Membrane potential of the stroma was recorded using standard electrophysiological recording techniques. The structure of the prostate was viewed using confocal or electron microscopy.
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Compared to normoxia, NS1619-induced vasodilation was significantly greater following hypoxia; however, NO-dependent vasodilation and BKCa-mediated vasodilation, in response to NS1619, were similar in the normoxic and hypoxic lungs. In contrast, direct activation of L-type Ca2+ and non-BKCa K+ channel was involved in the NS1619-induced vasodilation only in hypoxic lungs.
This study was carried out to characterize the set of voltage-dependent Ca2+ channel subtypes expressed by mouse adrenal chromaffin cells superfused with solutions containing low (2 mM) or high (10 mM) Ba2+ concentrations. Using 50-ms test pulses at 0 mV from a holding potential of -80 mV, averaged peak current in 10 mM Ba2+ was around 1 nA, and in 2 mM Ba2+ 0.36 nA. When using 2 mM Ba2+ as the charge carrier, nifedipine (3 microM) blocked IBa by 40-45%. omega-Conotoxin GVIA (1 microM) caused 26% inhibition, while omega-conotoxin MVIIC (3 microM) produced a 48% blockade. At low concentrations (20 nM), omega-agatoxin IVA caused 5-15% of current inhibition, while 2 microM gave rise to a 35-40% blockade. In 10 mM Ba2+, the blocking effects of nifedipine (40%) and omega-conotoxin GVIA (25%) were similar to those seen in 2 mM Ba2+. In contrast, blockade by omega-conotoxin MVIIC was markedly reduced in 10 mM Ba2+ (20-25%) as compared to 10 mM Ba2+ (48%). The blocking actions of omega-agatoxin IVA (2 microM) were also slowed down in 10 mM Ba2+, though the final blockade was unaffected. In 2 mM Ba2+, IBa was quickly inhibited by over 94% with combined nifedipine + omega-conotoxin MVIIC + omega-conotoxin GVIA; in 10 mM Ba2+, IBa was blocked by 70% with this combination. The data suggest that mouse chromaffin cells express L-type (40%) as well as non-L-type (60%) high-threshold voltage-dependent Ca2+ channels. The current carried by non-L-type Ca2+ channels consists of about 25% N-type and 35% P/Q-type; P-type channels, if anything, are poorly expressed. The data also indicate that the fraction of current blocked by omega-conotoxin MVIIC and omega-agatoxin IVA might considerably change as a function of the Ba2+ concentration of the extracellular solution; taking this fact into consideration, it seems that a residual R-type current is not expressed in mouse chromaffin cells.
Based on this evidence, we examined the role of BDNF release and the impact of L-type VDCCs on the behavioral actions of ketamine.
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Calcium antagonists normalize endothelial dysfunction and improve the clinical outcome in patients with hypertension. However, the mechanism underlying these beneficial effects remains to be elucidated. Here, we show that the calcium antagonist nifedipine upregulates the expression of manganese superoxide dismutase (Mn SOD), an endogenous antioxidant enzyme, in vascular smooth muscle cells (VSMC) via cellular interactions between VSMC and endothelial cells (EC). Nifedipine induced upregulation of Mn SOD activity and expression in VSMC when cocultured with EC but not when cultured individually. NG-Monomethyl-L-arginine (L-NMMA), an inhibitor of nitric oxide (NO) synthesis, inhibited the upregulation of Mn SOD expression induced by nifedipine. Additionally, N-ethyl-2-(1-ethyl-2-hydroxy-2-nitrosohydrazino) ethanamine, a NO donor, reversed this inhibition by L-NMMA, indicating that NO may be involved in the mechanism underlying the nifedipine-induced upregulation of Mn SOD in VSMC. Preincubation of VSMC with Mn SOD antisense oligodeoxyribonucleotides (ODN) blocked the suppressive effects of nifedipine on DNA synthesis in VSMC cocultured with EC, whereas sense ODN had no effect. We conclude that the calcium antagonist nifedipine induces upregulation of Mn SOD expression in VSMC via NO derived from EC. This finding may provide some insight into the mechanism underlying the beneficial effects of calcium antagonists in patients with hypertension.
