Spontaneous Voltage Research Articles

ADH increases apical Na+, K+, 2Cl- entry in mouse medullary thick ascending limbs of Henle.

These studies were designed to evaluate the mechanism for the ADH-dependent increase in transcellular conductance (Gc, mS X cm-2), which accompanies hormone-dependent increases in the spontaneous transepithelial voltage (Ve, mV) and in the net rate of Cl- absorption in single medullary thick ascending limbs of Henle (mTALH) isolated from mouse kidney. The total transepithelial conductance (Ge, mS X cm-2) was measured with perfusing solutions containing 5 mM K+, zero Ba2+; Gc was that component of Ge blocked by luminal 20 mM Ba2+, zero K+. In paired experiments, antidiuretic hormone (ADH) increased Gc from 44.5 +/- 5.6 to 58.9 +/- 8.9 mS X cm-2 (delta = 14.3 +/- 5.5; P less than 0.02); however, in the presence of 10(-4) M luminal furosemide, ADH had no significant effect on Gc (delta = 5.0 +/- 4.3; NS). A set of similarly paired measurements together with paired observations on the effects of bath Cl- deletion, permitted an assessment of the effect of ADH on the magnitude of the fall in Gc on bath Cl- removal (delta GClc, mS X cm-2). delta GClc was clearly larger with ADH, 29.6 +/- 4.3, than without ADH, 19.2 +/- 1.0 (delta = 10.4 +/- 4.9; P less than 0.05). However, with luminal furosemide, ADH had no significant effect on delta GClc (delta = 1.7 +/- 4.5; NS). These results indicate that the ADH-dependent increase in Gc is secondary to increased salt entry across the apical membrane. We computed apical (ga, mS X cm-2) and basolateral (gb, mS X cm-2) membrane conductances from the Gc measurements and apical-to-basolateral membrane resistance ratios (Ra/Rb) obtained from cell impalement: the ADH-dependent Gc increase was due to an increase in gb, which was blocked entirely by luminal furosemide. We propose that ADH increases the number of functioning apical membrane Na+,K+,2Cl- transport units, and that gb increases because cell Cl- activity rises and depolarizes the basolateral membrane. Thus the calculated cellular Cl- activity was 16.3 mM without ADH, and 25 mM with ADH.

Equilibrium Fluctuation Analysis of Potassium Ferro/Ferricyanide Redox System on Platinum Disk Microelectrodes Using Field Effect Transistors

Spontaneous voltage fluctuations of the equilibrium potential of the ferrocyanide/ferricyanide redox couple at a Pt disk microelectrode have been measured with field effect transistors in the range of . Heterogeneous rate constants of the charge transfer reaction as well as the Warburg coefficients have been calculated from these measurements using a crossa‐correlation analysis. Stochastic and deterministic techniques for determination of electrode kinetic parameters have been compared. The deterministic procedure was a modified impedance technique in which the electrochemical system was perturbed by a lowa‐amplitude random signal applied to the electrode and the real and the imaginary parts of the equivalent electrical circuit were evaluated from the transfer function. Despite the very different nature of the origin of the signal the results obtained by these two techniques are in excellent agreement. An unusual concentration dependence of the Warburg impedance has been observed which is probably related to the small size of the electrode.

Effects of (CO2 + HCO3-) on electrical conductance in cortical thick ascending limbs

These experiments in isolated mouse cortical thick ascending limbs (cTALH) provide information about: the relative contributions of cellular and paracellular pathways to the transepithelial electrical conductance Ge (mS cm-2); the effects of (CO2 + HCO3-) on Ge; the ratio of net K+ secretion (JKnet) to net Cl- absorption (JClnet); and the K+ requirement for apical membrane furosemide-sensitive NaCl entry. The combination of luminal Ba++, zero K+ reduced Ge; at 5 mM luminal Ba++, the residual conductance was about 75% of the control Ge. The Ba++-insensitive Ge of 73.1 +/- 6.4 mS cm-2 was only slightly greater than the shunt conductance of 57 mS cm-2 computed from the sum of the dissipative bath to lumen fluxes of 22Na+ and 36Cl-. Moreover, luminal 5 mM Ba++, zero K+ had no effect on the Na+/Cl- permselectivity ratio of the paracellular pathway. Thus, Ba++ blockaded transcellular conductance by blocking apical membrane K+ channels. The combination of (CO2 + HCO3-) in external solutions increased Ge solely by augmenting the Ba++-sensitive, that is, transcellular, component of Ge. Finally, in paired experiments, the ratio JKnet/JClnet was 0.27 +/- 0.05; and both Ve, the spontaneous transepithelial voltage (mV), and the equivalent short circuit current Je (pEq sec-1 cm-2) were reduced dramatically by luminal K+ omission. Thus, apical membranes of the cTALH appear to contain a pathway for net K+ secretion, and apical membrane NaCl entry may involve co-transport with K+. Transcellular conductance contributes at least 25% to the total Ge, and the combination (CO2 + HCO3-) augments transcellular conductance.

