Adrenergic agents stimulate and cholinergic agents inhibit H+ secretion by amphibian jejunum

1986 ◽  
Vol 251 (3) ◽  
pp. G405-G412
Author(s):  
J. F. White ◽  
R. Britanisky
Keyword(s):  
Acid Secretion ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Atpase Inhibitor ◽  
Adrenergic Agents ◽  
Cholinergic Agents ◽  
Ph Stat ◽  
Opposing Effects ◽  
Dose Dependent Increase

In vitro segments of Amphiuma jejunum secrete H+ spontaneously. This study explored the effect of cholinergic and adrenergic agents on H+ secretion. Segments of mucosa were short-circuited and exposed on their mucosal surface to HCO3- -buffered medium while the pH of the unbuffered serosal medium was held by the pH-stat technique. Methacholine added to the serosal medium nearly abolished the spontaneous short-circuit current (Isc) and serosal alkalinization (JHCO3-) with an EC50 of 3.7 X 10(-7) M. Subsequent addition of norepinephrine (NE) to the serosal medium caused a dose-dependent increase in Isc and JHCO3. For three catecholamines the order of potency was epinephrine greater than NE greater than isoproterenol. The spontaneous Isc was significantly reduced (P less than 0.05) by the gastric H+-K+-ATPase inhibitor omeprazole, while the NE-induced Isc was unaltered by the inhibitor. Replacement of medium Na+ with choline abolished the response to NE. The NE-induced Isc was also reduced by methacholine. Acetazolamide inhibited the spontaneous and NE-induced Isc and JHCO3. In summary, cholinergic and adrenergic agents have opposing effects on intestinal H+-HCO3- transport. Jejunal acid secretion may be controlled in part by these antagonistic influences. Adrenergically activated acid secretion occurs by a different mechanism than spontaneous acid secretion.

Sodium dependence of luminal alkalinization by rabbit ileal mucosa

1985 ◽  
Vol 249 (3) ◽  
pp. G358-G368 ◽  
Author(s):  
P. L. Smith ◽  
M. A. Cascairo ◽  
S. K. Sullivan
Keyword(s):  
Prostaglandin E1 ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Bathing Solution ◽  
Ileal Mucosa ◽  
Adrenergic Agents ◽  
Ussing Chambers ◽  
Sodium Removal ◽  
Ph Stat

Stripped rabbit ileal mucosa was studied in vitro in Ussing chambers under short-circuit conditions using the pH-stat technique to determine basal rates of luminal alkalinization; the contribution of the shunt pathway to the alkalinization process; the effects of Na, Cl, or HCO3 removal from the bathing solutions on luminal alkalinization; and the effects of epinephrine, ouabain, 4,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS), acetazolamide, prostaglandin E1 (PGE1), A23187, sugars, or amino acids on the alkalinization process. Results from these studies reveal that, under basal conditions, the rate of luminal alkalinization accounts for 81% of the basal short-circuit current (Isc), although there was no correlation between the rate of alkalinization and Isc. The contribution of the shunt to the alkalinization process accounts for less than 10% of the mucosal-to-serosal HCO3 flux. Removal of Cl from the bathing solutions increased the rate of luminal alkalinization and decreased Isc. Sodium removal from the bathing solutions reduced both Isc and the rate of luminal alkalinization. Addition of DIDS to the luminal or serosal bathing solution reduced luminal alkalinization less than 30%. Acetazolamide, PGE1, and A23187 were all without effect on luminal alkalinization. Addition of 3-O-methyl-D-glucose or L-alanine to the luminal bathing solution did not alter luminal alkalinization but increased Isc, D-Glucose added to the luminal bathing solution reduced luminal alkalinization. This effect appears to result from metabolic acid production since 1) it is not seen with L-alanine or 3-O-methyl-D-glucose; 2) in the absence of HCO3 in the bathing solutions, D-glucose increased luminal acidification; and 3) luminal addition of fructose also reduced the rate of luminal alkalinization. Addition of epinephrine to the serosal bathing solution stimulates a Na-dependent serosal alkalinization process. These results suggest that luminal alkalinization results from Na-dependent, transcellular HCO3 transport and that a Na-dependent, HCO3 absorptive process is stimulated by adrenergic agents.

