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PubMed1999

Endothelin-1 gene suppression by shear stress: pharmacological evaluation of the role of tyrosine kinase, intracellular calcium, cytoskeleton, and mechanosensitive channels.

Physiological fluid shear stress regulates endothelin-1 (ET-1) gene expression in endothelial cells by inducing an early transient upregulation followed by a sustained suppression, at times greater than 2 h in duration. We evaluated the mechanism of ET-1 mRNA downregulation in confluent monolayers of bovine aortic endothelial (BAE) cells by applying a 6 h steady laminar shear stress of magnitude 20 dyn/cm2. Inhibition of tyrosine kinases using herbimycin A (875 nM) abolished the shear-induced decrease in ET-1 mRNA expression. Similarly, chelation of intracellular calcium ([Ca2+]i) with quin 2-AM (10 microM) blocked the suppression of ET-1 mRNA by shear. To examine the role of the endothelial cytoskeleton in the response to flow, cytochalasin D was used to disrupt F-actin microfilaments. This treatment induced cell retraction and detachment under flow, whereas stabilization of F-actin with phalloidin (1 microM) did not affect shear-induced ET-1 downregulation. In contrast, disruption of the microtubule network with nocodazole (10 micrograms/ml) completely prevented, while microtubule stabilization with taxol (10 microM) did not affect the suppression of ET-1 mRNA by flow. To determine the possible contributions of mechanosensitive channels, barium (1 mM BaCl2), was added to confluent BAE monolayers in a low-sulfate/low-phosphate modified medium and was noted to abrogate the downregulation of ET-1 gene expression and to attenuate the shear-induced increase in cytoplasmic free calcium concentration. Tetraethylammonium (3 mM TEA) partially inhibited the suppression of ET-1 mRNA by shear; in contrast, gadolinium (10 microM GdCl3), an inhibitor of the stretch-activated cation channel ISA, had no effect. Membrane depolarization by elevated extracellular potassium ([K+]o) also attenuated the suppression of ET-1 mRNA by flow at [K+]o = 70 mM and completely inhibited it at [K+]o = 135 mM. In summary, the steady-state downregulation of ET-1 mRNA by physiological levels of fluid shear stress shares signaling features with the morphological and cytoskeletal response to shear stress. These include requirement for intracellular calcium, tyrosine kinase activity, an intact microtubule network, and independence from a Gd(3+)-sensitive ISA. Unlike shear-induced changes in cell morphology and the actin cytoskeleton, the shear-induced decrease in ET-1 mRNA level is blocked by cell depolarization and by Ba2+, a blocker of the shear-activated IKS which also decreases shear-induced cytoplasmic calcium increase.

Actins↗
PubMed1997

Evidence for K+ channels involvement in capillary sensing and for bidirectionality in capillary communication.

Although the capillary sensing and communication phenomenon has been characterized, its mechanism is not clear. It has been hypothesized that capillary sensing involves a membrane potential change in the capillary endothelium and/or pericyte and that communication represents an electrotonic spread of this change along the capillary. The goal of the present study was to address this hypothesis by examining the presence of K+ channels on the capillary and by determining bidirectionality of communication. Using intravital microscopy, we locally applied K+ (100 mM), acetylcholine (ACh; 3 mM), and norepinephrine (NE; 0.3 mM) on capillaries, 400-500 microns downstream from the arteriole, at the surface of the sartorius muscle in anesthetized frogs. Responses were measured in terms of red blood cell velocity (VRBC) changes in the stimulated capillary (control prestimulation VRBC ranged from 110 to 770 microns/sec). K+ and ACh caused significant 19 and 38% increases in VRBC, while NE caused a -46% decrease, respectively. The K+ response was blocked by local pretreatment with K+ channel blocker BaCl2 (1 microM) and by pretreatment with tetraethyl ammonium chloride (TEA; 5 mM). Responses to ACh and NE were attenuated by pretreatment with 1 microM BaCl2 (to 1%) and with 50 mM TEA (to -25%), respectively. In a separate experiment, NE (3 mM) application on the capillary 500 microns away from the draining venule (capillary occluded) caused a 19% venular constriction (i.e., similar to a reported 21% arteriolar constriction caused by the NE stimulus). We concluded that (i) K+ channels were present on the capillary and (ii) capillary communication was bidirectional. We interpreted these results to be consistent with the above hypothesis of membrane potential change and electrotonic spread.