Ionic conductance pathways in the mouse medullary thick ascending limb of Henle. The paracellular pathway and electrogenic Cl- absorption.

Net Cl- absorption in the mouse medullary thick ascending limb of Henle (mTALH) involves a furosemide-sensitive Na+:K+:2 Cl- apical membrane symport mechanism for salt entry into cells, which occurs in parallel with a Ba++-sensitive apical K+ conductance. The present studies, using the in vitro microperfused mouse mTALH, assessed the concentration dependence of blockade of this apical membrane K+-conductive pathway by Ba++ to provide estimates of the magnitudes of the transcellular (Gc) and paracellular (Gs) electrical conductances (millisiemens per square centimeter). These studies also evaluated the effects of luminal hypertonicity produced by urea on the paracellular electrical conductance, the electrical Na+/Cl- permselectivity ratio, and the morphology of in vitro mTALH segments exposed to peritubular antidiuretic hormone (ADH). Increasing luminal Ba++ concentrations, in the absence of luminal K+, produced a progressive reduction in the transcellular conductance that was maximal at 20 mM Ba++. The Ba++-sensitive transcellular conductance in the presence of ADH was 61.8 +/- 1.7 mS/cm2, or approximately 65% of the total transepithelial conductance. In phenomenological terms, the luminal Ba++-dependent blockade of the transcellular conductance exhibited negative cooperativity. The transepithelial osmotic gradient produced by luminal urea produced blebs on apical surfaces, a striking increase in shunt conductance, and a decrease in the shunt Na+/Cl- permselectivity (PNa/PCl), which approached that of free solution. The transepithelial conductance obtained with luminal 800 mM urea, 20 mM Ba++, and 0 K+ was 950 +/- 150 mS/cm2 and provided an estimate of the maximal diffusion resistance of intercellular spaces, exclusive of junctional complexes. The calculated range for junctional dilution voltages owing to interspace salt accumulation during ADH-dependent net NaCl absorption was 0.7-1.1 mV. Since the Ve accompanying ADH-dependent net NaCl absorption is 10 mV, lumen positive, virtually all of the spontaneous transepithelial voltage in the mouse mTALH is due to transcellular transport processes. Finally, we developed a series of expressions in which the ratio of net Cl- absorption to paracellular Na+ absorption could be expressed in terms of a series of electrical variables. Specifically, an analysis of paired measurement of PNa/PCl and Gs was in agreement with an electroneutral Na+:K+:2 Cl- apical entry step. Thus, for net NaCl absorption, approximately 50% of Na+ was absorbed via a paracellular route.

Voltage Noise in Acer pseudoplatanus Cells

The present contribution is devoted to studying the electrical noise of Acer pseudoplatanus cells in culture suspensions. Spontaneous voltage noise of the cells was recorded by means of a microelectrode inserted in the vacuole. The small signal impedance of the cell was measured so that it was possible to study the intensity spectra of the noise. We recorded intensity spectra with cells incubated in 10(-3) molar gramicidin A. Difference spectra showed characteristics of a channel noise. By using the calculated conductance of gramicidin A in an artificial membrane, and by simplifying assumptions for the ionic transports through plasmalemma and tonoplast, we were able to estimate the electrochemical potential difference for K(+) ions across the plasmalemma (3.2 +/- 1 millivolt).

Effects of antidiuretic hormone on cellular conductive pathways in mouse medullary thick ascending limbs of Henle: II. determinants of the ADH-mediated increases in transepithelial voltage and in net Cl-absorption.

