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Am J Physiol. 1984 Jan;246(1 Pt 1):C167-71.
Differing effects of cGMP and cAMP on ion transport across flounder intestine.

Rao MC, Nash NT, Field M.

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.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6320655&dopt=Abstract




Biochim Biophys Acta. 1984 Jun 27;773(2):207-18.
KCl loss and cell shrinkage in the Ehrlich ascites tumor cell induced by hypotonic media, 2-deoxyglucose and propranolol.

Thornhill WB, Laris PC.

Ehrlich ascites tumor cells lose KCl and shrink after swelling in hypotonic media and in response to the addition of 2-deoxyglucose, propranolol, or the Ca2+ ionophore, A23187, plus Ca2+ in isotonic media. All of these treatments activate cell shrinkage via a pathway with the following characteristics: (1) the KCl loss responsible for cell shrinkage does not alter the membrane potential; (2) NO3(-) does not substitute for Cl-; (3) the net KCl movements are not inhibited by quinine or DIDS; and (4) early in this study furosemide was effective in inhibiting cell shrinkage but this sensitivity was subsequently lost. This evidence suggests that the KCl loss in these cells occurs via a cotransport mechanism. In addition, hypotonic media and the other agents used here stimulate a Cl(-) - Cl(-) exchange, a net loss of K+ and a net gain of Na+ which are not responsible for cell shrinkage. The Ehrlich cell also appears to have a Ca2+-activated, quinine-sensitive K+ conductive pathway but this pathway is not part of the mechanism by which these cells regulate their volume following swelling or shrink in isotonic media in response to 2-deoxyglucose or propranolol. Shrinkage by the loss of K+ through the Ca2+ stimulated pathway appears to be limited by Cl- conductive movements; for when NO3(-), an anion demonstrated here to have a higher conductive movement than Cl-, is substituted for Cl-, the cells will shrink when the Ca2+-stimulated K+ pathway is activated.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6428451&dopt=Abstract




Pflugers Arch. 1984 Dec;402(4):364-75.
Mechanism of NaCl secretion in rectal gland tubules of spiny dogfish (Squalus acanthias). II. Effects of inhibitors.

Greger R, Schlatter E.

Rectal gland tubule (RGT) segments of the spiny dogfish (Squalus acanthias) were perfused in vitro. The effects of inhibitors of known mode of action on transepithelial PD (PDte resistance (Rte), the PD across the basolateral membrane (PDbl), the fractional resistance of this membrane (FRbl), and intracellular activities of NA+, Cl-, K+ (apha cell) were examined. Furosemide (5 x 10(-4) mol x 1(-1)) reduced PDte from -12 +/- 0.7 to -2.3 +/- 0.2 mV (n = 63), hyperpolarized PDbl from -71 +/- 1.3 to -79 +/- 0.9 mV (n = 59), FRbl decreased from 0.2 +/- 0.03 to 0.13 +/- 0.01 (n = 21), alpha cell cl- fell from 38 +/- 4 to 11 +/- 2 mmol x 1(-1) (n = 21), alpha cell Na+ fell from 37 +/- 4 to 17 +/- 2 mmol x 1(-1) (n = 12) and alpha cell K+ was constant [113 +/- 14 vs. 117 +/- 15 mmol x 1(-1) (n = 6)]. Furosemide exerted its effects within some 20-40s. Its action was completely reversible. Analysis of the time courses revealed that the furosemide induced initial fall in alpha cell cl- was approximately twice as rapid when compared to that of alpha cell Na+. Ba2+ 0.5 mmol x 1(-1) (bath) reduced PDte from -7.1 +/- 1.2 to -4.1 +/- 0.6 mV (n = 24), increased Rte from 18 +/- 2 to 22 +/- 2.5, omega cm2 (n = 14). PDbl depolarized from -75 +/- 2 to -48 +/- 2 mV (n = 42), FRbl increased from 0.2 +/- 0.02 to 0.34 +/- 0.04 (n = 14) and alpha cell K+ increased from 143 +/-28 to 188 +/- mmol x 1(-1) (n = 4). Ouabain (50 x 10(-6) mol x 1(-1), bath) reduced PDte from -12 +/-2 to -3 +/- 0.5 mV (n = 9), Rte increased from 18 +/- 3 to 21 +/- 3 omega cm2 (n = 5). PDbl depolarized from -67 +/- 4 to -26 + 3 mV (n = 14), FRbl increased from 0.23 +/- 0.04 to 0.45 +/- 0.05 (n = 6), alpha cell K+ fell only slightly from 135 +/- 15 to 112 +/- 30 mmol x 1(-1) (n = 4), but alpha cell cl- increased from 35 +/- 12 to 111 +/- 37 mmol x 1(-1) (n = 3). These effects of ouabain were slow when compared to those exerted by furosemide or Ba2+. The ouabain effects on PDte and PDbl were completely prevented if furosemide was applied first.(ABSTRACT TRUNCATED AT 400 WORDS)

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