inhibited by the extract. The data suggest that the extract from D. aromatica specifically inhibits catecholamine secretion by blocking nAChR in a noncompetitive manner.

Animals↗
PubMed2000

Role of titin in nonmuscle and smooth muscle cells.

Extensive investigation of vertebrate striated muscle titin has yielded significant insight into its structure and function in striated muscle. We have begun to investigate other members of the titin protein family found in vertebrate smooth muscle and nonmuscle cells. Smooth and nonmuscle titins resemble striated muscle titin in molecular size and morphology but differ in their interactions with myosin II filaments and in the structural contexts in which they exist in vivo. Divergence of these titins from the muscle titin paradigm demonstrates the versatility of this remarkable family of giant proteins.

Animals↗
PubMed2000

Differential stereoselectivity of D- and L-myo-inositol 1,2,4, 5-tetrakisphosphate binding to the inositol 1,4,5-trisphosphate receptor and 3-kinase.

D- and L-myo-inositol 1,2,4,5-tetrakisphosphate (Ins(1,2,4,5)P(4)) were investigated for their ability to bind to the D-myo-inositol 1, 4,5-trisphosphate (Ins(1,4,5)P(3)) receptor in a bovine adrenal cortical membrane fraction, to mobilize intracellular Ca(2+) stores in Xenopus oocytes, and to bind to the rat brain Ins(1,4,5)P(3) 3-kinase overexpressed and purified in E. coli. In competitive binding experiments with the Ins(1,4,5)P(3) receptor, D-Ins(1,2,4, 5)P(4) effectively displaced [(3)H]Ins(1,4,5)P(3) in a concentration-dependent manner with a potency comparable to that of D-Ins(1,4,5)P(3), while L-Ins(1,2,4,5)P(4) was approximately 50-fold less effective than D-Ins(1,4,5)P(3) and D-Ins(1,2,4,5)P(4). The DL-Ins(1,2,4,5)P(4) racemate bound to the Ins(1,4,5)P(3) receptor with an apparent intermediate efficiency. Injection of D-Ins(1,2,4, 5)P(4) into oocytes evoked a chloride current dependent on intracellular Ca(2+) mobilization in which the agonists ranked in a similar order of potency as in the Ins(1,4,5)P(3) receptor binding. On the other hand, D-Ins(1,2,4,5)P(4) only inhibited the binding of [(3)H]Ins(1,4,5)P(3) to 3-kinase very weakly with a markedly reduced potency compared to D-Ins(1,4,5)P(3), indicating that D-Ins(1,2,4, 5)P(4) is not an effective competitor in the phosphorylation of [(3)H]-Ins(1,4,5)P(3) by 3-kinase. The results, therefore, clearly indicate that D-Ins(1,2,4,5)P(4) is as effective as D-Ins(1,4,5)P(3) in the binding to the receptor but not 3-kinase, and access of Ins(1, 2,4,5)P(4) over the Ins(1,4,5)P(3) receptor calls for stringent stereospecificity with D-Ins(1,2,4,5)P(4) being the active form in DL-Ins(1,2,4,5)P(4)-mediated Ca(2+) mobilization.

Animals↗
PubMed2000

Fluticasone propionate versus zafirlukast: effect in patients previously receiving inhaled corticosteroid therapy.

BACKGROUND: The use of inhaled corticosteroids compared with leukotriene modifying drugs in the treatment of persistent asthma has not been extensively studied. OBJECTIVE: To compare the efficacy and safety of a low dose of fluticasone propionate (FP) and zafirlukast in patients previously maintained on inhaled corticosteroids. METHODS: Patients (> or = 12 years old; FEV1 = 60% to 85% of predicted) with persistent asthma who were previously treated with low doses of triamcinolone acetonide (TAA) 400 to 800 microg/day or beclomethasone dipropionate (BDP) 168 to 336 microg/day were randomized to treatment with FP aerosol 88 microg BID (FP, n = 221) or zafirlukast 20 mg BID (n = 216) over 6 weeks. RESULTS: Treatment with FP significantly increased the mean change at endpoint (the last post-baseline observation) in FEV1 (0.22 L versus 0.03 L, P < .001), morning PEF (17.8 versus 3.1 L/min, P = .004), evening PEF (16.7 versus 2.6 L/min, P = .002), the percentage of symptom-free days (16.2 versus 7.1%, P = .007), and the percentage of rescue-free days (23.4 versus 9.3%, P < .001), and significantly decreased rescue albuterol use (-0.66 puffs/day versus an increase of 0.27 puffs/day, P < .001) and combined symptom scores (-0.13 versus an increase of 0.08, P < .001) compared with zafirlukast. Treatment with FP maintained the percentage of awakening-free nights (-1.0 +/- 1.0); in contrast, treatment with zafirlukast reduced the percentage of awakening-free nights (-9.0 +/- 1.6, P < .001). A clinically meaningful difference (change of > or = 0.5; P < .001) was observed between FP and zafirlukast in the Asthma Quality of Life Questionnaire (AQLQ) global score and for each domain score except activity limitation (change of 0.3, P < .001). Significantly more patients in the zafirlukast group experienced an asthma exacerbation (n = 14) compared with FP-treated patients (n = 5, P = .035). Patients in the zafirlukast group were significantly more likely to be withdrawn due to lack of efficacy (P < .001). CONCLUSION: Switching patients from low doses of inhaled corticosteroids to a lower total microgram dose of FP improves pulmonary function, asthma symptoms, and quality of life, while switching to the leukotriene receptor antagonist zafirlukast may result in worsening of asthma control. This was indicated by the significant number of zafirlukast-treated patients who were dropped from the study due to lack of efficacy within 6 weeks of discontinuing inhaled corticosteroids.