Cellular impalements were used in combination with standard transepithelial electrical measurements to evaluate some of the determinants of the spontaneous lumen-positive voltage, Ve, which attends net Cl- absorption, JnetCl, and to assess how ADH might augment both JnetCl and Ve in the mouse medullary thick ascending limb of Henle microperfused in vitro. Substituting luminal 5 mM Ba++ for 5 mM K+ resulted in a tenfold increase in the apical-to-basal membrane resistance ratio, Ra/Rbl, and increasing luminal K+ from 5 to 50 mM in the presence of luminal 10(-4)M furosemide resulted in a 53-mV depolarization of apical membrane voltage, Va. Thus K+ accounted for at least 85% of apical membrane conductance. Either with or without ADH, 10(-4) M luminal furosemide reduced Ve and JnetCl to near zero values and hyperpolarized both Va and Vbl, the voltage across basolateral membranes; however, the depolarization of Vbl was greater in the presence than in the absence of hormone while the hormone had no significant effect on the depolarization of Va. Thus ADH-dependent increases in Ve were referable to greater depolarizations of Vbl in the presence of ADH than in the absence of ADH. 68% of the furosemide-induced hyperpolarization of Va was referable to a decrease in the K+ current across apical membranes, but, at a minimum, only 19% of the hyperpolarization of Vbl could be accounted for by a furosemide-induced reduction in basolateral membrane Cl- current. Thus an increase in intracellular Cl- activity may have contributed to the depolarization of Vbl during net Cl- absorption, and the intracellular Cl- activity was likely greater with ADH than without hormone. Since ADH increases apical K+ conductance and since the chemical driving force for electroneutral Na+, K+, 2Cl- cotransport from lumen to cell may have been less in the presence of ADH than in the absence of hormone, the cardinal effects of ADH may have been to increase the functional number of both Ba++-sensitive conductance K+ channels and electroneutral Na+, K+, 2Cl- cotransport units in apical plasma membranes.

Perturbations in the membrane potential of cultured heart cells: role of calcium.

Intracellular recordings were obtained from spheroidal aggregates of 7-day embryonic chick heart cells after 3 days in gyratory culture. Three types of perturbations in the membrane potential were observed under experimental conditions expected to increase intracellular calcium: 1) multiple oscillations (of 5-20 mV peak-to-peak amplitude) during diastole in aggregates exposed to 10-15 mM Ca, 5 microM strophanthidin, or K-free solutions; 2) less periodic spontaneous voltage fluctuations (of less than 1.5 mV peak-to-peak amplitude) in aggregates exposed to solutions containing 22% of the normal [Na], and 3) depolarizing afterpotentials (DAPs), following repolarization of the action potential, in aggregates treated with 20-50 microM A23187, a Ca ionophore, or 5-10 mM caffeine. The oscillations were reduced markedly by 0.03-3.0 microM tetrodotoxin (TTX) and were blocked by 5-10 mM caffeine. Spontaneous voltage fluctuations were increased by raising external Ca, were unaffected by 30 microM TTX, and were blocked by 5 mM caffeine. DAPs were not blocked by 5 mM caffeine or by 0.1 microM TTX and 1 microgram/ml D 600, concentrations that greatly reduced the action potential upstroke velocity and plateau, respectively. Two intracellular electrodes were employed to test for electrotonic coupling between cells within an aggregate. An electrotonic response in one cell could be recorded when current was injected into another cell during recordings of each of the perturbations but was somewhat less during spontaneous voltage fluctuations. Possible ionic mechanisms for the perturbations and for concomitant changes in the configuration of the action potential are discussed.

Electrographic recording from bovine vomeronasal capsule under spontaneous and stimulated conditions

The vomeronasal organ (VNO) is an accessory olfactory system which in many vertebrates seems to be involved in reproductive behavior, particularly in permitting males to detect estrus in conspecific females. We postulated that EEG-like field potentials could be recorded from the VNO because the organ has a sensory epithelium that can discharge in response to odorants, and because VNO receptor cells are structurally similar to cells in the olfactory mucosa that produce field potentials (the “electro-olfactogram”). We examined this postulate in male cattle by surgically implanting recording/perfusion cannulae into the ducts leading to each VNO. Both bipolar (between VNOs) and reference recording revealed continuous spontaneous voltage fluctuations that were similar to an EEG, except that amplitudes were larger and frequencies slower. Simultaneous recording of the EEG and VNO, using the same nasal reference electrode revealed that neither signal was “contaminated” by voltages from the other. Perfusions of one VNO with whole urine, urine condensate, or aqueous reconstituted urine extracts, whether from females in estrus or in anestrus, produced massive transient electrical responses from both VNOs. Perfusion with penicillin or local anesthetics caused more sustained large electrical responses from both VNOs, except that activity became quiescent about 15 min after local anesthesia. These results suggest that it is feasible to use direct recording of VNO responses to stimulation to investigate the behavioral physiology of the VNO. The cellular origin of these potentials is not self-evident, inasmuch as there are several probable sources: VNO receptor cells, cells of origin of the nervus terminalis, trigeminal afferents, vasomotor fibers, vascular erectile tissue, and fluid motion in the VNO. The experimental approach that is presented here could provide an assay system for exploring comparative functions and the behavioral significance of the various cell types that are associated with the mammalian VNO.