Acetylcholine↗
PubMed2000

Acetazolamide and enalapril combination offers complete protection from nitric oxide-deficient stroke in stroke-prone spontaneously hypertensive rats.

Chronic oral administration of l -NAME precipitates stroke in stroke-prone spontaneously hypertensive rats (SHRSP). The present study investigated whether acetazolamide (an acidotic agent) given alone or in combination with an angiotensin blocker (enalapril maleate) offers any protection from NO-deficient stroke in SHRSP. We also examined whether protection from NO-deficient stroke involves activation of K(+)channels. Five-week-old SHRSP drank saline (group I), l -NAME (group II), l -NAME+enalapril (group III), l -NAME+acetazolamide (group IV), and l -NAME+enalapril+acetazolamide (group V). Within a few hours following onset of stroke, rats were attached to a blood pressure recorder. In subsequent experiments, to investigate the involvement of K(+)channels, glibenclamide and BaCl(2)(K(+)channel blockers) were included in the drinking solutions that were given to the SHRSP groups receiving l -NAME, acetazolamide and enalapril. Group I of SHRSP did not develop stroke. Group II, III and IV developed stroke in 12+/-2, 29+/-2 and 20+/-2 days, respectively. SHRSP from group V did not develop stroke. However, they died in 70+/-2 days. The glibenclamide and BaCl(2)administration failed to prevent this protection from stroke. In conclusion, concurrent administration of acetazolamide and enalapril prevents onset of NO-deficient stroke in SHRSP. These stroke-protective effects are independent of reductions in mean or systolic blood pressures and do not involve an activation of K(+)channels.

Acetazolamide↗
PubMed1986

Cardiotoxic actions of doxepin and barium chloride in conscious rabbits.

Infusion of doxepin (Dx) i.v. to conscious rabbits induced dose dependently cardiac dysrhythmias of varying severity. Attempts to reduce sympathetic tone with diazepam or clonidine failed to modify Dx effects. Activation of the heart with aminophylline sensitized the animals to Dx effects. Infusion of barium chloride (Ba) caused severe ventricular dysrhythmias which were promptly abolished or reduced by verapamil. A subtoxic dose of Dx, but not diazepam, clonidine or taurine, counteracted Ba effects. Both the toxic and "therapeutic" effects of Dx might depend on its "quinidine-like" membrane effects.

Animals↗
PubMed1995

Effect of moderate cooling on contractile responses in mouse vas deferens and its relation to calcium.

Isolated mouse vas deferens preparations were used to study the effect of temperature on noradrenaline-induced contractions. Preparations were suspended in the organ bath containing Krebs-Henseleit solution for isometric tension recording. Contractile responses to noradrenaline were investigated in the mouse vas deferens after moderate cooling from 37 to 26 or 22 degrees C. A significant increase of the phasic contractions to noradrenaline was observed at 26 or 22 degrees C compared with responses obtained at 37 degrees C (about 12.3 and 35.6% increase at 26 and 22 degrees C, respectively). The secondary noradrenaline-induced sustained contraction was also significantly enhanced after moderate cooling to 26 degrees C. The potentiation of noradrenaline-induced contraction at 26 degrees C remained in a Ca(2+)-free EGTA (1 mM)-containing solution. However, sustained contraction was suppressed after removal of the calcium from the medium at 37 and 26 degrees C. Contraction to caffeine was significantly enhanced at 22 degrees C compared with 37 degrees C. By contrast, barium chloride-induced contraction of the vas deferens was markedly decreased after moderate cooling to 22 degrees C. In the presence of ouabain (0.1 mM), the noradrenaline-induced peak contraction was significantly increased at 37 degrees C. However, potentiation of the noradrenaline response at 22 degrees C was unaffected by the Na+/K+ pump inhibitor. Noradrenaline-induced peak contractions were depressed in the presence of vanadate (1 mM) and cyclopiazonic acid (10 microM), two Ca(2+)-ATPase inhibitors, at 37 degrees C and also at 22 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Analysis of the hyperpolarizing effects of forskolin in guinea-pig atrial heart muscle.

