Secretagogue-dependent and -independent transport of zinc hydration forms in rat parietal cells
Prolonged exposure to gastric acid is a leading cause of gastroesophageal reflux disease (GERD) and esophagitis. With the ever increasing number of patients showing insensitivity to proton-pump-inhibitor (PPI) therapy with recurrence of symptoms over time, alternative treatment options remain an imp...
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| Veröffentlicht in: | Pflügers Archiv 2016-11, Vol.468 (11-12), p.1877-1883 |
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| creator | Ferstl, Florentina Sophie Kitay, Alice Miriam Trattnig, Rebecca Marion Alsaihati, Abrar Geibel, John Peter |
| description | Prolonged exposure to gastric acid is a leading cause of gastroesophageal reflux disease (GERD) and esophagitis. With the ever increasing number of patients showing insensitivity to proton-pump-inhibitor (PPI) therapy with recurrence of symptoms over time, alternative treatment options remain an important issue. Previous studies from our laboratory have shown that a zinc sulfate salt can inhibit HCl generation at the cellular level of the parietal cell. In this paper, we examine the difference between two hydration forms of ZnSO
4
(monohydrate H
2
O and heptahydrate 7H
2
O) in their entry characteristics into the parietal cell under several physiological conditions associated with acid secretion. Using the Zn sensitive fluorochrome Newport Green, we examined the rate of Zn entry in Δfluorescent units/second (ΔFU/second), at two different concentrations for both hydration states on both fasted and non-fasted animals. In a separate series of studies, we examined the effects of secretagogues on the entry rates and transport mechanisms. Exposure of the secretagogue carbachol transformed the resting parietal cell to an activated state and represents a stimulated condition through the neuronal pathway. The hormonal activation of the parietal cell was achieved by using histamine. Non-fasted conditions were considered to be a state between hormonal and neuronal activation. To demonstrate that ZnSO
4
enters the parietal cell through the NKCC1 co-transporter, the inhibitor bumetanide was applied during secretagogue-stimulated acid secretion. Both salts, monohydrate and heptahydrate ZnSO
4
, show a concentration-dependent cell entry under all conditions studied. During stimulated acid secretion, induced through either the neuronal or the hormonal pathway, heptahydrate ZnSO
4
enters the parietal cell significantly faster than monohydrate ZnSO
4
, whereas monohydrate ZnSO
4
exhibits faster entry during resting conditions in fasted animals. At 30 μM following stimulation with histamine, heptahydrate ZnSO
4
enters the cell faster than monohydrate ZnSO
4
(ΔFU/second 30 μM
ZnSO4*7H2O + histamine
= 1.782, ΔFU/second 30 μM
ZnSO4*H2O+histamine
= 1.038, respectively). Three hundred micromolar, heptahydrate ZnSO
4
shows a faster entry into the cells (ΔFU/second
ZnSO4*7H2O300μM + carbachol
= 4.02407) compared to monohydrate ZnSO
4
(ΔFU/second
ZnSO4*H2O300μM + carbachol
= 3.225) following exposure to carbachol. The mechanism of entry of both salts was found to be predominantl |
| doi_str_mv | 10.1007/s00424-016-1889-3 |
| format | Article |
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4
(monohydrate H
2
O and heptahydrate 7H
2
O) in their entry characteristics into the parietal cell under several physiological conditions associated with acid secretion. Using the Zn sensitive fluorochrome Newport Green, we examined the rate of Zn entry in Δfluorescent units/second (ΔFU/second), at two different concentrations for both hydration states on both fasted and non-fasted animals. In a separate series of studies, we examined the effects of secretagogues on the entry rates and transport mechanisms. Exposure of the secretagogue carbachol transformed the resting parietal cell to an activated state and represents a stimulated condition through the neuronal pathway. The hormonal activation of the parietal cell was achieved by using histamine. Non-fasted conditions were considered to be a state between hormonal and neuronal activation. To demonstrate that ZnSO
4
enters the parietal cell through the NKCC1 co-transporter, the inhibitor bumetanide was applied during secretagogue-stimulated acid secretion. Both salts, monohydrate and heptahydrate ZnSO