Sch-28080 inhibits bafilomycin-sensitive H+ secretion in turtle bladder independently of luminal [K+]

1993 ◽  
Vol 265 (2) ◽  
pp. F174-F179
Author(s):  
O. F. Kohn ◽  
P. P. Mitchell ◽  
P. R. Steinmetz
Keyword(s):  
Competitive Inhibition ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Atpase Inhibitor ◽  
Turtle Bladder ◽  
High K ◽  
Ph Stat ◽  
Low Levels ◽  
K Concentration ◽  
Removal Studies

To explore the possible contribution of an H-K-adenosine-triphosphatase (H-K-ATPase) to H+ secretion (JH) in the isolated turtle bladder, we measured electrogenic JH (JeH) as short-circuit current and total JH (JTH) by pH stat titration in the presence of ouabain at different ambient K+ concentration ([K+]) and during luminal addition of a known gastric H-K-ATPase inhibitor, Schering (Sch)-28080. JH was not reduced by decreasing ambient [K+] to undetectable or very low levels (< 0.05 mM by atomic absorption) and luminal BaCl2 addition to further reduce local [K+] at the apical membrane. These K(+)-removal studies indicate that H+ transport is not coupled to countertransport of K+. JTH did not exceed JeH at any point: in K(+)-free solutions JTH was 0.73 +/- 0.05, and JeH was 0.95 +/- 0.08 mumol/h; in standard (3.5 mM) K+ solutions JTH was 0.72 +/- 0.05 and JeH 0.98 +/- 0.06 mumol/h; in high (118 mM) K+ solutions JTH was 0.65 +/- 0.07 and JeH 0.94 +/- 0.08 mumol/h. Sch-28080 caused a rapid inhibition of JH, with similar half-maximal inhibitory concentrations (IC50) in K(+)-free, standard [K+], and high [K+] solutions. Bafilomycin inhibited JeH and JTH with an IC50 of approximately 100 nM. The observed non-potassium-competitive inhibition of JH by Sch-28080 and the bafilomycin sensitivity distinguish the H-ATPase of the turtle bladder from the gastric H-K-ATPase. The rapidity of the inhibition by Sch-28080 suggests that it acts at an accessible luminal site of the ATPase.

Action of 2-deoxy-D-glucose on frog gastric mucosa

1965 ◽  
Vol 209 (3) ◽  
pp. 461-466 ◽  
Author(s):  
George Sachs ◽  
R. Shoemaker ◽  
B. I. Hirschowitz
Keyword(s):  
Gastric Mucosa ◽  
Acid Secretion ◽  
Glucose Uptake ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Potential Difference ◽  
Atp Levels

2-Deoxyglucose (2-DG) has been found to inhibit chloride and acid secretion by the in vitro frog mucosa, with a fall in short-circuit current and potential difference and a rise in resistance. The ATP levels and phosphohexoisomerase activity were essentially unchanged following 2-DG treatment. 3-Methyl-O-glucose uptake was reduced by about 50% following preincubation with 2-DG. The O2 consumption was only slightly reduced with 10 mmoles 2-DG, but the CO2 ratio from glucose-6-C14/glucose-1-C14 fell from 0.98 to 0.37, indicating activation of the hexosemonophosphate (HMP) shunt.