The effects of forskolin on action potential configuration and on both uptake and efflux of 86Rb+ were studied in guinea-pig left atria. The action potential was prolonged by forskolin in the plateau range but shortened at the end of repolarization; maximal upstroke velocity and amplitude of slow response potentials were enhanced. In partially depolarized preparations, the resting potential was increased by forskolin; this effect was not prevented by atropine 1 mumol/l. Forskolin augmented the rate constant of 86Rb+ efflux in beating and in resting preparations. The uptake of 86Rb+ was enhanced by forskolin in resting preparations. It is concluded that forskolin stimulates the Na+,K+-pump and activates a background potassium conductance. Both effects may account for the shortening effect of the drug on the action potential and the increase in resting potential seen in partially depolarized preparations.

Animals↗
PubMed1990

Pharmacological modification of mechanical and electrical responses of frog heart to thrombin.

The pharmacological modification of the thrombin effect on the mechanical and electrical responses of frog heart was examined in the Straub heart preparation and in single ventricular cells. Associated with the positive inotropic action thrombin increases voltage and duration of action potentials of isolated frog ventricular cells. As found by the patch-clamp technique in the cell-attached mode, thrombin stimulates single L-type Ca2+ channels, presumably mediated by a second messenger. The enhancement of contractility by thrombin depends on the proteolytic activity of the enzyme because enzymatically inactivated thrombin has no effect on frog hearts. The positive inotropic effect of thrombin as well as its stimulation of Ca2+ channel currents were inhibited by the protein kinase C blocker 1-(5-isoquinoline-sulfonyl)-2-methylpiperazine (H7). However, phorbol 12-myristate 13-acetate (PMA), a known stimulator of protein kinase C, was ineffective in stimulating the inotropic action of thrombin. The inhibition of the thrombin-induced enhancement of contractility by indometacin indicates an involvement of arachidonic acid in the action of thrombin on frog heart.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1992

Evidence that plasma membrane electrical potential is required for vesicular stomatitis virus infection of MDCK cells: a study using fluorescence measurements through polycarbonate supports.

We used fluorescence microscopy of Madin-Darby Canine Kidney (MDCK) cells grown on polycarbonate filters to study a possible link between plasma membrane electrical potential (delta psi pm) and infectivity of vesicular stomatitis virus (VSV). Complete substitution of K+ for extracellular Na+ blocks VSV infection of MDCK cells as well as baby hamster kidney (BHK) cells. When we independently perfused the apical and basal-lateral surfaces of high resistance monolayers, high K+ inhibited VSV infection of MDCK cells only when applied to the basal-lateral side; high K+ applied apically had no effect on VSV infection. This morphological specificity correlates with a large decrease in delta psi pm of MDCK cells when high K+ buffer is perfused across the basal-lateral surface. Depolarization of the plasma membrane by 130 mM basal K+ causes a sustained increase of cytosol pH in MDCK cells from 7.3 to 7.5 as reported by the fluorescent dye BCECF. Depolarization also causes a transient increase of cytosol Ca2+ from 70 to 300 nM as reported by the dye Fura-2. Neither increase could explain the block of VSV infectivity by plasma membrane depolarization. One alternative hypothesis is that delta psi pm facilitates membrane translocation of viral macromolecules as previously described for colicins, mitochondrial import proteins, and proteins secreted by Escherichia coli.

Animals↗
PubMed1980

Proteins in chromosome banding. II. Effect of R- and C-banding treatments on the proteins of isolated nuclei.