1. The contribution of endothelin-1 (ET-1) to angiotensin II (Ang II)-mediated contraction of the isolated rat tail artery was assessed with measurements of tension, and cytosolic calcium ([Ca(2+)](i)). The distribution of the AT(1) receptor was studied with RT - PCR and immunohistochemistry. 2. Ang II induced an endothelium-independent contraction (pEC(50) 7.95+/-0.06 and E(max): 0.46 g+/-0.05 with endothelium vs 7.81+/-0.02 and 0.41 g+/-0.07 without endothelium; P>0.05). Ang II (0.003 - 0.3 microM)-induced a non-sustained contraction of endothelium-intact preparations which was not antagonized by BQ-123 (1 microM), but was inhibited by losartan (10 nM). In addition, the maximal contraction induced by ET-1 (0.1 microM) could be further increased by the addition of 0.1 microM Ang II. 3. Ang II (0.001 - 0.3 microM) elevated [Ca(2+)](i) in single vascular smooth muscle cells (VSMCs) in a dose-dependent manner (pEC(50) 9.12+/-0.26) and the Ang II-induced increases in [Ca(2+)](i) were not affected by a Ca(2+)-free solution, but were abolished by pretreatment with caffeine (5 mM). Ang II did not increase [Ca(2+)](i) in endothelial cells. ET-1 (0.1 microM) increased [Ca(2+)](i) in single VSMCs in a normal Ca(2+) containing physiological saline solution (PSS), but not in a Ca(2+)-free solution. 4. Ang II-induced contraction was insensitive to inhibition by nifedipine (0.1 microM), an antagonist of L-type voltage-gated Ca(2+) channels, and SK&F96365 (10 microM), which blocks non-selective cation channels, whereas that to ET-1 was inhibited by SK&F69365. 5. RT - PCR data indicate the expression of AT(1A) and AT(1B) on both VSMCs and endothelial cells, but immunohistochemical evidence illustrates that the AT(1) is located primarily on VSMCs. 6. These results indicate that endothelium-derived ET-1 is not involved in the Ang II-mediated vasoconstriction of the rat tail artery and that Ang II- and ET-1-mediated VSM contractions utilize distinct pathways.
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The main problem of treatment of hypertension in this country as well as abroad is the fact that only less than one quarter of hypertensive patients are treated effectively and have thus normal blood pressure readings. More effective treatment of hypertension is thus one of the main tasks of health care systems in different countries. The objective of treatment of hypertension is to achieve a normal blood pressure. Evidence has been provided that diuretics and beta-blockers markedly reduce cerebrovascular and cardiovascular mortality, in particular in the elderly. ACE inhibitors are the drugs of choice in patients with heart failure or asymptomatic left ventricular dysfunction and in patients with diabetic nephropathy. Unsuitable for treatment of hypertension are short acting calcium channel blockers, in particular nifedipine. On the other hand, long-acting calcium channel blockers reduce the cerebrovascular mortality in elderly hypertensive patients. A number of questions still remain the subject of research: a) should diastolic pressure be reduced to values lower than 90 mm Hg; so far it is necessary only in hypertensive subjects with diabetes mellitus and in juvenile hypertensives; b) is the influence of new groups of antihypertensive drugs, in particular calcium channel blockers, similar, better or worse than that of diuretics and beta-blockers in the prevention of cardiovascular and cerebrovascular morbidity and mortality?; c) is it wise to recommend acetylsalicylic acid also to hypertensive patients without clinical signs of IHD or atherosclerotic affection of other vessels?; d) what is the value of combined antihypertensive and hypolipidaemic pharmacological treatment? Will this combination be not much more valuable in the prevention of IHD?; e) is the prognosis of hypertensive subjects with left ventricular hypertrophy better when ACE inhibitors are used as compared with other antihypertensive drugs?; f) do ACE inhibitors influence the prognosis of diabetic patients more favourably than beta-blockers?
