[Squamous epithelial carcinoma of the kidney pelvis--a rare tumor].
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Adult↗
Biomedical subjects
J Bernhardt
Publications and source records attributed to J Bernhardt.
Evidence for the involvement of G proteins in the modulation of 22Na and 45Ca fluxes in myogenic L6 and aortic smooth muscle cells.
Preincubation of rat skeletal muscle derived L6 myoblasts with 10 mM NaF increased, the activity of Na+/H+ exchanger, and the uptake of 45Ca by 2 and 5 folds, respectively. In cultured vascular smooth muscle cells (CVSMC) of rat aorta, NaF increased the activity of Na+,K(+)-pump, Na+/H+ exchanger, passive permeability for Na+, and 45Ca uptake by 1.6, 9, 2, and 9 folds, respectively. Both, in CVSMC and L6 cells, the effect of NaF on the Na+/H+ exchanger and 45Ca uptake were significantly augmented by 20 microM AlCl3. No effect of AlCl3 on the NaF dependent changes in ion flux was seen in rat erythrocytes. The results suggest that in L6 and CVSMC cells, the Na+/H+ exchanger and Ca++ uptake pathway(s) are activated by GTP-binding proteins.
Aluminum↗
Genes for ribosomal proteins S3, L16, L5 and S14 are clustered in the mitochondrial genome of Brassica napus L.
We have cloned and sequenced an 8.9-kb mitochondrial-DNA fragment from rapeseed (Brassica napus L.). The nucleotide sequence indicates a gene cluster that encodes four ribosomal proteins (S3, L16, L5, S14), two tRNA genes (trnD, trnK), and the 5' region of the cob gene. The arrangement of these seven genes is trnD-trnK-rps3-rpl16-rpl5-rps14-cob. The rps3 and rpl16 frames overlap by 131 bp. The rpl5 and rps14 genes are separated by a 4-bp spacer. A 1474-basepair intron is located in the rps3 gene. The tRNA(Asp) gene (trnD) is very similar to the corresponding gene from chloroplasts (cp-like-tRNA(Asp)). Gene-specific probes for each ribosomal protein gene, and for the cp-like-trnD, trnK and cob genes, hybridized to a common pre-mRNA of an estimated size of 10 kilobases, indicating that these seven genes may be expressed as a single transcription unit. The rps3-rpl16-rpl5-rps14 region of B. napus mtDNA may function as a ribosomal operon, similar to the S10 and SPC operons of Escherichia coli and to the ribosomal protein operon of the chloroplast genome from Euglena gracilis.
Amino Acid Sequence↗
Acetylsalicylic acid has no effects on various isolated immune cells in vitro.
In addition to the well known biological effects of acetylsalicylic acid (ASA), its stimulating effect on the immune system has recently been described. In the present study, therefore, the influence of ASA on isolated leucocytes was investigated in vitro. Various concentrations of ASA, representing therapeutic concentrations, had neither an inhibitory nor a stimulating influence on the cytotoxicity of CD16-positive cells. The phytohaemagglutinin-induced proliferation of lymphocytes and the phagocytosis activity of monocytes and neutrophilic granulocytes was similarly unaffected. These results would indicate that the immunostimulating effects already described for ASA cannot be examined in isolated leucocytes in vitro and should be attributed to an interaction of various effector cells in vivo.
Aspirin↗
Acetylsalicylic acid, at high concentrations, inhibits vascular smooth muscle cell proliferation.
The growth of human smooth muscle cells in culture is inhibited by acetylsalicylic acid (ASA). In comparison to control, the proliferation of cells treated with 270 mg/L lysinmono(acetylsalicylate)/30 mg/L glycine was inhibited by 50-90% under different culture conditions. Cell numbers per well (control vs. treated) were as follows: (a) 470,500 +/- 55,890 vs. 24,750 +/- 4,030 (p < 0.002) after 6 days in the presence of 10% fetal calf serum (FCS), (b) 160,500 +/- 9,920 vs. 74,000 (p < 0.001) after 8 days in the presence of 10% human serum; and (c) 387,000 +/- 29,420 vs. 35,250 +/- 1,110 (p < 0.001) after 8 days in the presence of 5% FCS. Significant inhibition of growth by lysinmono(acetylsalicylate) at 90 mg/L was noted only for cultures grown with 10% FCS. Lower concentrations of this drug were ineffective under all culture conditions. Higher dosages of ASA, which would prevent not only platelet aggregation but also smooth muscle cell growth, may therefore be indicated in therapy of patients who undergo percutaneous transluminal coronary angioplasty (PTCA) or coronary artery transplantation.
