Evidence for a Na+/K+/Cl− cotransport system in basolateral membrane vesicles from the rabbit parotid

Rj, Turner; Jn, George; Baum, Buzz

doi:10.1007/bf01871194

Cited by 77 publications

(60 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Since physiological studies with salivary glands have indicated that 99mTcO-is handled in a manner analogous to radioiodide (7,8), we also attempted to study the effect ofreplacing C1-in HBSS-H with I-. Although we observed a significant inhibition of 99mTcO-uptake (75%) when C1-was replaced with I-in HBSS-H, we found that non- (16) and is quite similar to comparably characterized C1-co-transport mechanisms found in the shark rectal gland (17,18) and the rabbit thick ascending limb of Henle's loop (19). We show here that "mTcO uptake by rat parotid cell aggregates is very rapid, mimicking closely the time course of 36C1-uptake in the same preparation (15).…”

Section: Resultscontrasting

confidence: 74%

99mTc-pertechnetate uptake in parotid acinar cells by the Na+/K+/Cl- co-transport system.

Helman¹,

Turner²,

Fox³

et al. 1987

J. Clin. Invest.

View full text Add to dashboard Cite

""Tc-Pertechnetate ("'rcO) has widespread clinical use in the diagnosis and evaluation of dysfunctions in many different tissues. However, despite the broad clinical application of this radionuclide, very little is known about the mechanism by which ""TcOi enters a cell. We report evidence here that ""'TcO4shares the Na+/K+/Cl co-transport system localized to the basolateral membrane of rat parotid acinar cells. " TcO. uptake by these cells was quite rapid (t1/2 30 s), was completely inhibited by the loop diuretics furosemide and bumetanide, and was markedly dependent on the presence of Na', K+, and Oin the extracellular medium. Relative to uptake measured in the presence of physiological extracellular salt concentrations (Hanks' salts), "'TcOj uptake was inhibited 80% by sodium replacement and 50% by potassium replacement. When Cl-was replaced with the physiologically inert anion gluconate a threefold stimulation in ""'TcO uptake resulted. These observations provide strong evidence that "'TcO4 can substitute for G-as a substrate for the Na+/K+/Cl-co-transporter and indicate that "'TcO4 uptake by salivary glands (e.g., as seen with salivary scintiscans), and possibly by a variety of other tissues, reflects the functional activity of this co-transport mechanism.

show abstract

Section: Resultscontrasting

confidence: 74%

99mTc-pertechnetate uptake in parotid acinar cells by the Na+/K+/Cl- co-transport system.

Helman¹,

Turner²,

Fox³

et al. 1987

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…These effects of bumetanide are duplicated by the removal of medium chloride (Fig. 2), a maneuver which would also result in suppression of Na'-K+-2Cr-cotransport activity (6). Furthermore, when the acinar cells are alkalinizedby propionate removal rather than NH' addition, as in Fig.…”

Section: Resultsmentioning

confidence: 96%

“…Studies from a number of laboratories, including our own, indicate that a Na+-K+-2Cl-cotransporter is responsible for driving the bulk ofthe acinar chloride secretion associated with fluid production in salivary glands (3)(4)(5)(6)(7). This process is thought to conform to the following scheme (8,9).…”

Section: Introductionmentioning

confidence: 98%

Beta-adrenergic upregulation of the Na(+)-K(+)-2Cl- cotransporter in rat parotid acinar cells.

Paulais¹,

Turner²

1992

J. Clin. Invest.

View full text Add to dashboard Cite

We used the pH-sensitive fluorescent dye 2',7'-bis(2-carboxyethyl)-5(6')-carboxyfluorescein to monitor the recovery of the intracellular pH (pH,) of rat parotid acini from an NH+-induced alkaline load. This recovery was markedly inhibited by the loop diuretic bumetanide and by Cl-removal, indicating that it is largely due to NH' entry via the basolateral Na'-K+-2Cl-cotransporter. The rate of recovery of pHi was enhanced threefold by pretreatment (37.5 s) with isoproterenol (K112 = 21.5 nM) or norepinephrine (in the presence of phentolamine), and blocked by the #,-specific antagonist atenolol, indicating an upregulation of cotransport activity by ,81-adrenergic stimulation. The effect of isoproterenol was prevented by protein kinase inhibitors and mimicked by cAMP analogues, and by maneuvers known to increase cytosolic cAMP levels in these cells, consistent with the involvement ofprotein kinase A. Physiologically, such an upregulation of the acinar Na'-K+-2CI-cotransporter would lead to an increase in acinar chloride uptake across the basolateral membrane, and consequently, an increase in overall chloride and fluid secretion. Prevention of this upregulation by t-blockers and possibly by other commonly used clinical agents may account for the dry mouth and dry eyes experienced by some patients taking these medications. (J.

