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Biomedical subjects

J Bijman

Publications and source records attributed to J Bijman.

51 records · Page 3Linked to original sources
PubMed1987

Permeability properties of cell membranes and tight junctions of normal and cystic fibrosis sweat ducts.

The transepithelial permeability properties to Na, K, and Cl in microperfused segments of human eccrine sweat ducts from normal (N) subjects and patients with cystic fibrosis (CF) were examined. Amiloride administered on the luminal surface caused the transepithelial potential (Vt) of normal ducts to depolarize to 0 mV, but in the absence of Cl in the medium or in CF ducts, amiloride caused the Vt to significantly reverse electrical polarity from lumen negative to lumen positive with respect to the serosal bath. The Vt responses to changes in Na concentration in the lumen and K concentration in the bath were similar in CF and N ducts and showed that the basolateral membrane of the duct is K permeable and the apical membrane (in the absence of an anion shunt) is an almost ideal Na electrode. The Vt of N ducts was insensitive to 10-fold changes in luminal K and contraluminal Na solution concentrations. These responses show that in normal ducts, the apical membrane and tight junctions are relatively impermeable to K, and the basal membrane and tight junctions are relatively impermeable to Na. The Vt was highly sensitive to Cl- changes on either surface before or after ouabain inhibition in N ducts, but in every case were insensitive to Cl- changes in CF ducts. By comparison to control ducts the cation selective properties of the CF duct are probably normal, but both cell membranes as well as the tight junctions of the CF duct are relatively impermeable to Cl. The present data are inconclusive as to whether the route of Cl movement across the N duct epithelium is trans- or paracellular.

Amiloride↗
PubMed1987

Characterization of human sweat duct chloride conductance by chloride channel blockers.

To characterize the chloride conductance of human sweat duct the effect of various analogues of diphenylamine-2-carboxylate was investigated on the transepithelial potential difference (PDT) and resistance (RT) of isolated microperfused sweat ducts. Although the most powerful analogues which block Cl- channels in various secretory and absorptive epithelia were ineffective, a number of analogues (in particular Cl substituted ones) were found which at high concentrations significantly and reversibly increased PDT and RT. The data suggest that the main chloride conductance pathway of sweat duct epithelium resides in the cell membranes rather than in the tight junctions. In addition the different blocking spectra of the chloride conductances of sweat duct and tracheal epithelium (Welsh MJ, Science 232:1648, 1986) suggest that the combined impairment of both conductances in cystic fibrosis does not result from a molecular defect in the Cl- channels.

Chlorides↗
PubMed1987

Lactate and bicarbonate uptake in the sweat duct of cystic fibrosis and normal subjects.

The sweat of single sweat glands of healthy individuals and cystic fibrosis patients was analyzed for differences in bicarbonate, lactate, and pH. These values were monitored as a function of sweat rate simultaneously with 1) the electrical potential difference at the duct orifice (with respect to the interstitial fluid) and 2) the concentrations of sodium, potassium, and chloride in surface sweat. Sweat in both groups contained about equal concentrations of lactate and bicarbonate at similar sweat rates. Similarly, the pH of sweat secreted at similar rates in the two populations was not significantly different. Acidification of sweat increased with decreasing sweat rate. In both populations, lactate and bicarbonate may be absorbed passively in the distal sweat duct in their nonionic form and, thus, not influenced by the increased electrical potential difference in the cystic fibrosis sweat duct. The uptake of these ions may involve active proton secretion by sweat duct cells.

Bicarbonates↗
PubMed1986

Direct demonstration of high transepithelial chloride-conductance in normal human sweat duct which is absent in cystic fibrosis.

The transepithelial electrical potential difference (Vt) and the transepithelial resistance (Rt) were measured across individual microdissected sweat ducts obtained from biopsies of the scapular region of normal human volunteers and of a Cystic Fibrosis (CF) patient. During luminal and contraluminal perfusion with NaCl Ringer solution Vt and Rt were -10.7 +/- 1.1 (mV, lumen negative) and 10.9 +/- 1.7 (omega X cm2). Bilateral substitution of Cl- by gluconate increased Vt and Rt to -42.7 +/- 5.1 (mV) and 98.0 +/- 12.0 (omega X cm2), respectively. Luminal application of amiloride (10(-4) mol/l) collapsed Vt and increased Rt to 11.4 +/- 1.7 and 159.7 +/- 12.0 omega X cm2 in Cl- and gluconate Ringer respectively. These data indicate that 90% of the total transepithelial conductance is attributed to Cl- and 5% to Na+ while the remaining 5% is unaccounted for at present. In CF ducts Vt and Rt were high already in Cl- Ringer solution (-78.9 +/- 9.9 mV and 91.2 +/- 15.6 omega X cm2) and did not change significantly after replacement of Cl- by gluconate. The data demonstrate that normal human sweat duct epithelium, despite its ability to generate high electric and osmotic gradients, is a low resistance epithelium, probably because of a high Cl(-)-permeability of its cell membranes. In addition, the data demonstrate that this Cl(-)-conductance is missing in CF, in conformation of what has been postulated previously from simple potential measurements.