Regulation of bicarbonate transport in rabbit ileum: pH stat studies

1989 ◽  
Vol 257 (4) ◽  
pp. G607-G615 ◽  
Author(s):  
J. H. Sellin ◽  
R. Desoignie
Keyword(s):  
Short Circuit ◽  
Exchange Process ◽  
Short Circuit Current ◽  
Ringer Solution ◽  
Bicarbonate Transport ◽  
Bicarbonate Secretion ◽  
Acid Base Balance ◽  
Rabbit Ileum ◽  
Ph Stat

Although it is well recognized that the ileum secretes bicarbonate, understanding of the mechanisms of the transport of this ion has been limited by the inability to measure fluxes in vitro. However, by clamping the bathing fluid at a set pH using a pH stat system, accurate measurements of bicarbonate movement can be made. Bicarbonate transport in rabbit ileum in vitro was measured by simultaneously employing both the pH stat and short-circuit techniques. The role of acid-base balance was assessed by systematically altering buffer bicarbonate concentration, pH, and partial pressure of CO2 (PCO2). Bicarbonate secretion was strongly correlated with both serosal [HCO3-] (r = 0.824, P less than 0.01) and serosal pH (r = 0.793, P less than 0.01). Bicarbonate absorption was not significantly altered by mucosal [HCO3-], pH, or PCO2. Paracellular movement of bicarbonate, as assessed by voltage clamping and diffusion potential experiments, did not appear to be a major component of transcellular transport. Epinephrine stimulated bicarbonate absorption significantly, both in Cl-containing and Cl-free Ringer solution but did not alter bicarbonate secretion. Epinephrine-induced decreases in short-circuit current were correlated with enhanced bicarbonate absorption. Bicarbonate secretion was inhibited by serosal chloride and serosal bumetanide; mucosal chloride stimulated bicarbonate secretion. Mucosal chloride did not affect bicarbonate absorption. Glucocorticoids enhanced both bicarbonate absorption and secretion. These results suggest that there are discrete apical and basolateral transport mechanisms that regulate bicarbonate transport. Bicarbonate secretion may be mediated by a basolateral bumetanide-sensitive, chloride-inhibitable transporter and by an apical chloride-bicarbonate exchange process.

Potassium secretion by rabbit descending colon: effects of adrenergic stimuli

1986 ◽  
Vol 250 (4) ◽  
pp. G432-G439 ◽  
Author(s):  
P. L. Smith ◽  
R. D. McCabe
Keyword(s):  
Short Circuit ◽  
Short Circuit Current ◽  
Maximal Effect ◽  
Dependent Manner ◽  
Adrenergic Stimulation ◽  
Adrenergic Agents ◽  
Ussing Chambers ◽  
K Secretion ◽  
Potassium Secretion

Stripped rabbit distal colonic mucosa was studied in vitro in Ussing chambers to investigate the effects of adrenergic stimuli on Na+, K+, and Cl- transport. The adrenergic stimuli epinephrine and norepinephrine decrease short-circuit current in a dose-dependent manner, with a half-maximal effect at 5 X 10(-7) M and a maximal effect between 10(-5) and 10(-4) M. The effects produced by norepinephrine and epinephrine can also be elicited by the beta 1-agonist dobutamine, but not by the beta 2-agonist terbutaline or the alpha-agonist phenylephrine. In addition, the effects of adrenergic stimulation can be inhibited by the beta-antagonist propranolol but not by the muscarinic antagonist atropine, the alpha 2-antagonist yohimbine, or tetrodotoxin. The decrease in short-circuit current elicited by adrenergic stimuli is accompanied by an increase in net K+ secretion with no change in net Cl- or Na+ transport. This increase in net K+ secretion elicited by beta-adrenergic stimulation can be inhibited by trifluoperazine but not by indomethacin. These studies suggest that K+ transport by the colon can be regulated by adrenergic agents acting via beta 1-receptors.

Relation between hydrogen ion secretion and oxygen uptake by gastric mucosa

1964 ◽  
Vol 206 (1) ◽  
pp. 218-222 ◽  
Author(s):  
J. G. Forte ◽  
R. E. Davies
Keyword(s):  
Gastric Mucosa ◽  
Acid Secretion ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Hydrogen Ion ◽  
Sodium Thiocyanate ◽  
Ph Stat ◽  
The Mean ◽  
Stat Method ◽  
Hydrogen Ion Transport