4
, show a concentration-dependent cell entry under all conditions studied. During stimulated acid secretion, induced through either the neuronal or the hormonal pathway, heptahydrate ZnSO
4
enters the parietal cell significantly faster than monohydrate ZnSO
4
, whereas monohydrate ZnSO
4
exhibits faster entry during resting conditions in fasted animals. At 30 μM following stimulation with histamine, heptahydrate ZnSO
4
enters the cell faster than monohydrate ZnSO
4
(ΔFU/second 30 μM
ZnSO4*7H2O + histamine
= 1.782, ΔFU/second 30 μM
ZnSO4*H2O+histamine
= 1.038, respectively). Three hundred micromolar, heptahydrate ZnSO
4
shows a faster entry into the cells (ΔFU/second
ZnSO4*7H2O300μM + carbachol
= 4.02407) compared to monohydrate ZnSO
4
(ΔFU/second
ZnSO4*H2O300μM + carbachol
= 3.225) following exposure to carbachol. The mechanism of entry of both salts was found to be predominantly via the basolateral NKCC1 transporter with the rate of zinc entry decreasing to minimal values (ΔFU/second = 0.275) after application of bumetanide during stimulated conditions.</description><identifier>ISSN: 0031-6768</identifier><identifier>EISSN: 1432-2013</identifier><identifier>DOI: 10.1007/s00424-016-1889-3</identifier><identifier>PMID: 27757581</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Animals ; Biological Transport ; Biomedical and Life Sciences ; Biomedicine ; Bumetanide - pharmacology ; Carbachol - pharmacology ; Cell Biology ; Gastric Acid - secretion ; Histamine - pharmacology ; Human Physiology ; Ion Channels ; Male ; Molecular Medicine ; Neurosciences ; Parietal Cells, Gastric - drug effects ; Parietal Cells, Gastric - metabolism ; Parietal Cells, Gastric - secretion ; Rats ; Rats, Sprague-Dawley ; Receptors ; Receptors and Transporters ; Solute Carrier Family 12, Member 2 - metabolism ; Zinc Sulfate - metabolism</subject><ispartof>Pflügers Archiv, 2016-11, Vol.468 (11-12), p.1877-1883</ispartof><rights>Springer-Verlag Berlin Heidelberg 2016</rights><rights>Pflugers Archiv - European Journal of Physiology is a copyright of Springer, 2016.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-f3518124e2f0fca330f3f98a5849356b40acb39e70f0da3fa7096521adccfae43</citedby><cites>FETCH-LOGICAL-c405t-f3518124e2f0fca330f3f98a5849356b40acb39e70f0da3fa7096521adccfae43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00424-016-1889-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00424-016-1889-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51298</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27757581$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ferstl, Florentina Sophie</creatorcontrib><creatorcontrib>Kitay, Alice Miriam</creatorcontrib><creatorcontrib>Trattnig, Rebecca Marion</creatorcontrib><creatorcontrib>Alsaihati, Abrar</creatorcontrib><creatorcontrib>Geibel, John Peter</creatorcontrib><title>Secretagogue-dependent and -independent transport of zinc hydration forms in rat parietal cells</title><title>Pflügers Archiv</title><addtitle>Pflugers Arch - Eur J Physiol</addtitle><addtitle>Pflugers Arch</addtitle><description>Prolonged exposure to gastric acid is a leading cause of gastroesophageal reflux disease (GERD) and esophagitis. With the ever increasing number of patients showing insensitivity to proton-pump-inhibitor (PPI) therapy with recurrence of symptoms over time, alternative treatment options remain an important issue. Previous studies from our laboratory have shown that a zinc sulfate salt can inhibit HCl generation at the cellular level of the parietal cell. In this paper, we examine the difference between two hydration forms of ZnSO
4
(monohydrate H
2
O and heptahydrate 7H
2
O) in their entry characteristics into the parietal cell under several physiological conditions associated with acid secretion. Using the Zn sensitive fluorochrome Newport Green, we examined the rate of Zn entry in Δfluorescent units/second (ΔFU/second), at two different concentrations for both hydration states on both fasted and non-fasted animals. In a separate series of studies, we examined the effects of secretagogues on the entry rates and transport mechanisms. Exposure of the secretagogue carbachol transformed the resting parietal cell to an activated state and represents a stimulated condition through the neuronal pathway. The hormonal activation of the parietal cell was achieved by using histamine. Non-fasted conditions were considered to be a state between hormonal and neuronal activation. To demonstrate that ZnSO