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Recently, we have shown that two biologically active, disulfated polyhydroxysteroids from the Pacific brittle star Ophiopholis aculeata stimulate Ca(2+) influx into different cell types. In the present study, 45Ca(2+) and two fluorescent calcium probes, quin-2/AM and fura-2/AM, were employed to investigate the course and amplitude of calcium signals induced in different mouse cells using an radio-isotope, spectrofluorimetry, and microcytofluorimetry techniques. The cytotoxic and hemolytic effects were not observed for both steroids at the wide range of concentrations. Steroids did not influence [3H]-uridine incorporation in a variety of cells. The investigated steroids stimulated a rapid increase in cytosolic Ca(2+) content in Ehrlich mouse carcinoma cells, mouse spleen lymphocytes, and mouse peritoneal macrophages in the concentration range 1-100 microg/ml on a dose-dependent basis. Blockers of L-type calcium channels, such as verapamil, diltiazem, nifedipine (1 x 10(-7)M), and 1mM EGTA, inhibited this process and reduced the response of cells to steroid application. The stimulatory effect of steroids on human fibroblast proliferation and mouse macrophage lysosome activity was observed also. It is suggested that the investigated compounds may act as Ca(2+)-agonists and increase Ca(2+)-transport across cell membranes.
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The chronic usage of nifedipine is associated with the appearance of gingival overgrowth (GO). The frequency of GO associated with chronic nifedipine therapy remains controversial and the possible subclinical effects of this drug on the gingival epithelium should be investigated. We investigated the epithelial proliferation index and apoptosis rate, and their association with epithelial enlargement. Proliferation (Ki67 and Cyclin B1) and apoptosis (BCL2, Bax and p53) markers were identified by immunohistochemistry in twenty-one samples of gingival tissue from patients undergoing chronic treatment with nifedipine and in eleven samples of gingival tissue from healthy patients who did not use drugs associated with GO (control). Our results show that the epithelial tissue of nifedipine users has considerably longer rete pegs compared to control (P = 0.01). However, the density of Ki67(+) and Cyclin B1(+) cells was similar in both groups. Regarding apoptosis, we found more BCL2(+) cells in the nifedipine group when compared to controls (P = 0.12). An increase in Bax(+) cells in the nifedipine group compared to control (P = 0.003) was also seen, and slightly lower levels of p53(+) expression were observed (P = 0.51). Our results suggest that the chronic use of nifedipine is not associated with subclinical changes in gingival tissue.
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The effects of cyclosporine and tacrolimus on cytochrome P450 (CYP) 1A2-mediated 7-ethoxyresorufin O-deethylation, CYP2C9-mediated tolbutamide hydroxylation, CYP2C19-mediated S-mephenytoin 4'-hydroxylation, CYP2D6-mediated debrisoquine 4-hydroxylation, CYP2E1-mediated chlorzoxazone 6-hydroxylation, CYP3A4-mediated nifedipine oxidation, and CYP3A4-mediated testosterone 6beta-hydroxylation activities in human liver microsomes were compared. Cyclosporine and tacrolimus, at concentrations of 0.2 or 2 muM, neither inhibited nor stimulated any of the metabolic activities except for those of CYP3A4. On the other hand, cyclosporine and tacrolimus competitively inhibited CYP3A4-mediated nifedipine oxidation activity, with inhibition constants (K(i)) of 1.42 and 0.36 muM, respectively. In addition, 20 muM cyclosporine inhibited CYP2C19 and CYP2D6 activities by 29% and 30%, respectively. These results suggest that tacrolimus would not cause clinically significant interactions with other drugs, which are metabolized by CYPs, via the inhibition of hepatic metabolism and that the reason why cyclosporine, but not tacrolimus, has a pharmacokinetic inhibitory effect might be that the dosage and/or the unbound concentrations around its metabolic enzymes are higher than those of tacrolimus, rather than the differences in the inhibition potential. Obvious substrate-dependent effects on CYP3A4-inhibition potential were not observed.