Spontaneous voltage and current fluctuations in tissue cultured mouse dorsal root ganglion cells

Fetal mouse dorsal root ganglion (DRG) neurons were maintained in primary dissociated cell culture for periods of 7 days to 3 months. Intracellular recordings from these cells revealed the presence of spontaneous subthreshold potentials in 101/177 neurons studied. When measured at the resting membrane potential, these spontaneous voltage events took two forms: (a) high frequency potential fluctuations several millivolts in peak-to-peak amplitude and (b) small, discrete hyperpolarizations. Neurons exhibiting either type of event were designated as ‘active’ DRG cells. No spontaneous potentials were seen in DRG cells hyperpolarized to membrane voltages more negative than −64 ± 11.5 mV (n= 5cells). Under voltage-clamp conditions, the subthreshold potentials of active DRG cells were replaced by fluctuations in outward current. The power spectral density, S(f) of these current fluctuations was approximated by an equation of the form S(f)= (S(o)/[1 + (f/f c) α] where 2 ⩽ α ⩽ 3 and the half-power frequency f c= 11.3 ± 3.1 Hz at 23°C ( n = 17 cells). The spontaneous voltage fluctuations of active DRG cells were abolished in Ca 2+-free saline, and of the divalent metal cations Sr 2+, Mg 2+, Ba 2+, Co 2+ and Mn 2+, only Sr 2+ could substitute for Ca 2+ in the maintenance of this activity. Tetraethylammonium ions (1–10 mM) reversibly blocked the spontaneous potentials, while caffeine (10 mM) increased the frequency of these events. The spontaneous voltage fluctuations were not dependent on the presence of spinal cord neurons in the culture plate, and they were also observed in cultured DRG cells derived from adult mice.

Bistable electro-optic switching of a ferroelectric liquid crystal (HOBACPC)

The article gives a brief review about our experimental investigations on ferroelectric liquid crystals. We have studied the electro-optic switching properties of thin homogeneous layers of the smectic liquid crystal HOBACPC. A complete set of data for some of the switching parameters (spontaneous polarization, switching angle, contrast ratio, threshold voltage and switching time) is given for the first time in all of the three ferroelectric phases of this material. It is shown that the switching behaviour is strongly sensitive to the alignment conditions. The article furthermore reports on ferroelectric bubble domains. Finally some remarks about applications in general as well as about recently constructed devices are given.

Furosemide-sensitive Cl transport in embryonic chicken retinal pigment epithelium

Retinal pigment epithelium- (RPE) choroid-sclera preparations from embryonic chickens were mounted in an Ussing chamber. A spontaneous transepithelial voltage (Ve) of 5.1 mV (retinal side positive) and a resistance of 114 omega . cm2 can be attributed to the RPE. Furosemide and ouabain inhibited the Ve without affecting the resistance when applied to the retinal surface of the preparation but had no effect when applied to the scleral surface. Acetazolamide and amiloride were without effect when applied to either surface. The Ve fell by 100% in Na-free medium, by 70% in Cl-free medium, and was unchanged in HCO3-free medium. When Na and Cl were returned to the medium, the Ve recovered. Dilution potentials and unidirectional flux studies indicated that the RPE is more permeable to Na than to Cl. Isotope flux studies performed under open-circuit conditions showed a net retina-to-choroid flux for both Na and Cl with the net Cl flux abolished by furosemide. Analysis of the Na+ and Cl- electrochemical gradients and the Na permeability across the RPE suggests that the net retina-to-choroid Na+ flux is largely passive, whereas the net retina-to-choroid Cl- flux results from active transport. These results indicate that embryonic chicken RPE possesses furosemide-sensitive Cl transport function. A model of embryonic chicken RPE transepithelial transport is presented.