Adult↗
PubMed1984

Influence of calcium and cyclic nucleotides on beta-adrenergic sweat secretion in equine sweat glands.

The effects of Ca2+, the cyclic nucleotides adenosine 3',5'-cyclic monophosphate (cAMP) and guanosine 3',5'-cyclic monophosphate (cGMP), and other parameters of sweat secretion from single equine sweat glands were examined in vitro. Extracellular Ca2+, the Ca2+ ionophore A23187, and the Ca2+ channel antagonist verapamil were all without effect on sweat secretion. Prolonged rinsing of the glands in Ca2+-free Ringer solution with 5 mM ethylenediaminetetraacetic acid decreased the secretion to 30% of the control sweat rate in response to the beta-adrenergic agonist isoproterenol; the sweat response was restored upon adding Ca2+ to the Ringer. cAMP but not cGMP analogues were as effective in stimulating sweat rates as isoproterenol, which elicited maximal secretory rates in vitro. cAMP stimulation was not inhibited by the beta-adrenergic antagonist propranolol. Because the equine sweat gland is predominantly stimulated via the beta-adrenergic receptor, we conclude that cAMP is a principal intracellular messenger in coupling this type of stimulus to the fluid secretion response in this tissue.

Animals↗
PubMed1984

Influence of abnormal Cl- impermeability on sweating in cystic fibrosis.

Parameters of electrolyte transport in single sweat glands in normal subjects and cystic fibrosis (CF) patients were monitored and compared. Results indicate that in both normal and CF sweat ducts, Na+ is reabsorbed by an active process in which Cl- follows passively while K+ is secreted. However, while net NaCl reabsorption is markedly lower, the electrical potential associated with sweat emerging from the sweat duct is significantly more negative in CF than in normal subjects. Comparison of the differences in apparent electrochemical potential experienced by ions in the sweat duct during secretion indicates that Na+ is held out of the lumen of both groups of ducts against a large but similar gradient, but that Cl- is held in the CF duct against a much larger gradient than in the normal duct. These results indicate that the mechanism for Na+ reabsorption is not inhibited in the CF duct, but that the decreased NaCl transport in the defective duct is due to an abnormally low permeability to Cl-. Analysis of the electrical potential as a function of the Cl- gradient in the sweat suggests that the normal and defective route of Cl- uptake may be transcellular.

Adolescent↗
PubMed1984

Predominantly beta-adrenergic control of equine sweating.

Single equine sweat glands were found to secrete for more than 1 h in vitro in response to pharmacologic secretagogues. The adrenergic agonists epinephrine and norepinephrine evoked maximal sweat rates of 2.0 nl X gland-1 X min-1. However, the concentration of norepinephrine (10(-5) M) required to evoke the maximal response was 10 times higher than that for epinephrine. Maximal sweat rates also were stimulated with the beta 2-adrenergic agonist terbutaline. This stimulation was blocked by the beta-adrenergic antagonist propranolol. Moderate sweating responses were also obtained with the alpha-adrenergic agonists phenylephrine and methoxamine, but these responses also were blocked by propranolol. Neither the muscarinic blocker atropine nor the alpha-adrenergic antagonist phentolamine inhibited any of the pharmacologically induced sweat responses. Unlike most other mammalian exocrine glands, cholinergic agonists were ineffective in stimulating sweat secretion. Therefore equine sweat glands apparently are under predominantly beta-adrenergic control.

Animals↗
PubMed1984

Apparent absence of cystic fibrosis sweat factor on ion-selective and transport properties of the perfused human sweat duct.

Several previous studies have reported that a substance in exocrine products from cystic fibrosis (CF) patients is inhibitory to the transport of NaCl in several biological preparations. We have recently developed techniques for studying a target CF tissue, the eccrine sweat duct, and determined that salt absorption in the CF sweat duct appears to be decreased due to an impermeability to Cl. To determine whether this property might be induced, we have examined the sweat from patients with CF for potential influences on the ion-reabsorptive and ion-selective properties of sweat ducts from normal subjects. Isolated segments of sweat ducts from healthy volunteers were microperfused in vitro with concentration-adjusted sweat collected after thermal stimulation from CF patients and from normal subjects. The eccrine sweat duct may be best considered as a tight epithelium through which the mucosal uptake of NaCl proceeds via separate Na+ and Cl- pathways. As such, inhibitory actions of CF fluids should be exerted via an inhibition on one, or both, pathways, and should be expected to inhibit the electrolyte transport activity and alter the ion-selective properties of normal ductal tissue. We were unable to detect any effect of CF sweat on either property of the normal duct.

