Transepithelial electrical potential of nonsensory region of gerbil utricle in vitro

1986 ◽  
Vol 251 (5) ◽  
pp. C662-C670 ◽  
Author(s):  
D. C. Marcus
Keyword(s):  
Electrical Potential ◽  
Potential Difference ◽  
Disulfonic Acid ◽  
Sensory Cells ◽  
Bathing Solution ◽  
Electrical Potential Difference ◽  
Bathing Medium ◽  
Direct Demonstration ◽  
Voltage Change

Transepithelial electrical potential difference (VT) was measured across the vestibular labyrinth of the inner ear in vitro by puncturing the epithelial wall of the utricle with a glass microelectrode. A region of nonsensory cells of the utricle was isolated from the sensory regions by introducing columns of liquid Sylgard 184. Under control conditions, the VT of this region was +7.5 +/- 0.3 mV (means +/- SE), lumen positive. This potential difference was rapidly reduced by either 1 mM ouabain, 10-100 microM bumetanide, 0.5-5.0 mM Ba (in the bathing solution), or cooling, but not by the disulfonic stilbene, 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid. Changes in VT due to reductions of Cl or Na or to increases of K in the bathing solution in exchange for presumably impermeant ions were observed in this region and were compared with those in a preparation in which the insulating seals were absent. The K-induced voltage change was significantly higher in the unblocked preparation, a finding consistent with a high K permeability of the sensory cells. The voltage change due to reduction of Cl was not inhibited by Cl channel blockers (9-anthracenecarboxylate and diphenylamine-2-carboxylate) in the bathing solution. These results represent the first direct demonstration that the nonsensory cells of the utricle produce a lumen-positive active-transport potential and characterize some of the properties of the cell membranes in terms of their pharmacological sensitivities and net voltage responses to changes in the bathing medium ions Na, K, and Cl.

Stimulation of HCO3- transport in isolated proximal bullfrog duodenum by prostaglandins

1980 ◽  
Vol 239 (3) ◽  
pp. G198-G203 ◽  
Author(s):  
G. Flemstrom
Keyword(s):  
Electrical Potential ◽  
Potential Difference ◽  
Electrical Potential Difference ◽  
Morphological Examination ◽  
Minimal Concentration ◽  
Dependent Transport ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Stimulation Of

An in vitro preparation of proximal duodenum from the bullfrog transported alkali into the luminal solution (approximately 1 mueq x h-1 x cm-2) and generated a transepithelial electrical potential difference (5-10 mV, lumen negative). Transport was inhibited by 2,4-dinitrophenol (10(-5) M), CN- (5 X 10(-3) M), indomethacin (5 X 10(-5) M), and acetazolamide (5 X 10(-3) M) indicating that metabolism is required. Both alkali transport and the electrical potential difference showed a dose-dependent increase on administration of the prostaglandins E2, 16,16-dimethyl E2, and F2 alpha. The minimal concentration stimulating transport was lower with the E-type prostaglandins (10(-8) M than with F2 alpha (10(-6) M), and the former also produced greater maximal responses. In addition to metabolic-dependent transport of alkali, there was passive transmucosal migration of HCO3-, amounting to approximately 40% of basal (unstimulated) transport and sensitive to variation of the transmucosal hydrostatic pressure. Morphological examination showed that the preparation is devoid of Brunner glands. Stimulation of duodenal epithelial HCO3- transport by prostaglandins may contribute to their previously demonstrated ability to prevent duodenal ulceration.