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Cytochrome P450s (P450) form a superfamily of membrane-bound proteins that play a key role in the primary metabolism of both xenobiotics and endogenous compounds such as drugs and hormones, respectively. To be enzymically active, they require the presence of a second membrane-bound protein, NADPH P450 reductase, which transfers electrons from NADPH to the P450. Because of the diversity of P450 enzymes, much of the work on individual forms has been carried out on purified proteins, in vitro, which requires the use of complex reconstitution mixtures to allow the P450 to associate correctly with the NADPH P450 reductase. There is strong evidence from such reconstitution experiments that, when cytochrome b5 is included, the turnover of some substrates with certain P450s is increased. Here we demonstrate that allowing human P450 reductase, CYP3A4, and cytochrome b5 to associate in an in vivo-like system, by coexpressing all three proteins together in Escherichia coli for the first time, the turnover of both nifedipine and testosterone by CYP3A4 is increased in the presence of cytochrome b5. The turnover of testosterone was increased by 166% in whole cells and by 167% in preparations of bacterial membranes. The coexpression of cytochrome b5 also resulted in the stabilization of the P450 during substrate turnover in whole E. coli, with 109% of spectrally active CYP3A4 remaining in cells after 30 min in the presence of cytochrome b5 compared with 43% of the original P450 remaining in cells in the absence of cytochrome b5.
Dinoflagellate bioluminescence serves as a whole-cell reporter of mechanical stress, which activates a signaling pathway that appears to involve the opening of voltage-sensitive ion channels and release of calcium from intracellular stores. However, little else is known about the initial signaling events that facilitate the transduction of mechanical stimuli. In the present study using the red tide dinoflagellate Lingulodinium polyedrum (Stein) Dodge, two forms of dinoflagellate bioluminescence, mechanically stimulated and spontaneous flashes, were used as reporter systems to pharmacological treatments that targeted various predicted signaling events at the plasma membrane level of the signaling pathway. Pretreatment with 200 μM Gadolinium III (Gd(3+) ), a nonspecific blocker of stretch-activated and some voltage-gated ion channels, resulted in strong inhibition of both forms of bioluminescence. Pretreatment with 50 μM nifedipine, an inhibitor of L-type voltage-gated Ca(2+) channels that inhibits mechanically stimulated bioluminescence, did not inhibit spontaneous bioluminescence. Treatment with 1 mM benzyl alcohol, a membrane fluidizer, was very effective in stimulating bioluminescence. Benzyl alcohol-stimulated bioluminescence was inhibited by Gd(3+) but not by nifedipine, suggesting that its role is through stretch activation via a change in plasma membrane fluidity. These results are consistent with the presence of stretch-activated and voltage-gated ion channels in the bioluminescence mechanotransduction signaling pathway, with spontaneous flashing associated with a stretch-activated component at the plasma membrane.