SDS polyacrylamide gel electrophoresis was used to study the proteins extracted from, and those remaining in isolated, fixed, air-dried nuclei subjected to a variety of R- and C-banding techniques. The R-banding procedures, involving exposure to hot Earle's BSS or NaH2PO4, had the least effect of any of the banding techniques on the extraction of proteins from isolated nuclei. Only small amounts of 5 nonhistone proteins were detected in the Earle's BSS extract, and no proteins were found in the NaH2PO4 solution after treatment. The residual proteins remaining in the nuclei after either treatment were virtually identical to those in control nuclei. The C-banding techniques, on the other hand, produced substantial changes in the nuclear proteins. These techniques involve several sequential steps, including HCl treatment, exposure to NaOH or Ba(OH)2, and an incubation in hot SSC. The HCl treatment extracted a large variety of nonhistones and some of each of the remaining histones. No proteins were detected in the SSC solution. Some of the proteins extracted by Ba(OH)2 appeared after the two complete C-banding treatments revealed both similarities and differences. The Ba(OH)2 technique appeared to have a more severe effect on the nuclear proteins than the NaOH technique. Fewer residual nuclear proteins were observed after the former technique, but all of these were also represented in nuclei after the NaOH technique. The results indicate that the different treatments producing a common type of banding generally have similar effects on the nuclear proteins, while the treatments producing different types of banding (G-, R-, C-banding) have substantially different effects on these proteins. Such alterations may have implications for chromosome banding.

Animals↗
PubMed1996

Creatine kinase release from regenerated muscles after eccentric contractions in rats.

The purpose of this study was to test the hypothesis that an increase in plasma creatine kinase (CK) activity after eccentric contractions (ECC) would be attenuated in regenerated muscle fibres. Adult male Wistar rats (aged 12-14 weeks) were randomly assigned to a treatment group (n = 14) or a control group (n = 10). In the treatment group, 1.2% barium chloride solution (BaCl2) was injected into the tibialis anterior (TA) and extensor digitorum longus (EDL) muscles to induce degeneration and subsequent regeneration. The same amount of isotonic saline solution was injected into TA and EDL for the control group. Histological observation showed that approximately 50% of the fibres in the transverse sections of both muscles underwent necrosis 2 days after BaCl2 injection. The CK activity increased about tenfold at 2-4 h after BaCl2 injection. At 4 weeks after BaCl2 injection, when the regeneration process was almost complete, the TA and EDL of anaesthetized rats from both groups were subjected to ECC in which maximal dorsiflexion was caused by nerve electrical stimulation and the flexed foot was forcibly extended by a lever arm connected to a motor. This action was performed in 2 sets of 30 repetitions. Maximal isometric torque of the dorsiflexors decreased to about 15% (P < 0.01) of the pre-ECC value immediately after the exercise. Blood samples were collected before and 2, 4, 12, 24, 48 h after ECC. The CK activity increased significantly (P < 0.01) and peaked at 2-4 h after ECC, and there was no significant difference in the amount of CK increase between the treatment [1007 (SEM 120) IU.l-1] and the control [1064 (SEM 120) IU.l-1] group. Contrary to the hypothesis, CK release after ECC was not attenuated in muscle regenerated from BaCl2-induced myonecrosis.

Animals↗
PubMed1991

The effect of hypo-osmolarity upon transepithelial ion transport in cultured renal epithelial layers (MDCK).

Regulatory volume decrease after exposure to hypo-osmotic media in MDCK epithelial cells results from activation of both K+ and Cl- conductances. Swelling-stimulated 86Rb(K) losses were observed only across the basal-lateral membrane and were relatively insensitive to 10 mM Ba2+. The effect of hypo-osmotic media upon MDCK epithelia mounted in Ussing chambers has been investigated. Exposure of the basal-lateral surfaces to hypo-osmotic media resulted in a transient stimulation of inward short-circuit current (Isc) followed by inhibition of inward Isc in both control layers and in layers where inward current (due to transepithelial Cl- secretion) was first stimulated by 5 microM prostaglandin E1 (PGE1). The transient stimulation of inward current by hypo-osmotic media was not markedly attenuated by 10 mM Ba2+ in PGE1-stimulated layers. After stimulation of inward (Cl(-)-secretory) current to high levels by 10 microM adrenaline, the predominant effect of basal-lateral exposure to hypo-osmotic media was an inhibition of the inward current. This inhibition was partially reversed by 40 microM 4,4'-diisothiocyanatostilbene-2,2'-disulphonate (DIDS). The stimulation, then inhibition, of inward Isc is likely to be the result of separate swelling-induced K+ and Cl- conductances (respectively) at the basal-lateral membrane. The swelling-stimulated Cl- conductance is distinct from the apical Cl- conductance regulated by PGE1 or adrenaline.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1994