show abstract

“…The new pellet was saved as fraction 2, and the supernatant was centrifuged at 200,000g for 1 h to yield a pellet that was saved as fraction 3. ␥-Glutamyltranspeptidase was used as a marker for the APM (Paul et al, 1992) and K ϩ -stimulated p-nitrophenyl phosphatase was used as a marker for the basolateral plasma membrane (Turner et al, 1986) as described previously. The specific activity of ␥-glutamyltranspeptidase for fractions 1, 2, and 3 was 375 Ϯ 5.6, 18.3 Ϯ 0.9, and 28.5 Ϯ 2.7 nmol/ min/mg of protein, respectively.…”

Section: Methodsmentioning

confidence: 99%

The Muscarinic Acetylcholine Receptor-Stimulated Increase in Aquaporin-5 Levels in the Apical Plasma Membrane in Rat Parotid Acinar Cells Is Coupled with Activation of Nitric Oxide/cGMP Signal Transduction

2002

View full text Add to dashboard Cite

The present study investigated the role of nitric oxide (NO)/cGMP signal transduction in the M 3 muscarinic acetylcholine receptor (mAChR)-stimulated increase in aquaporin-5 (AQP5) levels in the apical plasma membrane (APM) of rat parotid glands. Pretreatment of rat parotid tissue with the NO scavenger 2-(4carboxyphe-nyl)-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide potassium inhibited both acetylcholine (ACh)-and pilocarpine-induced increases in AQP5 in the APM. NO donors [3-morpholinosydnonimine (SIN-1) and (S)-nitroso-N-acetylpenicillamine (SNAP)] mimicked the effects of mAChR agonists. A selective protein kinase G inhibitor [(9S,10R,12R)-2,3,9,10,11,12-hexahydro-10-methoxy-2,9-dimethyl-1-oxo-9,12-epoxy-1H-diindolo-[1,2,3-fg-3Ј,2Ј,1Ј-kl]pyrrolo [3,4-i] . These results suggest that NO/cGMP signal transduction has a crucial role in Ca 2ϩ homeostasis in the mAChR-stimulated increase in AQP5 levels in the APM of rat parotid glands.Several aquaporins (AQPs), which form water channels that selectively transport water across the plasma membrane, have been cloned from a variety of mammalian tissues (King and Agre, 1996). In the gastrointestinal tract, more than seven AQPs are known to be expressed: AQP1 in intrahepatic cholangiocytes; AQP4 in gastric parietal cells; AQP3 and AQP4 in colonic surface epithelium; AQP5 in salivary glands; AQP7 in small intestine; AQP8 in liver, pancreas, colon, and salivary glands; and AQP9 in liver (Ma and Verkman, 1999). AQP5 was cloned from the rat submandibular gland (Raina et al., 1995). The nucleotide sequence of AQP5 reveals 45 and 63% homology with AQP1 and AQP2, respectively (Raina et al., 1995). Salivary fluid secretion is defective in transgenic mice lacking AQP5, indicating that AQP5 is important in salivary gland function Krane et al., 2001). The sympathetic and parasympathetic nerves in rat parotid glands regulate the role of AQP5. Acetylcholine (ACh) and epinephrine acting at M 3 muscarinic acetylcholine receptors (mAChR) and ␣ 1 -adrenoceptors, respectively, inThis work was supported in part by a grant-in-aid for scientific research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan.ABBREVIATIONS: AQP, aquaporin; ACh, acetylcholine; mAChR, muscarinic acetylcholine receptor; APM, apical plasma membrane; SNI-2011, cevimeline hydrochloride; PLC, phospholipase C; IP 3, inositol 1,4,5-trisphosphate; DAG, 1,2-diacylglycerol; PKC, protein kinase C; CaM, calmodulin; MLCK, myosin light chain kinase; NOS, nitric-oxide synthase; GC, guanylate cyclase; NO, nitric oxide; PKG, protein kinase G; BAPTA-AM, 1,2-bis(2-aminophenoxy)ethane-N,N,NЈ,NЈ-tetraacetic acid-acetoxymethyl ester; Carboxy-PTIO, 2-(4carboxyphenyl)-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide potassium; IBMX, 3-isobutyl-1-methylxanthine; SIN-1, 3-morpholinosydnonimine; SNAP, (S)-nitroso-N-acetylpenicillamine; KN-62; (8)-5-isoquinolinesulfonic acid, 4-[2-(5-isoquinolinyl-sulfonyl)methylamino]-3-oxo-(4-phenyl-1-piperazinyl)-propyl]phenyl ester; ML9, (5-chloronaphthalene-1-sulfonyl...

show abstract

Evidence for a Na+/K+/Cl− cotransport system in basolateral membrane vesicles from the rabbit parotid

Cited by 77 publications

References 36 publications

99mTc-pertechnetate uptake in parotid acinar cells by the Na+/K+/Cl- co-transport system.

99mTc-pertechnetate uptake in parotid acinar cells by the Na+/K+/Cl- co-transport system.

Beta-adrenergic upregulation of the Na(+)-K(+)-2Cl- cotransporter in rat parotid acinar cells.

The Muscarinic Acetylcholine Receptor-Stimulated Increase in Aquaporin-5 Levels in the Apical Plasma Membrane in Rat Parotid Acinar Cells Is Coupled with Activation of Nitric Oxide/cGMP Signal Transduction

Contact Info

Product

Resources

About