Anti-Inflammatory Agents, Non-Steroidal↗
Concerted effects of lipoproteins and angiotensin II on signal transduction processes in vascular smooth muscle cells.
Low-density (LDL) and high-density (HDL3) lipoproteins dose-dependently activate phosphoinositide turnover and elevate cytosolic free Ca2+ concentrations ([Ca2+]i) in cultured vascular smooth muscle cells (VSMCs) from either human (microarterioles and aorta) or rat (aorta) sources. High-performance liquid chromatography analysis of cell extracts revealed comparable spectra of inositol phosphate isomers generated in response to either LDL, HDL3, or angiotensin II (Ang II). Thus, lipoproteins and Ang II may use similar, if not identical, signal transduction pathways for the generation and metabolism of inositol phosphates and intracellular Ca2+ mobilization in VSMCs. When Ang II was added in combination with either LDL or HDL3, the phosphoinositide and [Ca2+]i responses of VSMCs were either equal to or even greater than the sum of the effects elicited by the agonists individually. This additivity/synergy between Ang II and the lipoproteins was not accompanied by alteration in the half-maximally effective dose requirements of VSMCs for either Ang II (approximately 2 nmol/L, with or without lipoproteins) or lipoproteins (approximately 50 micrograms/mL for LDL and HDL3, with or without Ang II). Neither short-term (up to 10 minutes) nor long-term (48 hours) exposure of VSMCs to lipoproteins caused desensitization of phospholipase C and intracellular Ca2+ mobilization responses to either Ang II or lipoproteins. Since constant exposure of VSMCs to lipoproteins is a physiological circumstance, and because elevation of [Ca2+]i and activation of phosphoinositide turnover are pivotal events for VSMC contraction and growth, we suggest that the low concentrations of lipoproteins in the vessel intima may play an important role in regulating the response of the vasculature to Ang II.
Angiotensin II↗
Vascular smooth muscle cell calcium fluxes. Regulation by angiotensin II and lipoproteins.
This study examined 45Ca uptake, 45Ca efflux, and the distribution of exchangeable 45Ca in confluent, quiescent cultures of aortic smooth muscle cells (VSMCs) from normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHRs). These parameters were investigated under basal conditions and after addition of angiotensin II (Ang II) and low (LDL) and high (HDL) density lipoproteins. Basal 45Ca uptake was approximately 50% greater in VSMCs from SHRs (p < 0.005 versus WKY). Calcium antagonists (diltiazem or nifedipine) abolished this difference. The 45Ca uptake response to Ang II was approximately twofold greater in SHR than in WKY VSMCs (p < 0.05), and Ang II-induced increments of 45Ca uptake were weakly inhibited (by approximately 15-25%) by calcium antagonists. Lipoproteins also stimulated 45Ca uptake in VSMCs, and the apparent affinity of this process was approximately fivefold greater for LDL than for HDL. Calcium antagonists did not inhibit either LDL- or HDL-induced 45Ca uptake. SHR and WKY VSMCs did not differ with respect to 45Ca uptake induced by either LDL or HDL. The initial size of the slowly exchangeable pool of intracellular Ca2+ was approximately 35% greater in SHR VSMCs (p < 0.05 versus WKY). Ang II-induced mobilization of intracellular calcium (measured as the decrease in 45Ca content of the slowly exchangeable pool) was threefold greater in SHR VSMCs (p < 0.005 versus WKY). LDL and HDL marginally stimulated 45Ca efflux from this pool (< or = 20% above control) and to comparable extents in both SHR and WKY VSMCs.(ABSTRACT TRUNCATED AT 250 WORDS)
Angiotensin II↗
[Dose-response relationship of nisoldipine in patients with stable angina pectoris and stress-induced myocardial ischemia].