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The study was performed as a randomized clinical trial on women who had been admitted in the hospital diagnosed with preterm labor. In one group, the NG dermal patch and in the other group, nifedipine was prescribed. Then the women of the two groups were followed up to delivery and were compared according to arrest of labor for 2 h, 48 h, 7 days, gestational age at the time of delivery and their adverse effects. The primary outcome was to postpone delivery for 48 h in order to have enough time for prescribing corticosteroids
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Endogenous generated hydrogen peroxide during eye bank storage limits viability. We determined in cultured human corneal endothelial cells (HCEC) whether: (1) this oxidant induces elevations in intracellular calcium concentration [Ca2+]i; (2) epidermal growth factor (EGF) medium supplementation has a protective effect against peroxide mediated rises in [Ca2+]i. Whereas pathophysiological concentrations of H2O2 (10 mM) induced irreversible large increases in [Ca2+]i, lower concentrations (up to 1 mM) had smaller effects, which were further reduced by exposure to either 5 microM nifedipine or EGF (10 ng ml(-1)). EGF had a larger protective effect against H2O2-induced rises in [Ca2+]i than nifedipine. In addition, icilin, the agonist for the temperature sensitive transient receptor potential protein, TRPM8, had complex dose-dependent effects (i.e. 10 and 50 microM) on [Ca2+]i. At 10 microM, it reversibly elevated [Ca2+]i whereas at 50 microM an opposite effect occurred suggesting complex effects of temperature on endothelial viability. Taken together, H2O2 induces rises in [Ca2+]i that occur through increases in Ca2+ permeation along plasma membrane pathways that include L-type Ca2+ channels as well as other EGF-sensitive pathways. As EGF overcomes H2O2-induced rises in [Ca2+]i, its presence during eye bank storage could improve the outcome of corneal transplant surgery.
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We compared the risk of preterm delivery in fFN pos and fFN neg women and in women with a CL <15 mm and ≥15 mm, by using the Cox regression. Differences between the effectiveness of maintenance tocolysis in high- and low-risk women were assessed by using an interaction term.
Endothelin-1 (ET-1) has been proven to activate two types of Ca2+-permeable nonselective cation channels (designated NSCC-1 and NSCC-2) and a store-operated Ca2+ channel (SOCC) in rabbit internal carotid artery vascular smooth muscle cells (ICA VSMCs). Ca2+ influx through these channels plays an essential role for ET-1-induced mitogenesis in ICA VSMCs. The purpose of the current study was to investigate the effects of Ca2+ influx on intracellular pathways of ET-1-induced mitogenesis in ICA VSMCs using receptor-operated Ca2+ channel blockers, SK&F 96365 and LOE 908. We focused on extracellular-signal regulated kinase 1 and 2 (ERK1/2) in this context. PD 98059, an inhibitor of mitogen-activated protein kinase kinase, abolished the ET-1-induced increase in ERK1/2 activity, but only partially suppressed the mitogenesis. ERK1/2 activation by ET-1 was partially suppressed in the absence of extracellular Ca2+. Moreover, based on the sensitivity to SK&F 96365 and LOE 908, Ca2+ influx through NSCC-1, NSCC-2 and SOCC plays essential roles in the extracellular Ca2+-dependent component of ERK1/2 activity. In addition, Ca2+ influx through these channels was also involved in the PD 98059-resistant component of ET-1-induced mitogenesis. These results indicate that (1) the ET-1-induced mitogenesis involves both ERK1/2-dependent and -independent mechanisms in ICA VSMCs (2), ERK1/2 activation by ET-1 involves a Ca2+ influx-dependent cascade as well as a Ca2+ influx-independent cascade (3), Ca2+ influx through NSCC-1, NSCC-2 and SOCC has important roles in the Ca2+ influx-dependent component of ERK1/2-dependent mitogenesis, and (4) Ca2+ influx through these channels also plays important roles in mitogenic pathways downstream of ERK1/2.
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The effects of glycyrrhizic acid (GLZ) on protein binding of diltiazem, verapamil, and nifedipine were investigated. Protein binding studies (human serum, human serum albumin (HSA) and alpha1-acid glycoprotein (AAG)) were conducted using the equilibrium dialysis method with and without addition of GLZ. The binding parameters, such as the number of moles of bound drug per mole of protein, the number of binding sites per protein molecule, and the association constant, were estimated using the Scatchard plot. The serum binding of nifedipine, verapamil, and diltiazem was displaced with addition of GLZ, and the decreases of Ks for serum were observed. GLZ decreased the association constants of three drugs for HSA and AAG, while the binding capacity remained similar with addition of GLZ. Although the characteristics of interaction were not clear, GLZ seemed to mainly affect HSA binding of nifedipine rather than AAG binding, while GLZ seemed to affect both AAG- and HSA-bindings of verapamil and diltiazem resulting in a serum binding displacement.