Interactions among prostaglandin E2, antidiuretic hormone, and cyclic adenosine monophosphate in modulating Cl- absorption in single mouse medullary thick ascending limbs of Henle.

This paper describes the inhibitory effect of prostaglandin E2 (PGE2) on antidiuretic hormone (ADH)-stimulated net Cl- absorption and spontaneous transepithelial voltage (Ve) in single medullary thick ascending limbs of Henle (TALH, thick ascending limb; mTALH, medullary segment; cTALH, cortical segment) obtained from mouse kidney. The experimental data indicate that PGE2 reduced the ADH-dependent values of net Cl- absorption (JnetCl, eq cm-2 s-1) and Ve (mV) in a dose-dependent manner; that increasing concentrations of peritubular ADH reversed the PGE2-mediated reductions in the ADH-dependent moiety of Ve in the mouse mTALH; that PGE2 had no effect on cyclic AMP-stimulated increments in Ve in the mouse mTALH; and that PGE2 had no effect on Ve in the cTALH, where Ve is unaffected either by ADH or by cyclic AMP. These effects might be obtained because of a direct competition between ADH and PGE2 for receptor binding on basolateral membranes. Alternatively, PGE2 might have reduced the affinities between ADH-receptor units and a component(s) of the series of processes leading to adenyl cyclase activation. The latter argument requires that basolateral membranes of the mouse mTALH exhibit receptor reserve, i.e., at the minimum concentration of ADH required to enhance Ve and JnetCl maximally, a fraction of basolateral membrane ADH receptors were unoccupied. According to this view, increasing peritubular ADH concentrations might reverse the PGE2-mediated reduction in ADH-dependent salt transport by increasing the number of basolateral membrane receptors occupied by ADH.

CO2-stimulated NaCl absorption in the mouse renal cortical thick ascending limb of Henle. Evidence for synchronous Na +/H+ and Cl-/HCO3- exchange in apical plasma membranes.

These experiments evaluated salt transport processes in isolated cortical thick limbs of Henle (cTALH) obtained from mouse kidney. When the external solutions consisted of Krebs-Ringer bicarbonate (KRB), pH 7.4, and a 95% O2-5% CO2 gas phase, the spontaneous transepithelial voltage (Ve, mV, lumen-to-bath) was approximately mV; the net rate of Cl- absorption (JnetCl) was approximately 3,600 pmols s-1 cm-2; the net rate of osmotic solute absorption Jnetosm was twice JnetCl; and the net rate of total CO2 transport (JnetCO2) was indistinguishable from zero. Thus, net Cl- absorption was accompanied by the net absorption of a monovalent cation, presumably Na+, and net HCO3- absorption was negligible. This salt transport process was stimulated by (CO2 + HCO3-): omission of CO2 from the gas phase and HCO3- from external solutions reduced JnetCl, Jnetosm, and Ve by 50%. Furthermore, 10(-4) M luminal furosemide abolished JnetCl and Ve entirely. The lipophilic carbonic anhydrase inhibitor ethoxzolamide (10(-4) M, either luminal or peritubular) inhibited (CO2 + HCO3-)-stimulated JnetCl, Jnetosm, and Ve by approximately 50%; however, when the combination (CO2 + HCO3-) was absent, ethoxzolamide had no detectable effect on salt transport. Ve was reduced or abolished entirely by omission of either Na+ or Cl- from external solutions, by peritubular K+ removal, by 10(-3) M peritubular ouabain, and by 10(-4) M luminal SITS. However, Ve was unaffected by 10(-3) M peritubular SITS, or by the hydrophilic carbonic anhydrase inhibitor acetazolamide (2.2 x 10(-4) M, lumen plus bath). We interpret these data to indicate that (CO2 + HCO3-)-stimulated NaCl absorption in the cTALH involved two synchronous apical membrane antiport processes: one exchanging luminal Na+ for cellular H+; and the other exchanging luminal Cl- for cellular HCO3- or OH-, operating in parallel with a (CO2+ HCO3-)-independent apical membrane NaCl cotransport mechanism.