The dose-effect relation of nisoldipine in 3 single oral doses (5 mg, 10 mg, 20 mg) on exercise induced ST-segment depression, blood pressure and peripheral vascular response was evaluated in 16 patients with angiographically proven coronary artery disease and stable exertional myocardial in ischemia. The study was conducted according to a single-blind, randomized, placebo-controlled protocol with intraindividual cross-over. Maximal ST-segment depression and ischemia-score (ST-segment depression, workload time) under a constant submaximal workload exercise-protocol were analyzed with blood pressure, heart rate and the index b/a of digital pulse-plethysmography. 2 hours after medication nisoldipine led to a dose-dependent reduction of ST-segment depression by 12% (n.s.), 29% (p < 0.05) and 43% (p < 0.01), respectively. 8 hours after medication the ischemia-score decreased from 2.98 to 2.34 with the 20 mg-dose (p < 0.05). Systolic and diastolic blood pressure were reduced dose-dependent by 7%, 9%, and 14% with no change of heart rate at 2 h after medication. Digital pulse-plethysmography showed an acute reduction of the index b/a from 0.72 (placebo) to 0.63 (-12.5%, p < 0.01) with 10 mg and to 0.56 (-22%, p < 0.01) with 20 mg. Thus nisoldipine showed a dose-related antiischemic efficacy lasting for at least 8 h with the 20 mg dose. A small but significant peripheral vasodilatation 2 h after medication was observed.
Adult↗
Agricultural hazards in North Carolina.
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Accidents, Occupational↗
Volume-dependent regulation of sodium and potassium fluxes in cultured vascular smooth muscle cells: dependence on medium osmolality and regulation by signalling systems.
To identify ion transport systems involved in the maintenance of vascular smooth muscle cell volume the effects of incubation medium osmolality and ion transport inhibitors on the volume and 86Rb and 22Na transport in cultured smooth muscle cells from rat aorta (VSMC) have been studied. A decrease of medium osmolality from 605 to 180 mosm increased intracellular water volume from 0.6 to 1.3 microliters per 10(6) cells. Under isosmotic conditions, cell volume was decreased by ouabain (by 10%, P less than 0.005) but was not influenced by bumetanide, furosemide, EIPA and quinidine. These latter compounds were also ineffective in cell volume regulation under hypotonic buffer conditions. Under hyperosmotic conditions, cell volume was decreased by bumetanide (by approximately 7%, P less than 0.05) and by ethylisopropyl amiloride (by approximately 13%, P less than 0.005). Ouabain-sensitive 86Rb influx was decreased by 30-40% under hypoosmotic conditions. An increase in medium osmolality from 275 to 410 mosm resulted in an approximately eightfold increase in bumetanide-inhibited 86Rb influx and 86Rb efflux. The (ouabain and bumetanide)-insensitive component of 86Rb influx was not dependent on the osmolality of the incubation medium. However (ouabain and bumetanide)-insensitive 86Rb efflux was increased by approximately 1.5-2 fold in VSMC incubated in hypotonic medium. Ethylisopropyl amiloride-inhibited 22Na influx was increased by approximately sixfold following osmotic-shrinkage of VSMC. The data show that both Na+/H+ exchange and Na+/K+/2Cl- cotransport may play a major role in the regulatory volume increase in VSMC. Basal and shrinkage-induced activities of Na+/K+/2Cl- cotransport in VSMC were similarly sensitive to inhibition by either staurosporin, forskolin, R24571 or 2-nitro-4-carboxyphenyl N,N-diphenylcarbomate (NCDC). In contrast basal and shrinkage-induced Na+/K+/2Cl- cotransport were differentially inhibited by NaF (by 30 and 65%, respectively), suggesting an involvement of guanine nucleotide binding proteins in the volume-sensitive activity of this carrier. Neither staurosporin, forskolin, R24571 nor NCDC influenced shrinkage-induced Na+/H+ exchange activity. NaF increased Na+/H+ exchanger activity under both isosmotic and hyperosmotic conditions. These data demonstrate that different intracellular signalling mechanisms are involved in the volume-dependent activation of the Na+/K+/2Cl- cotransporter and the Na+/H+ exchanger.
Alkaloids↗
Oxidized low density lipoproteins stimulate phosphoinositide turnover in cultured vascular smooth muscle cells.