4
enters the parietal cell through the NKCC1 co-transporter, the inhibitor bumetanide was applied during secretagogue-stimulated acid secretion. Both salts, monohydrate and heptahydrate ZnSO
4
, show a concentration-dependent cell entry under all conditions studied. During stimulated acid secretion, induced through either the neuronal or the hormonal pathway, heptahydrate ZnSO
4
enters the parietal cell significantly faster than monohydrate ZnSO
4
, whereas monohydrate ZnSO
4
exhibits faster entry during resting conditions in fasted animals. At 30 μM following stimulation with histamine, heptahydrate ZnSO
4
enters the cell faster than monohydrate ZnSO
4
(ΔFU/second 30 μM
ZnSO4*7H2O + histamine
= 1.782, ΔFU/second 30 μM
ZnSO4*H2O+histamine
= 1.038, respectively). Three hundred micromolar, heptahydrate ZnSO
4
shows a faster entry into the cells (ΔFU/second
ZnSO4*7H2O300μM + carbachol
= 4.02407) compared to monohydrate ZnSO
4
(ΔFU/second
ZnSO4*H2O300μM + carbachol
= 3.225) following exposure to carbachol. The mechanism of entry of both salts was found to be predominantly via the basolateral NKCC1 transporter with the rate of zinc entry decreasing to minimal values (ΔFU/second = 0.275) after application of bumetanide during stimulated conditions.</description><subject>Animals</subject><subject>Biological Transport</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Bumetanide - pharmacology</subject><subject>Carbachol - pharmacology</subject><subject>Cell Biology</subject><subject>Gastric Acid - secretion</subject><subject>Histamine - pharmacology</subject><subject>Human Physiology</subject><subject>Ion Channels</subject><subject>Male</subject><subject>Molecular Medicine</subject><subject>Neurosciences</subject><subject>Parietal Cells, Gastric - drug effects</subject><subject>Parietal Cells, Gastric - metabolism</subject><subject>Parietal Cells, Gastric - secretion</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors</subject><subject>Receptors and Transporters</subject><subject>Solute Carrier Family 12, Member 2 - metabolism</subject><subject>Zinc Sulfate - metabolism</subject><issn>0031-6768</issn><issn>1432-2013</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkU1LBCEYgCWK2rZ-QJcQunSxXr9mnGNEXxB0qM7iOrpN7OqkM4f69blsXwRBJ1EfH5UHoQMKJxSgPs0AggkCtCJUqYbwDTShgjPCgPJNNAHglFR1pXbQbs7PAMCEYttoh9W1rKWiE6TvnU1uMPM4Hx1pXe9C68KATWgx6cL3wpBMyH1MA44ev3XB4qfXNpmhiwH7mJYZdwGXOe5N6opwga1bLPIe2vJmkd3-xzhFj5cXD-fX5Pbu6ub87JZYAXIgnkuqKBOOefDWcA6e-0YZqUTDZTUTYOyMN64GD63h3tTQVJJR01rrjRN8io7X3j7Fl9HlQS-7vHqBCS6OWVMlJdSqUvAPlEuhmorzgh79Qp_jmEL5SKGEbIQAKgtF15RNMefkvO5TtzTpVVPQq1B6HUqXUHoVSq_Mhx_mcbZ07deJzzIFYGsgl60wd-nH1X9a3wFZmp3E</recordid><startdate>20161101</startdate><enddate>20161101</enddate><creator>Ferstl, Florentina Sophie</creator><creator>Kitay, Alice Miriam</creator><creator>Trattnig, Rebecca Marion</creator><creator>Alsaihati, Abrar</creator><creator>Geibel, John Peter</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>20161101</creationdate><title>Secretagogue-dependent and -independent transport of zinc hydration forms in rat parietal cells</title><author>Ferstl, Florentina Sophie ; Kitay, Alice Miriam ; Trattnig, Rebecca Marion ; Alsaihati, Abrar ; Geibel, John Peter</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c405t-f3518124e2f0fca330f3f98a5849356b40acb39e70f0da3fa7096521adccfae43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Biological Transport</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Bumetanide - pharmacology</topic><topic>Carbachol - pharmacology</topic><topic>Cell Biology</topic><topic>Gastric Acid - secretion</topic><topic>Histamine - pharmacology</topic><topic>Human Physiology</topic><topic>Ion Channels</topic><topic>Male</topic><topic>Molecular Medicine</topic><topic>Neurosciences</topic><topic>Parietal Cells, Gastric - drug effects</topic><topic>Parietal Cells, Gastric - metabolism</topic><topic>Parietal Cells, Gastric - secretion</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors</topic><topic>Receptors and Transporters</topic><topic>Solute Carrier Family 12, Member 2 - metabolism</topic><topic>Zinc Sulfate - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ferstl, Florentina Sophie</creatorcontrib><creatorcontrib>Kitay, Alice