Administration, Inhalation↗
PubMed2000

Differential regulation of P2Y(11) receptor-mediated signalling to phospholipase C and adenylyl cyclase by protein kinase C in HL-60 promyelocytes.

The regulatory mode of the P2Y(11) purinoceptor-mediated signalling cascades towards phospholipase C and adenylyl cyclase was studied in HL-60 promyelocytes. Treatment with the potent P2Y(11) receptor activator dATP evoked an elevated intracellular Ca(2+) concentration ([Ca(2+)](i)) and inositol 1,4,5-trisphosphate (IP(3)) production that was sustained for longer than 30 min. However, the dATP-induced responses were significantly inhibited by the activation of protein kinase C after a short exposure to phorbol 12-myristate 13-acetate (PMA). dATP also potently stimulated cyclic AMP production with half maximum effect seen at 23+/-7 microM dATP. In addition, a 5-min pretreatment with PMA enhanced the dATP-stimulated cyclic AMP accumulation. PMA potentiated the cyclic AMP production when adenylyl cyclase was activated directly by forskolin or indirectly by G protein activation after cholera toxin treatment. dATP also enhanced the forskolin-mediated cyclic AMP generation. Treatment of the cells with 10 microM U-73122, which almost completely blocked the dATP-stimulated IP(3) production and [Ca(2+)](i) rise, had no effect on cyclic AMP accumulation, while 10 microM 9-(tetrahydro-2-furyl)adenine (SQ 22536), which inhibited the adenylyl cyclase activation, did not effect the dATP-stimulated phosphoinositide turnover. Taken together, the results indicate that P2Y(11) receptor-mediated activation of phospholipase C and adenylyl cyclase occurs through independent pathways and is differentially regulated by protein kinase C in HL-60 cells.

Adenylyl Cyclases↗
PubMed2000

Nongenomic inhibition of catecholamine secretion by 17beta-estradiol in PC12 cells.

We investigated the effects of 17beta-estradiol, an estrogen, on [(3)H]norepinephrine ([(3)H]NE) secretion in PC12 cells. Pretreatment with 17beta-estradiol reduced 70 mM K(+)-induced [(3)H]NE secretion in a concentration-dependent manner with a half-maximal inhibitory concentration (IC(50)) of 2 +/- 1 microM. The 70 mM K(+)-induced cytosolic free Ca(2+) concentration ([Ca(2+)](i)) rise was also reduced when the cells were treated with 17beta-estradiol (IC(50) = 15 +/- 2 microM). Studies with voltage-sensitive calcium channel (VSCC) antagonists such as nifedipine and omega-conotoxin GVIA revealed that both L- and N-type VSCCs were affected by 17beta-estradiol treatment. The 17beta-estradiol effect was not changed by pretreatment of the cells with actinomycin D and cycloheximide for 5 h. In addition, treatment with pertussis or cholera toxin did not affect the inhibitory effect of 17beta-estradiol. 17beta-Estradiol also inhibited the ATP-induced [(3)H]NE secretion and [Ca(2+)](i) rise. In PC12 cells, the ATP-induced [Ca(2+)](i) rise is known to occur through P2X(2) receptors, the P2Y(2)-mediated phospholipase C (PLC) pathway, and VSCCs. 17beta-Estradiol pretreatment during complete inhibition of the PLC pathway and VSCCs inhibited the ATP-induced [Ca(2+)](i) rise. Our results suggest that 17beta-estradiol inhibits catecholamine secretion by inhibiting L- and N-type Ca(2+) channels and P2X(2) receptors in a nongenomic manner.