Atherogenesis is associated with alterations in the properties of different cell types, including monocytes/macrophages (foam cell formation), platelets (increased aggregation), endothelial cells (injury), and smooth muscle cells (SMCs) (lipid accumulation or foam cell formation). Oxidized low density lipoproteins (ox-LDL) play a key role in this vascular pathology. This study investigated the ability of ox-LDL to elicit chemical signaling events in cultured human vascular smooth muscle cells (VSMCs). Ox-LDL was found to stimulate phospholipase C-mediated phosphoinositide turnover in human VSMCs. This response occurred rapidly (within 1 minute) and at low concentrations of ox-LDL (half-maximal effective concentration, approximately 5 micrograms/ml). Ox-LDL-stimulated inositol phosphate accumulation in human VSMCs was inhibited by pretreatment of cells with phorbol 12-myristate 13-acetate and with compounds that elevate cyclic AMP or cyclic GMP. Ca2+ antagonists also blocked the effects of ox-LDL on phosphoinositide turnover. Inhibitors of receptor-endocytotic processes (including receptor clustering, cross-linking, and cytoskeleton-dependent internalization) effectively prevented ox-LDL-induced inositol phosphate generation. The data suggest that ox-LDL promotes phospholipase C-mediated phosphoinositide turnover in a manner analogous to that for other Ca(2+)-mobilizing hormones. The results also support an association between phosphoinositide turnover and receptor-mediated endocytosis. Prevention of the direct effects of ox-LDL on SMCs could prove an interesting therapeutic avenue for the prevention of atherosclerosis.
Calcium Channel Blockers↗
Na(+)-K+ pump and Na(+)-K+ co-transport in cultured vascular smooth muscle cells from spontaneously hypertensive and normotensive rats: baseline activity and regulation.
OBJECTIVE: This paper examines the hypothesis that aberrations in vascular smooth muscle univalent ion transport systems play an important role in the pathogenesis of hypertension. DESIGN: Baseline Na(+)-K+ pump and Na(+)-K(+)-2Cl- co-transport activities and the regulation of these ion transport systems by angiotensin II and second messenger molecules have been studied in cultured aortic smooth muscle cells (VSMC) from normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). METHODS: Ion transport was studied using isotopic univalent cations (86Rb and 22Na). RESULTS: Baseline Na(+)-K+ pump activity was comparable between SHR- and WKY-derived VSMC. Baseline Na(+)-K(+)-2Cl- and K(+)-Cl- co-transport activity as well as K+ leakage were significantly greater in SHR VSMC. Baseline Na(+)-K(+)-2Cl- co-transport was sensitive to inhibition by forskolin and ethyleneglycol-bis-(beta-amino ethylester)-N,N,N',N'-tetraacetic acid, whereas cyclic guanosine monophosphate and phorbol 12-myristate, 13-acetate had no effect. Angiotensin II-stimulated Na(+)-K(+)-2Cl- co-transport activity did not differ between WKY and SHR VSMC. Angiotensin II increased Na(+)-K(+)-pump activity to a significantly greater extent in SHR VSMC. The stimulatory effect of angiotensin II upon Na(+)-K+ pump activity was reduced under Na(+)-free buffer conditions and in the presence of the Na(+)-H+ exchange inhibitor, ethylisopropyl amiloride. Na(+)-K+ pump activity was also stimulated by the protein kinase C activator, phorbol 12-myristate, 13-acetate, and this was completely inhibited under Na(+)-free buffer conditions. CONCLUSIONS: SHR VSMC exhibit anomalous Na(+)-K(+)-pump and Na(+)-K(+)-2Cl- co-transport activities. The influence of these univalent ion transport systems upon cellular Na+ and Ca2+ homeostasis invoke their participation in the pathogenesis of hypertension.
Angiotensin II↗
Expression of tenascin by vascular smooth muscle cells. Alterations in hypertensive rats and stimulation by angiotensin II.
The extracellular matrix glycoprotein tenascin is associated with remodeling events in many embryonic and pathologic tissues. The expression of tenascin has been investigated by immunohistochemistry in blood vessels of Wistar-Kyoto (normotensive) and spontaneously hypertensive rats. Weak tenascin staining was present throughout the tunica media of large and small arteries from normotensive animals; strong staining was only detectable at branching sites. In arteries from hypertensive animals, foci of strong tenascin staining were scattered throughout the tunica media. The expression of tenascin mRNA and protein by rat aortic smooth muscle cells cultured in serum-free medium was induced by the vasoconstrictor peptide angiotensin II. Transforming growth factor-beta and platelet-derived growth factor also stimulated tenascin mRNA expression. Vascular smooth muscle cells attached specifically to a substratum of tenascin, but remained rounded. Thus, increased focal tenascin expression by vascular smooth muscle cells is associated with hypertension, and may mediate angiotensin II-induced changes in vascular structure in hypertension.
