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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 319 (1970), S. 185-199 
    ISSN: 1432-2013
    Keywords: Submaxillary Gland ; Bicarbonate Secretion ; Microperfusion ; Acetazolamide ; Carbachol ; Submaxillardrüse ; Bicarbonatsekretion ; Mikroperfusion ; Acetazolamid ; Carbachol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Bicarbonate transport in the rat submaxillary main duct has been studied by microperfusion. Bicarbonate was concentrated in the duct lumen against an electrochemical gradient and the equilibrium concentration was estimated to be 56.5 mEq/l±3.1 (S.E.M.,n=11). The secretory mechanism could not be inhibited by 6 mMolar cyanide although such concentrations caused marked inhibition of both net sodium efflux and net potassium influx. Bicarbonate secretion in the main duct was not inhibited by acetazolamide whether applied from the duct lumen or given intravenously. Similarly, the drug was without effect on bicarbonate excretion by the intact gland even when maximum excretory rates had been induced with carbachol. It was concluded that catalytic hydration of carbon dioxide to carbonic acid was not a rate-limiting step in the bicarbonate secretory process. The data did not permit a distinction to be made between a bicarbonate secretory processper se and a process of either H+ reabsorption or OH− secretion. The parasympathomimetic agent, carbachol, when given parenterally was found to increase sharply the net influx of bicarbonate into the microperfused main duct as well as to reduce net sodium efflux and net potassium influx. Previously it had been postulated that final saliva was formed in two stages. First a plasma-like primary secretion was formed at a rate depending on the degree of stimulation, and second, the primary secretion was modified in the gland duct system by reabsorptive and secretory processes whose transport rates were presumed to be independent of the degree of stimulus. It now becomes necessary to postulate that stimulation can act on electrolyte transport at both primary and secondary levels; at present, however, no data are available to show whether appreciable net water influx can ever occur at the secondary level.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2013
    Keywords: Parasympathicomimetic ; Sympathicomimetics ; Submaxillary Gland ; Potassium Secretion ; Bicarbonate Secretion ; Isoproterenol ; Carbachol ; Parasympathomimetica ; Sympathomimetica ; Glandula submaxillaris ; Kalium-Sekretion ; bicarbonat-Sekretion ; Isoproterenol ; Carbachol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Salivary glands are generally supposed to produce their secretions in 2 stages: 1. A plasma-like secretion is formed in the acinar-intercalated duct region of the gland, the rate of production but not the electrolyte composition of this fluid being increased by gland stimulation. 2. This primary saliva is then modified during its passage along the gland duct system by processes of Na reabsorption and K and HCO3 secretion. In general terms this hypothesis accounts for the behaviour of salivary glands undergoing parasympathetic or parasympathomimetic stimulation. However, when sympathetic or sympathomimetic stimulation occurs the electrolyte excretory patterns are anomalous and the 2-stage hypothesis cannot easily account for them. Thus, after sympathomimetic stimulation the rat submaxillary saliva was found to be nearly isotonic with [K]=150 mEq/l and [HCO3]=135 mEq/l, the concentrations being independent of flow rate. To elucidate this problem the Na, K and HCO3 excretory curves in rat submaxillary saliva have been studied in animals undergoing parasympathomimetic, sympathomimetic and combined sympatho- and parasympathomimetic stimulation and these have been compared with the electrolyte concentrations of primary saliva obtained at rest and after stimulation. The results suggest: 1. That both types of drug stimulate formation of an approximately plasma-like primary secretion whose composition changes only slightly with stimulation. Parasympathomimetics, however, cause production of 6–8 times more primary fluid per unit time than sympathomimetics. 2. That contrary to all previous opinion, the drugs have a direct action at the ductal level where they stimulate secretion of K and HCO3. At this site the effects of the two types of drug are approximately equal which explains why sympathetic saliva is so rich in K and HCO3. The ductal action of parasympathomimetics may also explain why ductal secretion of both K and HCO3 do not undergo saturation as gland stimulation is progressively increased.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-2013
    Keywords: Carbachol ; Parasympathomimetic Drug ; Sodium Conductance ; Submaxillary Gland ; Microperfusion ; Electrolyte Transport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of carbachol on transepithelial potential difference and transepithelial nett electrolyte transport has been studied in the rabbit submaxillary main duct perfusedin vivo andin vitro with bicarbonate saline. The two preparations function similarly, reabsorbing Na, Cl and water and secreting K. In control ducts nett Na reabsorption was 683±55 nmol · cm−2 · min−1 and K secretion was 31.2±2.4 nmol · cm−2 · min−1. Nett water reabsorption was 970±71 nl · cm−2 · min−1 and the hydraulic conductivity was (14.0±1.6)×10−6 ml · cm−2 · s−1 · atm−1. The mean transepithelial potential difference was 13.1±0.8 mV (lumen negative) and, assuming no active transport of Cl, the partial conductance of the duct to Cl was (12.7±2.6)×10−2 mho · cm−2. Carbachol,in vivo andin vitro, caused partial depolarization of the transepithelial potential difference and reduction of nett Na and Cl reabsorption. It was without effect on duct K and HCO3 transport.In vitro, the drug was effective in concentrations as low as 10−7 M and perhaps lower. Atropine was able completely to block the effects of carbachol present at twice the atropine concentration. The results are consistent with the hypothesis that carbachol acts in some way to reduce the sodium conductance of the luminal face of the duct epithelial cell, this response being secondary to an undefined primary action of carbachol on the interstitial face of the cell.
    Type of Medium: Electronic Resource
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