Functional differentiation of the medullary collecting tubule: Influence of vasopressin

Medullary collecting tubules of rabbits were dissected from the outer zone at different stages of ontogenetic evolution and perfused in vitro. The hydraulic conductivity coefficient (Lp) was measured in the presence of either hypotonic perfusate and isotonic bath or isotonic perfusate and hypertonic bath. Basal Lp (cm s-1 atm-1 10(-7) was 85 +/- 34 (N = 17) during early functional differentiation of the outer medullary collecting tubule (e-OMCT), 36 +/- 6 (N = 8) in the intermediate state (i-OMCT), and 10 +/- 7 (N = 11) in the final, mature state of function (m-OMCT). Addition of supramaximal concentrations of arginine-vasopressin (AVP) to the bath increased Lp in i-OMCT (250 +/- 36) and m-OMCT (327 +/- 63) but did not activate the osmotic hydraulic conductance in e-OMCT (105 +/- 27). In 11 studies, OMCT were analyzed using isotonic solutions as the perfusate and bath medium. The spontaneous transtubular voltage (PD) was lumen positive, 1.71 +/- 0.3 in e-OMCT, lumen negative 2.43 +/- 0.3 in i-OMCT, and 6.1 +/- 0.4 in m-OMCT. AVP had no effect on PD in e- and i-OMCT but increased the PD significantly (P less than 0.025) to 9.2 +/- 0.6 in m-OMCT. The results indicate that both hydraulic conductivity coefficient and transtubular voltage in the medullary collecting tubule are dependent upon epithelial ontogeny and, particularly, display differential responses to the antidiuretic hormone. The data suggest that the differentiation of water and ion transport in the medullary collecting tubule may contribute to the increasing efficacy of the medullary countercurrent system.

Sodium transport in the rabbit connecting tubule.

Connecting tubules were dissected from rabbit kidneys and perfused in vitro with a solution identical to that in the bath. Transepithelial sodium fluxes were measured with 22Na. The mean lumen-to-bath flux was 33.7 +/- 3.4 peq . cm-1 . s-1 and the mean bath-to-lumen flux was 13.4 +/- 3.4 peq . cm-1 . s-1. Thus, the net sodium transport was 20.3 peq . cm-1 . s-1, which is approximately 3--4 times higher than the one previously measured in cortical collecting ducts under similar conditions. The sodium permeability calculated from the bath-to-lumen measurements corrected for mean voltage was 1.22 x 10(-5) cm .s-1. The mean transepithelial electrical resistance was 31 omega . cm2. This sodium permeability is much higher and the electrical resistance much lower than those in cortical collecting ducts. Spontaneous transepithelial voltage was oriented negative in the lumen and ranged up to -42 mV at low perfusion pressures. When the perfusion pressure was increased, the voltage decreased to approximately -5 mV without any measurable change in the electrical resistance or the lumen-to-bath sodium flux.

Transient depolarization and spontaneous voltage fluctuations in isolated single cells from guinea pig ventricles. Calcium-mediated membrane potential fluctuations.

Under the influence of cardiotonic steroids, single ventricular cells exhibit transient depolarization after a train of driven action potentials or, in voltage clamp experiments, transient inward current after a depolarizing clamp pulse. Transient depolarization or transient inward current was abolished by an intracellular injection of ethyleneglycol-bis (beta-aminoethyl ether)-N,N'-tetraacetic acid (EGTA) or by superfusion of 5 mM caffeine. Transient depolarization was elicited even in the control Tyrode's solution by an intracellular injection of CaCl2 or augmented by an injection of adenosine 3',5'-cyclic monophosphoric acid (cAMP). Along with transient depolarization or transient inward current, digitalis intoxication promoted spontaneous oscillatory fluctuations in membrane potential or in membrane current. Their power spectra showed peaks at frequencies ranging from 2 to 7 Hz, which coincided well with the frequency of repetitive transient depolarization or transient inward current. The fluctuations were eliminated by intracellular injections of EGTA and decreased in amplitude by 5 mM caffeine with a shift toward higher frequencies. Depolarization of the membrane caused a shift of the spectrum peak toward higher frequencies. These results suggest that an oscillatory release of Ca from intracellular storage sites is the common basis underlying both the transient events (depolarization or inward current) and the spontaneous miniature fluctuations in membrane potential or current.

NaCl transport in mouse medullary thick ascending limbs. III. Modulation of the ADH effect by peritubular osmolality.