Modulation of Ca(2+) channels has been shown to alter cellular functions. It can play an important role in the amplification of signals in the endocrine system, including the pleiotropically regulated pituitary lactotropes. Prolactin (PRL) secretion is tonically inhibited by dopamine (DA), the escape from which triggers acute episodes of hormone secretion. The magnitude of these episodes is explained by a potentiation of the PRL-releasing action of secretagogues such as thyrotropin-releasing hormone (TRH). While the mechanisms of this potentiation are not fully understood, it is known to be mimicked by the dihydropyridine, L-type Ca(2+) channel agonist Bay K 8644 and blocked by nifedipine and methoxyverapamil. The potentiation is also blocked by inhibitors of cyclic AMP-dependent protein kinase and protein kinase C. We recently described that the escape from tonic actions of DA results in increased macroscopic Ca(2+) currents in GH(4)C(1) lactotropic clonal cells transfected with a cDNA encoding the long form of the human D(2)-DA receptor. Here we show that the withdrawal from DA potentiates the PRL-releasing action of TRH in GH(4)C(1)/D(2)-DAR cells to the same extent as in enriched lactotropes in primary culture. In both experimental models a low density of dihydropyridine receptors was shown by (+)-[(3)H]PN200-110 binding. Photoaffinity labelling with the dihydropyridine [(3)H]azidopine revealed a protein consistent with the alpha(1) subunit of L-type Ca(2+) channels of 165-170 kDa. In both experimental models, the facilitation of TRH action triggered by the escape from DA was correlated with an enhanced rate of phosphorylation of this putative alpha(1) subunit, the nature of which was further supported by immunoprecipitation with selective antibodies directed against the alpha(1C) and alpha(1D) subunit of voltage-gated calcium channels. We propose that PKA- and PKC-dependent phosphorylation of the alpha(1) subunit of high voltage activated, L-type Ca(2+) channels is responsible for the facilitation of Ca(2+) currents in lactotropes, and hence for the potentiation of secretagogue-mediated PRL secretion. Thus, phosphorylation of Ca(2+) channels in endocrine cells may be a mechanism for the regulation of various functions including amplification of hormone secretion.
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Preconditioning with brief ischemia before a sustained period of ischemia reduces infarct size in the perfused heart. A cultured chick ventricular myocyte model was developed to investigate the role of adenosine receptor subtypes in cardiac preconditioning. Brief hypoxic exposure, termed preconditioning hypoxia, prior to prolonged hypoxia, protected myocytes against injury induced by the prolonged hypoxia. Activation of the adenosine A1 receptor with CCPA or the A3 receptor with C1-IB-MECA can replace preconditioning hypoxia and simulate preconditioning, with a maximal effect at 100 nM. While activation of the A2a receptor by 1 microM CGS21680 could not mimic preconditioning, its stimulation during preconditioning hypoxia, however, attenuated the protection against hypoxia-induced injury. Blockade of A2a receptors with the selective antagonist CSC (1 microM) during preconditioning hypoxia enhanced the protective effect of preconditioning. Nifedipine, which blocked the A2a receptor-mediated calcium entry, abolished the A2a agonist-induced attenuation of preconditioning. Isoproterenol, forskolin, and BayK 8644, which stimulated calcium entry, also attenuated preconditioning. Nifedipine blocked the increase in calcium uptake by these agents as well as their attenuating effect on preconditioning. The present study provides the first evidence that the adenosine A3 receptor is present on ventricular myocytes and can mediate simulation of preconditioning. The data demonstrate, for the first time, that activation of the A2a receptor antagonizes the preconditioning effect of adenosine, with increased calcium entry during the preconditioning stimuli as a novel mechanism.
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Nifedipine has been reported to cause impairment of insulin sensitivity. But recently a controlled-released formulation of nifedipine (nifedipine-GITS) has been reported that it could improve insulin sensitivity.
