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Biomedical subjects

M Field

Publications and source records attributed to M Field.

At least 73 records · Page 4Linked to original sources
PubMed1985

Phorbol ester inhibition of Na-H exchange in rabbit proximal colon.

In rabbit proximal colon, in vitro addition of phorbol 12,13-dibutyrate (PDB, 10(-7) M) to the serosal bathing medium inhibits mucosal (m)-to-serosal (s) unidirectional Na flux (JsmNa) without altering JsmNa or unidirectional Cl fluxes. Similar results were obtained when amiloride (2 X 10(-4) M) was added to the mucosal bathing medium. No additivity of effect was seen when tissues were exposed to both agents. Measurements with carboxyfluorescein reveal that the two agents cause equal decreases of intracellular pH (pHi), an effect that is dependent on the presence of extracellular Na (Na replacement also decreases pHi). No additivity of pHi effects is seen when both agents are added together. To determine the membrane site of this PDB-inhibitable Na-H exchange, Na influx across the luminal border of proximal colon was measured and was found to be inhibited equally by PDB and amiloride. We conclude that PDB, by activation of protein kinase C, inhibits electro-neutral amiloride-sensitive Na-H exchange in the luminal membrane of proximal colon.

Animals↗
PubMed1985

Atrial natriuretic factor inhibits Na-K-Cl cotransport in teleost intestine.

Addition of atrial natriuretic factor (ANF) to the contraluminal side of the intestinal mucosa of a marine teleost, the winter flounder Pseudopleuronectes americanus, inhibits short-circuit current, net transepithelial fluxes of Na and Cl, and the unidirectional influx of Rb across the brush border membrane. This action of ANF is closely mimicked by addition of 8-bromo-guanosine 3',5'-cyclic monophosphate (8-BrcGMP). In contrast to the intestine, the opercular epithelium of the flounder did not respond to the in vitro addition of either ANF or 8-BrcGMP. Because intestinal salt and water absorption diminishes when marine fish enter water of lower salinity, ANF may be an important hormonal regulator through which euryhaline fish adapt to varying salinities.

Animals↗
PubMed1985

Diarrhea in streptozocin-treated rats. Loss of adrenergic regulation of intestinal fluid and electrolyte transport.

Diarrhea was noted in rats with streptozocin-induced chronic diabetes. We have investigated the possibility that this diarrhea is a consequence of altered neuronal control of water and electrolyte absorption in the intestinal epithelium. In particular, we examined noradrenergic control because alpha-2-adrenergic agonists are known to stimulate intestinal fluid absorption. When compared with nondiabetic littermates, chronically diabetic rats exhibited significant impairment of fluid absorption by the ileum and colon, but not the jejunum. This impairment of intestinal fluid absorption was not found in either insulin-treated or untreated acutely diabetic (7 d) animals. Mucosal histology appeared normal in all of the above groups. Mucosal norepinephrine stores in the jejunum and ileum of chronically diabetic rats were estimated in vitro by the short-circuit current (Isc) response to tyramine, an agent that effectively releases stored norepinephrine. Pargyline was added to inhibit enzymatic destruction of the added tyramine. In chronically diabetic rats, the Isc response to tyramine was significantly decreased in ileum, but not in jejunum. However, when these responses were expressed as a fraction of the maximal Isc tissue response to exogenously added epinephrine, significant decreases were noted in both ileum and jejunum. In tissues from acutely diabetic rats, Isc responses to tyramine and epinephrine were no different from controls. When sympathetic denervation was produced in nondiabetic rats by treatment with 6-OH-dopamine, the pattern of impaired fluid absorption that developed was the same as that observed in chronically diabetic rats. We conclude that impaired intestinal mucosal absorption of fluid and electrolytes slowly develops in rats made diabetic with streptozocin and that this absorptive impairment is due to a loss of normally present noradrenergic innervation of enterocytes.

Animals↗
PubMed1985

Treatment of diabetic diarrhea with clonidine.

Stimulation of alpha 2-adrenergic receptors on enterocytes promotes fluid and electrolyte absorption and inhibits anion secretion. Loss of adrenergic innervation may play a role in impaired intestinal fluid and electrolyte absorption in diabetic patients with autonomic neuropathy. Clonidine, an alpha 2-adrenergic agonist, was used to treat three patients with "idiopathic" diabetic diarrhea after other treatments had failed: The volume of diarrhea declined significantly (p less than 0.01). Diarrhea recurred when the drug was withdrawn, but the patient's condition improved again when clonidine treatment was reintroduced. Hypotension did not occur as a side effect presumably because of the autonomic neuropathy of these patients.

Chronic Disease↗
PubMed1985

MRL mice show an age-related impairment of IgG aggregate removal from the circulation.