H2O2 induced hyperpolarization of pancreatic B-cells.

Conventional electrophysiology and the whole-cell patch-clamp technique have been applied to elucidate the effects of H2O2 on pancreatic B-cells of the mouse. In these cells, addition of 15 mmol/l glucose leads to depolarization and oscillation of the cell membrane potential. Subsequent addition of H2O2 (1 mmol/l) in the presence of glucose was followed by a marked and rapid hyperpolarization of the cell membrane with suppression of the electrical activity. Accordingly, in slow whole-cell patch-clamp experiments (with nystatin in the pipette solution) H2O2 induced a marked increase of cell membrane conductance. Tolbutamide, a blocker of K+ ATP channels, only partially blocked the effect of H2O2 even at high concentrations. The H2O2-induced, tolbutamide-insensitive current component, however, was largely abolished by a high concentration of TEA+ (80 mmol/l) or BaCl2 (10 mmol/l). It is concluded that in B-cells H2O2 stimulates a K+ current and that this effect leads to marked hyperpolarization and reversal of glucose-induced oscillations of cell membrane potential.

Animals↗
PubMed1989

Characterization of the calcium channel state transitions induced by the enantiomers of the 1,4-dihydropyridine Sandoz 202 791 in neonatal rat heart cells. A nonmodulated receptor model.

The actions of the optical enantiomers of Sandoz 202 791 were studied in barium inward currents recorded from single cultured neonatal rat ventricular heart cells, using the whole-cell configuration of the patch clamp technique. The enantiomers were applied by bath perfusion or rapidly by the technique of concentration jumps during single voltage clamp steps. (1) (-)-202 791 reduced the barium current in response to depolarizations positive to 0 mV. The peak current amplitude in the threshold range (-40 to 0 mV) was either not affected or slightly increased by the substance. (2) The agonist enantiomer (+)-202 791 increased the inward current over the whole voltage range, where the increase in peak inward current amplitude was most prominent in the voltage range from -40 mV to 0 mV. (3) The antagonist enantiomer (10(-6) M) induced a 18.2 +/- 2.1 mV (n = 6) shift of the midpoint of the steady state inactivation curve in the hyperpolarizing direction; in contrast (+)-202 791 at the same concentration did cause only a small but not significant shift of the Ca-channel availability curve (n = 5). (4) Rapid extracellular application of (-)-202 791 (10(-6) M), during the sustained current component at a test potential of 0 mV was followed by a sudden acceleration in barium current decay. The drug-induced barium current block developed with a mean time constant of 214.7 +/- 20.6 ms (n = 5). (5) (+)-202 791 (10(-6) M) rapidly applied during test pulses to 0 and -20 mV caused an increase in barium current with a mono- or biexponential time course. The estimated mean time constant of the drug activated Ba2+ current at 0 mV membrane potential was 617.3 +/- 49.3 ms (n = 4). (6) The interaction of Sandoz 202 791 with the Ca-channels is discussed in terms of a "nonmodulated receptor" model.

Animals↗
PubMed1989

Electrophysiological characterization of rabbit distal convoluted tubule cell.