Water and electrolyte transport by rabbit esophagus

1975 ◽  
Vol 229 (2) ◽  
pp. 438-443 ◽  
Author(s):  
DW Powell ◽  
SM Morris ◽  
DD Boyd
Keyword(s):  
Sodium Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Electrolyte Transport ◽  
Potential Difference ◽  
Sodium Absorption ◽  
Bathing Solution ◽  
Electrical Potential Difference

The nature of the transmural electrical potential difference and the characteristics of water and electrolyte transport by rabbit esophagus were determined with in vivo and in vitro studies. The potential difference of the perfused esophagus in vivo was -28 +/- 3 mV (lumen negative). In vitro the potential difference was -17.9 +/- 0.6 mV, the short-circuit current 12.9 +/- 0.6 muA/cm2, and the resistance 1,466 +/- 43 ohm-cm2. Net mucosal-to-serosal sodium transport from Ringer solution in the short-circuited esophagus in vitro accounted for 77% of the simultaneously measured short-circuit current and net serosal-to-mucosal chloride transport for 14%. Studies with bicarbonate-free, chloride-free, and bicarbonate-chloride-free solutions suggested that the net serosal-to mucosal transport of these two anions accounts for the short-circuit current not due to sodium absorption. The potential difference and short-circuit current were saturating functions of bathing solution sodium concentration and were inhibited by serosal ouabain and by amiloride. Thus active mucosal-to-serosal sodium transport is the major determinant of the potential difference and short-circuit current in this epithelium.

Active Transport of Sulphate Ions by the Malpighian Tubules of Larvae of the Mosquito Aedes Campestris

1975 ◽  
Vol 62 (2) ◽  
pp. 367-378
Author(s):  
S. H. P. MADDRELL ◽  
J. E. PHILLIPS
Keyword(s):  
Active Transport ◽  
Concentration Gradient ◽  
Electrical Potential ◽  
Malpighian Tubules ◽  
Potential Difference ◽  
Electrical Potential Difference ◽  
Sulphate Content ◽  
Anal Papillae ◽  
Tracer Experiments

1. Larvae of Aedes campestris ingest and absorb into their haemolymph large quantities of the sulphate-rich water in which they live, yet they are able to maintain the sulphate content of the haemolymph well below that of the environment. 2. Tracer experiments showed that sulphate regulation was not achieved by deposition of precipitates in the tissues. 3. In vitro preparations of Malpighian tubules secrete sulphate ions actively against both a three times concentration gradient and an electrical potential difference of 20 mV. This transport is half saturated at about 10 mM. 4. The rate of sulphate secretion by the Malpighian tubules is sufficient to remove all of the sulphate ingested by larvae living in waters which contain less than 100 mM of this anion. At higher concentrations, sulphate ions are probably also excreted elsewhere, perhaps by the rectum or anal papillae.

Endometrial transport generates the maternal-fetal electrical potential difference in guinea pigs

1991 ◽  
Vol 261 (2) ◽  
pp. R466-R472 ◽  
Author(s):  
T. G. McNaughton ◽  
L. A. Power ◽  
R. D. Gilbert ◽  
G. G. Power
Keyword(s):  
Guinea Pigs ◽  
Short Circuit ◽  
Electrical Potential ◽  
Uterine Wall ◽  
Late Gestation ◽  
Potential Difference ◽  
Fetal Membranes ◽  
Electrical Potential Difference

These studies examined the transport characteristics of the uterine endometrium with respect to the origin and mechanism of generation of the maternal-fetal electrical potential difference (PD) in pregnant guinea pigs. Late-gestation animals were used in two experimental preparations. In vivo, a sealed uterine pouch that preserved blood flow to the endometrium was prepared by removal of the fetus, placenta, and fetal membranes from the uterus and replacement with Earle's solution, a balanced electrolyte solution. In vitro, sections of uterine wall comprised of myometrium and endometrium without fetal membranes were mounted in Ussing chambers. Transuterine PDs (fetal side negative) were indistinguishable in vivo and in vitro, averaging 29.6 +/- 4.5 and 32.6 +/- 6.1 (95% confidence interval) mV in the respective preparations. Both values are within the range of maternal-fetal PD measured in intact guinea pigs, indicating that the fetoplacental unit is not essential in generating an intrauterine PD. The maternal-fetal PD, therefore, is likely a passive result of the fetus and placenta being immersed in fluids at the intrauterine potential. In vitro, both PD and short-circuit current (Isc) were completely inhibited by ouabain (10(-3) M) at the serosal (maternal) side of the uterine wall but unaffected by the inhibitor from the luminal (fetal) side. Amiloride (10(-5) M) and valinomycin (10(-5) M) caused decreases in the PD when added to the luminal side, both in vivo and in vitro, and were both ineffective from the serosal side in vitro. Isc was reduced 83% from 315 +/- 24 to 53 +/- 6 (SE) microA/cm2 after luminal amiloride (5 x 10(-4) M), indicating that Na+ is the predominant ion actively transported.(ABSTRACT TRUNCATED AT 250 WORDS)