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The aims of this review paper are: (1) to identify the pharmacological basis of interference of a variety of substances with MIBG uptake; and (2) to update the list of drugs that definitely interfere with MIBG on the grounds of evidence in the literature.
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The oviposition of female locusts requires longitudinal muscles to tolerate remarkable lengthening. Whether this ability together with concomitant properties develops during maturation or is present throughout life was investigated. The properties of the locust abdominal muscles involved in oviposition behaviour were investigated with respect to their maturation, segment- and gender-specificity and regulation by juvenile hormone (JH). Muscles from the sixth abdominal segment (an oviposition segment) of mature females (>18 days old) were able to tolerate large extensions (>8 mm). At this length, muscles were still able to generate considerable neurally evoked twitch tension. In contrast, muscle fibres from females less than 5 days old did not tolerate extension of more than 4 mm. At this length, tension generation was negligible. The maximum tension generated at different stimulus frequencies was significantly higher in muscles of females more than 18 days old than in females less than 5 days old. Furthermore, the cross-sectional area of muscle fibres increased significantly during reproductive development. Current-clamp recordings from denervated muscle fibres of females more than 18 days old revealed their ability to generate overshooting action potentials. The potentials were tetrodotoxin (TTX)-insensitive (0.5 micromol l(-1) TTX), but were blocked by Cd(2+) (50 micromol l(-1)) or nifedipine (50 micromol l(-1)), which suggests the involvement of L-type Ca(2+) channels. Action potentials recorded from females less than 5 days old differed considerably in amplitude and shape from those recorded from females more than 18 days old, suggesting their maturation during the first 2 weeks of adult life. Inactivation of the corpora allata (CA) by precocene inhibited the maturation of these muscle properties, whereas injection of JH into precocene-treated females reversed this effect. Homologous muscles from the third abdominal segment (a non-oviposition segment, M169) and muscles from males (M214) revealed no comparable changes, although some minor changes occurred during reproductive development. The results suggest a gender- and segment-specific maturation of muscle properties that is related to reproductive behaviour and controlled by JH.
PKG activators, SNP, diazoxide, nifedipine, isoprenaline, forskolin, and Sp-8-Br-cAMP were used to inhibit alpha(1)-adrenoceptor-induced contractions in tissue from transurethral resections of the prostate (TURP). The selective K(ATP) and large conductance Ca(2+) activated K(+) (BK(Ca)) channel inhibitors, glibenclamide and charybdotoxin, respectively were used to inhibit responses to PKG activators. RT-PCR identified the K(ATP) channel subunits present in TURP tissue and cultured cells.
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A randomised double-blind cross-over study enrolled 17 patients suffering from coronary heart disease (CHD) with stable angina of effort (SAE). For 1 month, each patient received diltiazem and nifedipine (60-90 mg 4 times a day and 20-30 mg 4 times a day, respectively). The effect was assessed by the pharmacodynamic test after the initial dose and in the end of each treatment course.
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The incidence and prevalence of diaper dermatitis varies widely between published studies. It is a condition which causes considerable parental anxiety. To better understand the frequency of diaper dermatitis, treatment practices, and the current importance of previously identified etiologic factors, a questionnaire survey of parents who had children wearing diapers (n = 532) attending a large United Kingdom district general hospital was undertaken. At the time of survey, only 16% of the study population had diaper dermatitis. Forty-eight percent of the study population had never had an episode of diaper dermatitis. In a multivariate analysis, current diaper dermatitis was independently associated with four factors: presence of oral thrush, number of previous episodes, frequency of diaper changes, and diarrhea. Recurrent episodes of diaper dermatitis were associated with increasing age, lack of barrier cream use, current diaper rash, and frequency of diaper changes. In the majority of children with diaper dermatitis at the time of survey, treatment had been instituted in the community. Diaper dermatitis usually presents and is treated successfully outside the hospital setting and is not a common clinical problem in secondary care.