We evaluated the effects of increasing bath osmolality on both the passive permeability properties and the ADH-dependent rates of net Cl- absorption in isolated mouse medullary thick ascending limbs of Henle (mTALH). Increases in both osmolality to 900 mosmol/kg H2O with 600 mM urea had no effect on either the electrical (PNa/PCl ratio, 1.7 and 1.9 with and without peritubular urea, respectively) or tracer (PNa, 0.21 and 0.22 micrometers . s-1 with and without peritubular urea, respectively) ionic permeability characteristics of the mTALH. However, this degree of urea bath hypertonicity reduced reversibly both JnetNaCl, the net rate of transepithelial NaCl absorption, and Ve, the spontaneous transepithelial voltage: JnetNaCl fell by 85% and Ve by 70%. Both of these latter effects could be accounted for quantitatively by an 85% reduction in tau NaCl, the rate of conservative transcellular NaCl transport. The inhibition of Ve by peritubular medium urea hypertonicity was not altered by supramaximal bath concentrations of ADH, supramaximal bath concentrations of cAMP analogues, or symmetrical addition of urea to perfusate and bath. Increases in peritubular medium mannitol concentrations also reduced Ve; the inhibition of Ve was not reversed by supramaximal bath concentrations of aDH. Cell volume remained unchanged with peritubular urea but was reduced by peritubular mannitol. These data indicate that in the mTALH increases in bath osmolality with nonelectrolytes inhibit tau NaCl noncompetitively with respect to ADH or cAMP and independently of cell volume. JnetCl was also reduced with increases in peritubular medium NaCl concentration and was associated with a reduction in cell volume.

Suppression of noise in a photoreceptor by oxidative metabolism

1. Intracellular recordings were made, using glass micropipettes, from retinula cells in a superfused, isolated locust compound eye. Spontaneous voltage noise, generated across the photoreceptors' membranes, increases when a cell's metabolism is suppressed by anoxia or by superfusion with saline containing 1 mM azide. 2. The increase in the voltage noise develops from a noisy afterpotential, which follows each response to light flashes delivered during treatment with azide. The noise may reach a peak-to-peak amplitude of 2 mV in severely affected cells. 3. Upon removal of azide, or re-oxygenation, the increased noise level and the depolarization are abolished within 15 min. 4. The noise is shown to arise from the summation of depolarizing shot events of amplitude 40 μV. 5. It is proposed that the voltage noise results from the residual random activation of sodium channels that were open during the response to light.

Transport of water and solutes across sheep visceral pleura.

The fluid and solute transport properties of pleural tissue were studied using specimens of intact visceral pleura from adult sheep lungs. After thoracotomy, a shallow incision through the pleural surface permitted 10-cm2 by 10-micrometer pieces of visceral pleura free of lung parenchyma to be peeled off the lung surface. The pleura was then mounted as a planar sheet separating 2 reservoirs of Krebs-Ringer solution. Electrical potential and resistance, hydraulic water permeability, and diffusional permeability to water and several hydrophilic solutes were measured. The results showed that (1) no spontaneous voltage difference was present across the pleura; (2) electrical resistance (27.1 omega/cm2) was very low; (3) hydraulic water permeability was extremely high (1.64 X 10(-8) ml/dyne-s); and (4) diffusional permeability was high, varying from 5.24 X 10(-4) cm/s for water to 4 X 10(-5) cm/s for hemoglobin. Blue dextran (molecular weight, 2 X 10(6) daltons) did not cross the pleura in measurable quantities. We concluded that the isolated visceral pleura of the adult sheep is an extremely "leaky" tissue that probably does not actively transport salt and water. These findings are consistent with a passive model of pleural fluid formation and reabsorption, and suggest that the transport properties of normal pleural tissue are unlikely to be responsible for any differences in composition between interstitial and pleural fluids.

An anomalous electrical property of CoSiF6.6H2O near its transition temperature

The electrical resistance of the CoSiF6.6H2O crystal along its three axes and of the powdered material has been measured in the vicinity of the transition temperature. The resistance of the crystal passes through a peak at 246K, the transition temperature in the cooling cycle, during heating the resistance jumps to a much lower value at about 265K. At and above 265K in the heating cycle the DC (i- nu ) characteristics show non-linear variation. A spontaneous voltage of approximately 0.6 V, of opposite polarity to the applied voltage, is developed across the crystal after a current of a few milliamperes is passed through the crystal via Aquadag electrodes and the applied voltage withdrawn. The value of the spontaneous voltage depends on the electrode material and the temperature. The non-linearity in the (i- nu ) characteristics is absent when AC measurements are made. The powdered sample does not show any anomaly in its resistance.