Bullfrog gastric mucosae were isolated, mounted between two glass chambers, and bathed with physiological salt solutions equilibrated with 5% CO2 and 95% O2. Oxygen consumption (qO2; measured polarographically) and acid secretion (qH+; pH stat method) were measured along with the transmucosal potential difference (p.d.) and current passing through the mucosa. Histamine (4 x 10–4 m) caused an increase in qH+ and qO2. In measurements on nine short-circuited mucosae the mean ratio for the ΔqH+/ΔqO2 was 2.1. Sodium thiocyanate (0.5–15 mm) caused a decrease in qH+ and qO2 and an increase in short-circuit current. These effects were reversible. The ratio of ΔqH+/ΔqO2 induced by thiocyanate varied from 5.0 to 12.0. Current (0.5 to 1.0 ma/cm2) passed through the mucosae, which reversed the normally observed p.d. to values between +70 and +240 mv (secretory side with respect to nutrient side in an external circuit), caused a decrease in qH+ and qO2; the average ΔqH+/ΔqO2 was approximately 13. Using either thiocyanate or electric current the ratio of the induced ΔqH+/ΔqO2 can really exceed 4.0, the electrochemical equivalent of oxygen, and thus if this extra oxygen provides the energy for the extra acid secretion these results invalidate a simple redox pump hypothesis of hydrogen ion transport by gastric mucosa.

Bicarbonate absorption by in vitro amphibian small intestine

1981 ◽  
Vol 241 (5) ◽  
pp. G389-G396 ◽  
Author(s):  
J. F. White ◽  
M. A. Imon
Keyword(s):  
Small Intestine ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Mucosal Surface ◽  
Electrical Potentials ◽  
The Media ◽  
Transepithelial Voltage ◽  
Ph Stat ◽  
Voltage Gradients

Isolated segments of jejunum from Amphiuma bathed in Cl--free (SO42(-)) media usually generated serosa-negative electrical potentials when HCO3(-) was present in the media. Bidirectional isotope fluxes under short circuit revealed a negligible absorption of Na+ and a residual flux consistent with anion absorption. Acetazolamide (10(-4) M) eliminated the short-circuit current and the residual flux. Segments of jejunum exposed on the mucosal surface to HCO3(-) (pH 7.4) alkalinized the unbuffered serosal fluid at a rate of about 1.1 mueq . h-1 . cm-2, as measured by the pH-stat while clamped at zero transepithelial potential. Acetazolamide, anoxia, and 2,4-dinitrophenol lowered the rate of alkalinization and simultaneously reduced the short-circuit current by an equal amount. Absorption was constant above a [HCO3(-)] of 35 meq/l and uninfluenced by applied transepithelial voltage gradients. HCO3(-) absorption was not reduced after replacement of media Na+ or Cl- but was reduced on addition of ouabain or removal of K+. It is concluded that the jejunum actively absorbs HCO3(-) by an electrogenic process that does not involve Na+-H+ exchange.

Bioelectric properties and ion transport of excised rabbit trachea

1983 ◽  
Vol 55 (6) ◽  
pp. 1884-1892 ◽  
Author(s):  
F. Jarnigan ◽  
J. D. Davis ◽  
P. A. Bromberg ◽  
J. T. Gatzy ◽  
R. C. Boucher
Keyword(s):  
Cell Function ◽  
Short Circuit ◽  
Species Difference ◽  
Short Circuit Current ◽  
Open Circuit ◽  
Adrenergic Agents ◽  
Beta Adrenergic Agonists ◽  
Submucosal Glands ◽  
Cl Conductance