The distal convoluted tubule (DCT) from rabbit kidney were perfused in vitro to study the conductive properties of the cell membranes by using electrophysiological methods. When the lumen and the bath were perfused with a bicarbonate free solution buffered with HEPES, the transepithelial voltage (VT) averaged -2.8 +/- 0.6 mV (n = 20), lumen negative. The basolateral membrane voltage (VB) averaged -77.8 +/- 1.1 mV (n = 33) obtained by intracellular impalement of microelectrodes. Cable analysis performed by injecting a current from perfusion pipette revealed that the transepithelial resistance was 21.8 +/- 1.7 omega.cm2 and the fractional resistance of the luminal membrane was 0.78 +/- 0.03 (n = 8), indicating the existence of ionic conductances in the luminal membrane. Addition of amiloride (10(-5) mol/l) to the luminal perfusate or Na+ removal from the lumen abolished the lumen negative VT and hyperpolarized the apical membrane. An increase in luminal K+ concentration from 5 to 50 mmol/l reduced the apical membrane potential (VA) by 37.5 +/- 2.6 mV (n = 7), whereas a reduction of Cl- in the luminal perfusate did not change VA significantly (0.5 +/- 0.5 mV, n = 4). Addition of Ba2+ to the lumen reduced VA by 42.6 +/- 1.0 mV (n = 4). When the bathing fluid was perfused with 50 mmol/l K+ solution, the basolateral membrane voltage (VB) fell from -76.8 +/- 1.5 to -31.0 +/- 1.3 mV (n = 18), and addition of Ba2+ to the bath reduced VB by 18.3 +/- 4.8 mV (n = 7).(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗
PubMed1986

Electrical properties of renal collecting duct principal cell epithelium in tissue culture.

Whereas collecting duct epithelium in vivo is composed of principal and intercalated cells, we grew a pure principal cell epithelium using a new technique involving tissue culture. These principal cells were derived from collecting duct anlagen of newborn rabbits. We investigated the electrical properties of such epithelia in a newly designed lucite double-chamber with an inner opening of 0.08 cm2. Our observations were: mean transepithelial resistance Rte was 0.83 +/- 0.2 k omega cm2 at 37 degrees C and after preincubation in aldosterone; mean transepithelial potential difference Vte was low and variable under standard conditions and at room temperature but increased to -59.5 +/- 4.4 mV (sign referring to polarity of apical surface) after preincubation in 10(-6) mol/l aldosterone and at 37 degrees C; 10(-6) mol/l amiloride added to the apical perfusion fluid largely abolished this Vte while increasing Rte by 120%; experiments with 5 X 10(-3) mol/l BaCl2 in the apical perfusion fluid failed to change Rte and Vte significantly. This principal cell epithelium therefore has characteristics of a "tight" epithelium with active sodium transport; however, its electrical properties differ from those of the isolated perfused collecting duct segment.

Aldosterone↗
PubMed1986

Ca2+-channel current and its modification by the dihydropyridine agonist BAY k 8644 in isolated smooth muscle cells.

The electrophysiological properties of single smooth muscle cells isolated from the longitudinal layer of the guinea-pig ileum were studied with the whole-cell patch-clamp technique. The finding of resting potentials between -45 and -50 mV and the occurrence of spontaneous electrical activity when K+ was the predominant intracellular cation indicated that the cells were not leaky or hyperpermeable. The existence of an inward Ca2+ current overlapping in time with an outward rectifying K+ current was demonstrated. The latter could be selectively blocked by replacing internal K+ with Cs+ and external Ca2+ with Ba2+. Depolarizations to potentials between -40 and +50 mV evoked time-dependent inward currents, with a maximum peak value between -20 and 0 mV. For depolarizations beyond +50 mV time-dependent outward currents appeared. These currents were inhibited by 0.1 mM CdCl2. The activation of the inward current showed a sigmoidal time course, and the rate of onset of the current increased at more positive potentials. Inactivation could be described by two exponentials. The threshold for activation was about -40 mV, and full activation was reached at 0 mV. Inactivation was complete near 0 mV, whereas the channels were fully available at -80 mV. The fully-activated Ca2+-channel current was strongly voltage dependent. The conductance decreased for potentials close to the reversal potential, and showed rectification for hyperpolarizing potentials. The Ca2+ agonist BAY k 8644 enhanced the Ca2+-channel current without a significant effect on its kinetics. The fully-activated current and the steady-state activation were enhanced in a rather voltage-independent way.

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