The fate of heat-aggregated human IgG (HAGG) was examined in young and old autoimmune MRL-lpr/lpr and MRL-+/+ mice and compared to BALB/c mice of different ages. Following iv injection of [125I] HAGG the older MRL-lpr/lpr and MRL-+/+ mice showed impaired hepatic and splenic uptake of this material. In addition the clearance rate of HAGG was significantly slower in the older MRL-lpr/lpr mice (t1/2 = 50 min) when compared to younger controls (t1/2 = 13 min) although this age-related retardation of clearance was not observed in the MRL-+/+ mice. No difference was seen in the clearance rate or organ uptake studies of the two age groups of BALB/c mice. Catabolic studies using trichloracetic acid suggested that the HAGG was catabolized to smaller fragments with time but not to such a great extent in the older diseased animals, again no age-related difference was seen in the BALB/c mice. Our studies suggest that with age both autoimmune strains of MRL mice show some saturation of the mononuclear phagocytic system (MPS) and that this process is more obvious in the MRL-lpr/lpr mice. MPS saturation may play a role in the pathogenesis of autoimmune disease in these mice.

Aging↗
PubMed1984

Cl- transport in apical plasma membrane vesicles isolated from bovine tracheal epithelium.

The Cl- transport properties of the luminal border of bovine tracheal epithelium have been investigated using a highly purified preparation of apical plasma membrane vesicles. Transport of Cl- into an intravesicular space was demonstrated by (1) a linear inverse correlation between Cl- uptake and medium osmolarity and (2) complete release of accumulated Cl- by treatment with detergent. The rate of Cl- uptake was highly temperature-sensitive and was enhanced by exchange diffusion, providing evidence for a carrier-mediated transport mechanism. Transport of Cl- was not affected by the 'loop' diuretic bumetanide or by the stilbene-derivative anion-exchange inhibitors SITS (4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid) and DIDS (4,4'-diisothiocyanostilbene-2,2'-disulfonic acid). In the presence of the impermeant cation, tetramethylammonium (TMA+), uptake of Cl- was minimal; transport was stimulated equally by the substitution of either K+ or Na+ for TMA+. Valinomycin in the presence of K+ enhanced further Cl- uptake, while amiloride reduced Na+-stimulated Cl- uptake towards the minimal level observed with TMA+. These results suggest the following conclusions: (1) the tracheal vesicle membrane has a finite permeability to both Na+ and K+; (2) the membrane permeability to the medium counterion determines the rate of Cl- uptake; (3) Cl- transport is not specifically coupled with either Na+ or K+; and, finally (4) Cl- crosses the tracheal luminal membrane via an electrogenic transport mechanism.

Amiloride↗
PubMed1984

Chloride and sodium transport across bovine tracheal epithelium: effects of secretagogues and indomethacin.

The regulation of ion transport in bovine tracheal epithelium was studied in vitro. In the absence of exogenous modifiers of ion transport, average values for transepithelial electrical potential difference (psi t), short-circuit-current (Isc) and tissue resistance (Rt) were 35.4 mV (lumen negative), 5.4 muEq X h-1 X cm-2 and 187 omega X cm2 respectively; net Cl secretion (3.2 muEq X h-1 X cm-2) and net Na absorption (1.3 muEq X h-1 X cm2) accounted for 82% of the Isc. Amiloride reduced psi t and Isc, and increased Rt. The values of psi t, Rt and Isc obtained following addition of theophylline, epinephrine or prostaglandin E1 (PGE1) were not different from control values. Theophylline also did not alter Na and Cl fluxes but it increased tissue cAMP content 3-fold. Indomethacin did not affect psi t but it increased Rt and net Na absorption, and decreased Isc and net Cl secretion; it did not significantly reduce tissue cAMP. When added to indomethacin-treated tissues, epinephrine restored Isc, Rt and Na and Cl fluxes to control levels and increased tissue cAMP 3-fold. Similarly, when PGE1 was added to indomethacin-treated tissues, Isc and Rt were restored to control levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Alprostadil↗
PubMed1984

Mechanism of Cl secretion in canine trachea: changes in intracellular chloride activity with secretion.

Cl-sensitive microelectrodes were employed to investigate the mechanism of Cl secretion by canine tracheal epithelium. In control tissues with a mean calculated short-circuit current (Isc) of 18.1 microA/cm2, the intracellular Cl activity (aiCl) was 47.2 mM. This value is 30.1 mM (or 27.0 mV) above the electrochemical equilibrium for Cl across the apical membrane. Epinephrine, which stimulates Cl secretion, increased the calculated Isc to 160 microA/cm2 and decreased aiCl to 32.2 mM, a value only 11.2 mM (or 10.9 mV) above equilibrium for the apical membrane. These results indicate a secretagogue induced decrease in the impedance to Cl exist from the cell via the apical membrane. From these and prior measurements we calculate that epinephrine-induced Cl efflux from the cell can occur by simple diffusion across the apical membrane. Further implications of these calculations are also discussed.

Animals↗
PubMed1984

Regulation of epithelial electrolyte transport by metabolites of arachidonic acid.