Adult↗
PubMed1983

Higher bioelectric potentials due to decreased chloride absorption in the sweat glands of patients with cystic fibrosis.

Patients with cystic fibrosis have characteristic disturbances in the electrolyte composition of their sweat, saliva, and pancreatic secretions. We studied the electrical properties of sweat glands in eight patients with cystic fibrosis and in seven normal volunteers to determine the basis of the well-documented inhibition of sodium absorption in this disease. The average electrical potential across 47 sweat glands in the patients was -66.3 +/- 2.1 mV, as compared with -29.8 +/- 3.2 mV for 39 glands in the normal controls (P less than 0.001). The average sweat-secretion rate in 33 glands from six patients was not significantly different from that in 34 glands from six controls, but average concentrations of sodium, chloride, and potassium were significantly higher in sweat droplets from the patients. Calculated rates of both sodium and chloride reabsorption were lower in sweat glands of patients than of normal controls, but chloride reabsorption was more markedly reduced than sodium reabsorption. We conclude that a decrease in epithelial permeability to chloride may explain the characteristic changes in sweat electrolytes in cystic fibrosis and could be a generalized abnormality in the disease.

Absorption↗
PubMed1983

Effect of amiloride on electrolyte transport parameters of the main duct of the rabbit mandibular salivary gland.

We have studied the response of the rabbit mandibular main duct perfused in vitro to luminally administered amiloride. The half-maximal inhibitory concentrations (KI) when the duct was bathed in Cl solutions were: for net Na+ transport, 3 X 10(-6) mol l-1; for transepithelial potential difference, 6 X 10(-6) mol l-1; and for transepithelial conductance, 3 X 10(-7) mol l-1. Substitution of the impermeant SO2-(4) anion for Cl- changed the KI for conductance to 3 X 10(-6) mol l-1. Within Cl- -containing media, the time course of the amiloride effect on potential difference showed an early rapid fall of 10 mV with a half-time 2 s, followed by a slower depolarization of 9 mV, and the conductance change followed the slower component of the potential change. In SO2-(4)-containing media, the potential difference and conductance changes followed time courses similar to one another. Finally, experiments on the effect of serosal applications of ouabain revealed that, although, in general, ouabain reduced resistance, it caused an increase in resistance in those ducts where the initial resistance was low. We conclude that: i) luminal Na+ transport occurs via amiloride-sensitive, conductive Na+ channels; ii) the Cl- conductance is the major determinant of transepithelial conductance; iii) the first phase of the potential response is due to blocking of the Na+ conductive channels, whilst the slow phase reflects secondary inhibition of an electrogenic Na+ pump; and iv) duct resistance changes are secondary to alterations in intracellular Cl- concentration.

Amiloride↗
PubMed1978

Electrical resistance of rabbit submaxillary main duct: a tight epithelium with leaky cell membranes.

The electrical resistance of rabbit salivary main duct epithelium has been measured. A small axial electrode, which passed current and measured potential simultaneously, was placed inside the ductal lumen. A cylindrical spiral was wound around the main duct and served as outside current electrode. The instantaneous current voltage relations were linearly up to current densities of 1.5 mA/cm2, independently of the Cl concentration in the bathing solutions. Strong polarization effects were observed in low Cl solutions. There was a significant inverse correlation between the spontaneous potential difference across the epithelium and the epithelial resistance in solutions with either high or low Cl concentrations. In high Cl solutions the epithelial resistance was 12.2 + 1.8 (n = 7) omegacm2. The resistance increased when the mucosal Na and Cl concentrations decreased. After addition of ouabain the resistance always decreased. The temperature dependence of the resistance was determined, and apparent activation energies were calculated. Values for activation energies ranged from 3.2 to 6.5 kcal/mol, depending on the ionic composition of the bathing solutions. Addition of amiloride to the mucosal solution led to an increase in resistance by a factor of 2.1 in high Cl solutions and of 4.1 in low Cl solutions. When ouabain was applied before amiloride, there was no effect on the resistance in high Cl solutions and a smaller increase in the resistance in low Cl solutions. The results of this study support the conclusion that the low resistance of main duct epithelium resides in the cell membranes and is not due to a paracellular pathway.

Amiloride↗