Adenosine↗
PubMed2000

A new method for aesthetic reduction of labia minora (the deepithelialized reduction of labioplasty).

An enlarged labium minus can be bothersome for functional, aesthetic, and social reasons. Labia minora hypertrophy can be congenital or acquired by chronic irritation, exogenous androgenic hormones, or stretching with weights. This can cause inflammation, poor hygiene, interference with sexual intercourse, or intermittent urinary self-catheterization in myelodysplastic women. Aesthetically, an asymmetric or enlarged labium minus causes self-consciousness sexually and when the subject wears tight pants. Previously, labia minora reduction was performed by amputation of the protuberant segment and oversewing the edge, or a wedge of protuberant labial tissue was excised and reapproximated. However, the former technique removes the natural contour and color of the edge of the labium minus, and the latter can result in an incomplete or tight reduction. Therefore, rather than an amputation or a wedge resection, we preserved the natural contour and anatomy of the labium minus by simply reducing its central width through bilateral deepithelialization and reapproximation of the central portion with preservation of the neurovascular supply to the edge. Six patients have undergone this reduction method with excellent results without specific complications.

Adolescent↗
PubMed2000

Primary peritoneal pregnancy implanted on the uterosacral ligament: a case report.

Peritoneal pregnancies are classified as primary and secondary. Primary implantation on the peritoneum is extremely rare in extrauterine pregnancy and is a potentially life-threatening variation of ectopic pregnancy within the peritoneal cavity, representing a grave risk to maternal health. Secondary abdominal pregnancies are by far the most common and result from tubal abortion or rupture, or less often, after uterine rupture with subsequent implantation within abdomen. Early diagnosis and appropriate surgical management, regardless of stage of gestation, appear to be important in achieving good results. We report a case of primary peritoneal pregnancy in a 28-year-old woman, who had severe lower abdominal pain one day before laparotomy for a preoperative diagnosis of ectopic pregnancy. The conceptus was implanted on the left uterosacral ligament. A fresh embryo of approximately 8 weeks' gestation was found in the conceptus.

Adult↗
PubMed1999

B-myb proto-oncogene products interact in vivo with each other via the carboxy-terminal conserved region.

Using the yeast two-hybrid assay and in vivo binding assay, we investigated whether B-myb oncogene products (B-myb) can associate with each other. Specificity tests of the yeast two-hybrid system showed a self-association of B-myb proteins in yeast. Cotransfection experiments demonstrated that B-myb proteins form a complex in vivo. Deletion analysis revealed that this binding was sufficiently mediated by the carboxy-terminal conserved region of B-myb. In addition, the B-myb self-association is directly dependent on the amount of expressed B-myb in cells and slightly increased by the dephosphorylation state. These results suggested that B-myb could form a complex and influence its transcriptional activity.

Cell Line↗
PubMed1999

Chlorpromazine-induced inhibition of catecholamine secretion by a differential blockade of nicotinic receptors and L-type Ca2+ channels in rat pheochromocytoma cells.

We investigated the effect of chlorpromazine (CPZ), a phenothiazine neuroleptic, on catecholamine secretion in rat pheochromocytoma (PC12) cells. CPZ inhibited [3H]norepinephrine ([3H]NE) secretion induced by 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP), an agonist of nicotinic acetylcholine receptors (nAChRs) with an IC50 value of 1.0 +/- 0.2 microM. The DMPP-induced rise in cytosolic free Ca2+ concentration [Ca2+]i was inhibited by CPZ with an IC50 of 1.9 +/- 0.1 microM. The DMPP-induced increase in cytosolic free Na+ concentration [Na+]i was also inhibited by CPZ with a similar potency. Furthermore, the binding of [3H]nicotine to PC12 cells was inhibited by CPZ with an IC50 value of 2.7 +/- 0.6 microM, suggesting that the nAChRs themselves are inhibited by CPZ. In addition, both 70 mM K+-induced [3H]NE secretion and [Ca2+]i increase were inhibited by CPZ with IC50 of 7.9 +/- 1.1 and 6.2 +/- 0.3 microM, respectively. Experiments with Ca2+ channel antagonists suggest that L-type Ca2+ channels are mainly responsible for the inhibition. We conclude that CPZ inhibits catecholamine secretion by blocking nAChRs and L-type Ca2+ channels, with the former being more sensitive to CPZ.

Animals↗