Intestine (both small and large) secretes chloride in response to prostaglandins and agents, such as bradykinin, that increase prostaglandin synthesis. The colon, but not the small intestine, can also be stimulated to secrete chloride by certain lipoxygenase products, such as 5-hydroperoxy-eicosatetraenoic acid and 5-hydroxy-eicosatetraenoic acid, but not by leukotrienes. Intestine generates these compounds and leukotriene B4 (but not C, D, and E) and their synthesis is increased by melittin, calcium ionophore A23187, and bradykinin.

Animals↗
PubMed1984

Differing effects of cGMP and cAMP on ion transport across flounder intestine.

The intestinal epithelium of the winter flounder is highly cation selective and actively absorbs NaCl via a bumetanide-sensitive (Na + K + 2Cl) cotransport system; it also actively secretes K+. Combined addition of adenosine 3',5'-cyclic monophosphate (cAMP) and theophylline was previously shown to partially inhibit NaCl absorption and to increase passive Cl- permeability. Because theophylline increases cyclic GMP (cGMP) and cAMP concentrations, we compared the effects of the 8-Bromo analogues of these two nucleotides on ion transport. cGMP inhibits Cl- absorption, K+ secretion, and Cl- and K+ influx across the brush border as effectively as do furosemide and bumetanide. Even at maximal doses, cAMP is less effective than cGMP in inhibiting ion transport; however, unlike cGMP, it abolishes the cation selectivity of the epithelium by greatly increasing Cl- permeability. The effects of the two nucleotides are not additive with each other or with those of bumetanide, although cGMP or bumetanide can further inhibit transport in cAMP-treated tissues.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1984

Potassium transport by flounder intestinal mucosa.

We studied the mechanisms of K transport across an epithelium in which NaCl absorption is mediated primarily by Na/K/Cl cotransport at the apical membrane. Rubidium served as a reliable K substitute; under control conditions, both K and Rb were actively secreted. During secretion, K (Rb) enters across the basolateral membrane via the Na/K pump and exits across the apical membrane through K conductance pathways, since serosal ouabain or mucosal barium abolished K secretion, mucosal furosemide or Cl-free media blocked K secretion by interfering with access of Na to the pump, and elevated mucosal solution [K] or [Rb] depolarized the apical membrane electrical potential difference. Mucosal Ba unmasked active Rb absorption that could be blocked by mucosal furosemide. These findings illustrate active K absorption and secretion across an epithelium that comprises a single cell type in which opposing K fluxes across the apical membrane are mediated by Na/K/Cl cotransport entry and conductive K exit. The direction of transepithelial K transport is determined by the relative activities of these pathways.

Animals↗
PubMed1984

Placentophagy.

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Female↗
PubMed1984

An antiabsorptive basis for precipitated withdrawal diarrhea in morphine-dependent rats.

Diarrhea is a common manifestation of withdrawal from opiates in dependent subjects. This study examined the possibility that this diarrhea results in part from alterations in intestinal fluid transport. Isolated loops of jejunum, ileum and colon were created in morphine-dependent and nondependent rats implanted s.c. with morphine or lactose pellets, respectively. The administration of naltrexone (1 mg/kg s.c.) or its quaternary analog methylnaltrexone (0.01-3 mg/kg i.v.), which does not readily cross the blood-brain barrier, produced a dose-related reduction in fluid absorption from the jejunum and colon of dependent animals only. Similar effects were observed after the i.c.v. injection of quaternary naltrexone (1.0-10 microgram/rat). Both narcotic antagonists, given by any route, produced no change in ileal absorption. Pretreatment with hexamethonium (10 mg/kg i.v.) or atropine (4 mg/kg i.v.) attenuated the antiabsorptive effects of quaternary naltrexone on the jejunum. Serosal addition of naltrexone (10 microM) had no effect on Na or Cl fluxes, short-circuit current or tissue conductance across isolated segments of intestinal mucosa from dependent and nondependent rats. These results indicate that precipitated opiate withdrawal is associated with decreases in jejunal and colonic fluid absorption mediated at sites within both the central nervous system and periphery. Moreover, these effects are not a consequence of a direct opiate action on enterocytes.

Animals↗
PubMed1983

Isolation of transporting plasma membrane vesicles from bovine tracheal epithelium.

A method is described for isolating plasma membrane vesicles from bovine tracheal epithelium. The procedure yields highly purified apical membranes which are enriched 19-fold in the marker enzyme, alkaline phosphatase. Contamination of this fraction by other organelles is minimal. Basolateral membranes isolated from the same preparation have a 4-fold enrichment of (Na+ + K+)-ATPase and a 2-fold reduction in alkaline phosphatase specific activity compared to the starting material. Assays of Na+ uptake by the apical membrane vesicles demonstrate their suitability for transport studies. Transport of Na+ into an intravesicular space was demonstrated by (1) a linear inverse correlation between Na+ uptake and medium osmolarity; (2) complete release of accumulated Na+ by treatment with detergent; and (3) a marked temperature-dependence of Na+ uptake rate. Other features of Na+ transport were (1) inhibition by amiloride; (2) insensitivity to furosemide; and (3) anion-dependence of uptake rate with the following selectivity:SCN- greater than Cl- greater than gluconate-.

Alkaline Phosphatase↗