Ionic conductive properties of rabbit proximal straight tubule basolateral membrane

1990 ◽  
Vol 258 (4) ◽  
pp. F940-F950 ◽  
Author(s):  
P. A. Welling ◽  
R. G. O'Neil
Keyword(s):  
Basolateral Membrane ◽  
Electrical Potential ◽  
Disulfonic Acid ◽  
Electrical Potential Difference ◽  
Bicarbonate Buffer ◽  
Bathing Medium ◽  
Straight Tubule ◽  
Proximal Straight Tubule ◽  
K Concentration ◽  
Conductive Properties

The ionic conductive properties of the nonperfused rabbit proximal straight tubule (S2) basolateral membrane were assessed by microelectrode techniques. The response of the basolateral membrane electrical potential difference, Vbl, to rapid changes in the peritubular bath concentration of K, HCO3, Na, and Cl were monitored with microelectrodes. The control steady-state Vbl averaged -41 mV (cell negative). An increase in peritubular bathing medium K concentration from 5 to 40 mM resulted in an instantaneous and sustained depolarization of +14.6 mV (27% of delta EK). Addition of barium (2 mM) depolarized the Vbl by +15.8 mV and abolished the Vbl response to the high-K medium. In other studies, reduction of peritubular bicarbonate at constant pH from 25 to 2.5 mM instantaneously and transiently depolarized Vbl by +15.8 mV (26% of delta EHCO3). In these same tubules reduction of peritubular Na from 126 to 2.2 mM resulted in an instantaneous and paradoxical depolarization of Vbl of +21.5 mV. Both depolarization transients resulting from reduction of Na and HCO3 were simultaneously inhibited by the addition of 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS; 0.5 mM), consistent with the presence of a SITS-sensitive Na-HCO3-coupled conductive pathway. In the absence of the bicarbonate buffer, reduction of Na resulted in a small sustained hyperpolarization of -5.8 mV (5% of delta ENa). Reduction of peritubular Cl from 120 to 4 mM resulted in an instantaneous and sustained depolarization of Vbl of +5.3 mV (6% of ECl) and was not affected by the addition of bumetanide (0.1 mM). It is concluded that the basolateral membrane of the nonperfused proximal straight tubule is characterized by a major barium-sensitive K conductance and a SITS-sensitive Na-coupled HCO3 conductance that carries net negative charge. These pathways are paralleled by relatively minor, but important, Na-conductive and Cl-conductive pathways.

Effect of acetylcholine on Cl- and Na+ fluxes across dog tracheal epithelium in vitro

1976 ◽  
Vol 231 (5) ◽  
pp. 1546-1549 ◽  
Author(s):  
MG Marin ◽  
B Davis ◽  
JA Nadel
Keyword(s):  
Short Circuit ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Atropine Sulfate ◽  
Open Circuit ◽  
Ion Flux ◽  
Potential Difference ◽  
Tracheal Epithelium ◽  
Electrical Potential Difference

Electrical potential difference is generated across canine tracheal epithelium by active transport of Cl- toward and Na+ away from the lumen. The present study examines the effects of acetylcholine on short-circuit current, potential difference, resistance, and fluxes of 36Cl and 24Na measured across pieces of canine tracheal epithelium mounted in Ussing-type chambers. Under short-circuit conditions, acetylcholine (5 X 10(-5) M) increased significantly net ion flux toward the lumen of Cl- (n equals 7) from +1.7 +/- SE 0.5 TO +3.3 +/- SE 0.5 mueq/cm2 - h, and of Na+ (n equals 7) from -0.8 +/- SE 0.2 to +0.5 +/- SE 0.2 mueq/cm2 - h. Under open-circuit conditions, acetylcholine (5 X 10(-5) M) increased significantly the unidirectional flux of Cl- (n equals 6) toward the lumen from 4.7 +/- SE 1.3 to 5.9 +/- SE 1.4 mueq/cm2 - h, while the other measured fluxes did not change significantly, suggesting that net Cl- flux had increased toward the lumen. Atropine sulfate (10(-8) M) prevented the response to acetylcholine (5 X 10(-5) M). The increased ion flux due to acetylcholine may mediate water secretion into the airway lumen, and this secretion may have important effects on the physical properties of the liquid through which the respiratory cilia beat.