Bioelectric properties and 22Na+ and 36Cl- isotopic flows across rabbit trachea, an airway epithelium without submucosal glands, were measured in vitro. One hundred twenty-two excised tracheas exhibited a mean transepithelial electric potential difference (PD) of 12 mV (lumen negative), a conductance (G) of 8.5 mS X cm-2, and a short-circuit current (Isc) of 90 microA X cm-2. G remained stable for more than 3 h, but Isc and PD fell slowly (10%/h). G was inversely correlated with PD, but Isc and G were not correlated. Na+ was absorbed under both open-circuit (1.7 mueq. cm-2 X h-1) and short-circuit (2.2 mueq X cm-2 X h-1) conditions. Net Na+ transport accounted for 70% of Isc of the short-circuited trachea. Net Cl- flow in the absorptive direction approximated that of Na+ under open-circuit conditions (1.6 mueq X cm-2 X h-1). Under short-circuit conditions the small net flow of Cl- in the direction of secretion (0.4 mueq X cm-2 X h-1) was not significant. Both unidirectional Cl- fluxes were correlated with G; [14C]-mannitol permeability and Na+ flows were weakly or not correlated with G. We found no evidence of net HCO-3 or proton transport. Acetylcholine (10(-4) M), phenylephrine (10(-5) M), or isoproterenol (10(-5) M) induced no change in bioelectric properties or ion flows. We conclude that the rabbit trachea is primarily a Na+ absorbing epithelium. The absence of a correlation between mannitol permeability and G suggests that much of the Cl- conductance is transcellular. Whereas insensitivity of rabbit trachea to cholinergic and alpha-adrenergic agents is compatible with the absence of glands, the lack of response to beta-adrenergic agonists denotes a species difference (compared with canine trachea) in airway-surface epithelial cell function.

Acid secretion, potential difference, and resistance of elasmobranch stomach

1962 ◽  
Vol 203 (6) ◽  
pp. 1091-1093 ◽  
Author(s):  
Warren S. Rehm
Keyword(s):  
Gastric Mucosa ◽  
Acid Secretion ◽  
Present Report ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Potential Difference ◽  
Secretory Rate ◽  
Negaprion Brevirostris ◽  
Ion Secretion

The present report is concerned with in vitro studies on gastric mucosa of the skate, Raja eglentaria, the electric ray, Narcine braziliensis, and the shark, Negaprion brevirostris. Maximum secretory rates of from 0.65 to 2.7 µEq hr–1 cm–2 were found. An increase in the secretory rate from an initial low level was associated with an increase in potential difference (PD), a decrease in resistance, and an increase in the calculated short-circuit current. The average PD and resistance before the increase in the secretory rate was 2.2 mv (nutrient positive) and 268 ohms cm2. After the increase they were 6.4 mv and 199 ohms cm2. Thiocyanate (10–2 m) to nutrient resulted in a decrease of secretory rate to zero and an increase in PD and resistance. The results can be explained on the basis of the separate mechanisms theory of H+ and Cl– ion secretion on the assumption that the resistance in the Cl– ion limb of the circuit is considerably lower than that in the H+ ion limb of the circuit.

Cholinergic-adrenergic interactions on intestinal ion transport.

1978 ◽  
Vol 235 (4) ◽  
pp. E402 ◽  
Author(s):  
E J Tapper ◽  
D W Powell ◽  
S M Morris
Keyword(s):  
Low Dose ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Potential Difference ◽  
Initial Increase ◽  
High Dose ◽  
Intestinal Epithelial ◽  
Rabbit Ileum ◽  
Adrenergic Agents

The autonomic control of intestinal electrolyte transport has been investigated in the in vitro, short-circuited rabbit ileum with varying doses of carbachol and with neuroeffector blocking agents. Low-dose carbachol (less than 10(-6) M) and high-dose carbachol (greater than 10(-4) M) had different effects on Na and Cl transport. Low-dose carbachol caused a transient increase in the potential difference and short-circult current, stimulated Cl secretion, and inhibited the residual flux (probably HCO3 secretion). This is a muscarinic response since it is inhibited by atropine (10(-6) M). After an initial increase of the potential difference and short-circuit current, high-dose carbachol reduced these electrical parameters, stimulated Na and Cl absorption, and abolished the residual flux. This is a nicotinic response since it is inhibited by hexamethonium (10(-5) M). This nicotinic response is identical to that reported by others with alpha-adrenergic agents and it was inhibited also by phentolamine (10(-7) M). We propose that high-dose carbachol stimulates nicotinic receptors on postganglionic sympathetic fibers present in our preparations causing a release of catecholamines and a resulting alpha-adrenergic response by the intestinal epithelial cell. The physiological significance of this response in the gut remains to be determined.

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