Angiotensin II↗
Release of nitric oxide from human vascular smooth muscle cells.
It has recently been shown that nitric oxide (NO) or a labile NO-releasing compound is produced in endothelial cells. In the present study we measured the NO-release from human vascular smooth muscle cells in culture. The cells released an average 2.2 x 10(-9) moles nitric oxide per 10(8) cells in ten minutes with a large variation between different cell lines and passages without stimulators. The NO-release was markedly reduced by the inhibitor of NO-formation NG-momomethyl-L-arginine (L-NMMA, 10(-5) M) to 3% of the control levels (p less than 0.02, n = 4), but unaffected by acetylcholine, bradykinin or endothelin -1, -2 or -3. In a microperfusion system the compound released from human vascular smooth muscle cells caused profound relaxation of isolated rat mesenteric resistance arteries. Thus, human vascular smooth muscle cells in culture produce and release biologically active NO from L-arginine.
Animals↗
Stimulation of autocrine platelet--derived growth factor AA-homodimer and transforming growth factor beta in vascular smooth muscle cells.
We have investigated the interrelationship between growth factors and vasoconstrictor peptides in terms of their possible paracrine/autocrine regulation of vascular smooth muscle cell differentiation/proliferation. Responses of quiescent cells from spontaneously hypertensive and Wistar-Kyoto rats to stimulation with a selected number of growth factors- and vasoconstrictor peptides were established (induction of mRNA as well as secretion of immunoreactive peptides). A single exposure of quiescent vascular smooth muscle cells to the vasoconstrictor peptides Angiotensin II and Endothelin-1 (10(-8) M each) resulted in a prolonged induction of platelet- derived growth factor A-chain and transforming growth factor beta transcripts (maximal at 5-6 hrs poststimulatory). The interrelationship between platelet- derived growth factor AA and transforming growth factor beta was investigated in experiments using the pure peptides individually for stimulation of mRNA and peptide secretion. Both growth factors enhanced their own and one anothers transcript expression. The results demonstrated that in spontaneously hypertensive rats, an established animal model of hypertension, the steady state balance of this set of growth factors may be disturbed. Defects involved may be attributable to alterations in the secretory machinery and/or amount of autocrine growth factor produced.
Angiotensin II↗
Percutaneous nephrostomy tubes in the neonate with obstructive uropathy.
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Humans↗
Making a difference: an educational advisory committee in the NICU.
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Critical Care↗
Rapid kinetics of agonist binding and permeability response analyzed in parallel on acetylcholine receptor rich membranes from Torpedo marmorata.
Excitable acetylcholine receptor rich membrane fragments from Torpedo marmorata have been used to measure, in parallel, (1) the permeability response to the fluorescent cholinergic agonist Dns-C6-Cho (in the 0.1 microM to millimolar concentration range) characterized by both the initial rate of Li+ transport and the rate of channel closure using the rapid-mixing quench-flow technique and (2) the kinetics of interaction of Dns-C6-Cho with the acetylcholine receptor sites using the rapid-mixing stopped-flow technique. Analysis of the kinetics of Dns-C6-Cho binding in the millisecond to minute time scale leads to the identification of at least three conformational states of the acetylcholine receptor: a "low-affinity" one (approximately 50 microM) that can be interconverted in the fraction of a second to a transient state of "intermediate affinity" (approximately 1 microM), followed by the final stabilization, in the second to minute time range, of a state of "high affinity" (approximately 3 nM). Comparison of Dns-C6-Cho binding data with the permeability response to the same agonist demonstrates that the binding to the low-affinity conformation(s) of the acetylcholine receptor sites coincides with the triggering of the permeability increase--or "activation"--and the transitions to the intermediate- and high-affinity states with the two-step process of channel closing--or "desensitization". The data are interpreted in terms of a minimum four-state "allosteric" model for the acetylcholine receptor.
Animals↗