Role of calcium in monitor peptide-stimulated cholecystokinin release from perifused intestinal cells

1992 ◽  
Vol 262 (5) ◽  
pp. G791-G796 ◽  
Author(s):  
E. P. Bouras ◽  
M. A. Misukonis ◽  
R. A. Liddle
Keyword(s):  
Calcium Influx ◽  
Hormone Secretion ◽  
Electrical Potential ◽  
Potential Difference ◽  
Electrical Potential Difference ◽  
Dependent Manner ◽  
Cellular Mechanisms ◽  
Free Environment ◽  
Cck Release

Monitor peptide stimulates cholecystokinin (CCK) release from the intestine, but the cellular mechanisms responsible for this effect are uncertain. In the present study, the roles of membrane potential difference and calcium influx in monitor peptide-mediated CCK release were examined in a perifusion system containing isolated mucosal cells from the rat duodenum. This method represents an in vitro system in which CCK-releasing cells can be challenged with secretagogues or other maneuvers to study the dynamics of hormone secretion. High concentrations of KCl (50 mM), which reduce electrical potential difference across the cell membrane, caused the release of CCK. This effect was inhibited by the calcium channel blocker MnCl2. Monitor peptide stimulated CCK release in a dose-dependent manner at concentrations from 3 x 10(-12) to 3 x 10(-8) M. The requirement for extracellular calcium in secretagogue-stimulated release of CCK was investigated using ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA), a calcium chelator, and MnCl2. A calcium-free environment supplemented with 2 mM EGTA completely inhibited CCK secretion in response to stimulatory doses of monitor peptide. CCK secretion was restored when calcium was reintroduced into the system. Similarly, MnCl2 completely blocked monitor peptide-stimulated CCK release. These data indicate that membrane depolarization and monitor peptide stimulate the release of CCK through calcium-dependent mechanisms, suggesting that increases in intracellular calcium within CCK cells are likely to be important in CCK release.

OSMOTIC INHIBITION OF THE NATRIFERIC RESPONSE OF THE TOAD URINARY BLADDER TO VASOPRESSIN

1975 ◽  
Vol 67 (1) ◽  
pp. 119-125
Author(s):  
P. J. BENTLEY
Keyword(s):  
Urinary Bladder ◽  
Water Movement ◽  
Short Circuit ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Toad Bladder ◽  
Toad Urinary Bladder ◽  
Electrical Potential Difference ◽  
Osmotic Gradient

SUMMARY The electrical potential difference and short-circuit current (scc, reflecting active transmural sodium transport) across the toad urinary bladder in vitro was unaffected by the presence of hypo-osmotic solutions bathing the mucosal (urinary) surface, providing that the transmural flow of water was small. Vasopressin increased the scc across the toad bladder (the natriferic response), but this stimulation was considerably reduced in the presence of a hypo-osmotic solution on the mucosal side, conditions under which water transfer across the membrane was also increased. This inhibition of the natriferic response did not depend on the direction of the water movement, for if the osmotic gradient was the opposite way to that which normally occurs, the response to vasopressin was still reduced. The natriferic response to cyclic AMP was also inhibited in the presence of an osmotic gradient. Aldosterone increased the scc and Na+ transport across the toad bladder but this response was not changed when an osmotic gradient was present. The physiological implications of these observations and the possible mechanisms involved are discussed.

Sign in / Sign up

Export Citation Format

Share Document