Miriam</creatorcontrib><creatorcontrib>Trattnig, Rebecca Marion</creatorcontrib><creatorcontrib>Alsaihati, Abrar</creatorcontrib><creatorcontrib>Geibel, John Peter</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Biological Science Journals</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Pflügers Archiv</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ferstl, Florentina Sophie</au><au>Kitay, Alice Miriam</au><au>Trattnig, Rebecca Marion</au><au>Alsaihati, Abrar</au><au>Geibel, John Peter</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Secretagogue-dependent and -independent transport of zinc hydration forms in rat parietal cells</atitle><jtitle>Pflügers Archiv</jtitle><stitle>Pflugers Arch - Eur J Physiol</stitle><addtitle>Pflugers Arch</addtitle><date>2016-11-01</date><risdate>2016</risdate><volume>468</volume><issue>11-12</issue><spage>1877</spage><epage>1883</epage><pages>1877-1883</pages><issn>0031-6768</issn><eissn>1432-2013</eissn><abstract>Prolonged exposure to gastric acid is a leading cause of gastroesophageal reflux disease (GERD) and esophagitis. With the ever increasing number of patients showing insensitivity to proton-pump-inhibitor (PPI) therapy with recurrence of symptoms over time, alternative treatment options remain an important issue. Previous studies from our laboratory have shown that a zinc sulfate salt can inhibit HCl generation at the cellular level of the parietal cell. In this paper, we examine the difference between two hydration forms of ZnSO
4
(monohydrate H
2
O and heptahydrate 7H
2
O) in their entry characteristics into the parietal cell under several physiological conditions associated with acid secretion. Using the Zn sensitive fluorochrome Newport Green, we examined the rate of Zn entry in Δfluorescent units/second (ΔFU/second), at two different concentrations for both hydration states on both fasted and non-fasted animals. In a separate series of studies, we examined the effects of secretagogues on the entry rates and transport mechanisms. Exposure of the secretagogue carbachol transformed the resting parietal cell to an activated state and represents a stimulated condition through the neuronal pathway. The hormonal activation of the parietal cell was achieved by using histamine. Non-fasted conditions were considered to be a state between hormonal and neuronal activation. To demonstrate that ZnSO
4
enters the parietal cell through the NKCC1 co-transporter, the inhibitor bumetanide was applied during secretagogue-stimulated acid secretion. Both salts, monohydrate and heptahydrate ZnSO
4
, show a concentration-dependent cell entry under all conditions studied. During stimulated acid secretion, induced through either the neuronal or the hormonal pathway, heptahydrate ZnSO
4
enters the parietal cell significantly faster than monohydrate ZnSO
4
, whereas monohydrate ZnSO
4
exhibits faster entry during resting conditions in fasted animals. At 30 μM following stimulation with histamine, heptahydrate ZnSO
4
enters the cell faster than monohydrate ZnSO
4
(ΔFU/second 30 μM
ZnSO4*7H2O + histamine
= 1.782, ΔFU/second 30 μM
ZnSO4*H2O+histamine
= 1.038, respectively). Three hundred micromolar, heptahydrate ZnSO
4
shows a faster entry into the cells (ΔFU/second
ZnSO4*7H2O300μM + carbachol
= 4.02407) compared to monohydrate ZnSO
4
(ΔFU/second
ZnSO4*H2O300μM + carbachol
= 3.225) following exposure to carbachol. The mechanism of entry of both salts was found to be predominantly via the basolateral NKCC1 transporter with the rate of zinc entry decreasing to minimal values (ΔFU/second = 0.275) after application of bumetanide during stimulated conditions.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>27757581</pmid><doi>10.1007/s00424-016-1889-3</doi><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0031-6768 |
| ispartof | Pflügers Archiv, 2016-11, Vol.468 (11-12), p.1877-1883 |
| issn | 0031-6768 1432-2013 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1855078680 |
| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Animals Biological Transport Biomedical and Life Sciences Biomedicine Bumetanide - pharmacology Carbachol - pharmacology Cell Biology Gastric Acid - secretion Histamine - pharmacology Human Physiology Ion Channels Male Molecular Medicine Neurosciences Parietal Cells, Gastric - drug effects Parietal Cells, Gastric - metabolism Parietal Cells, Gastric - secretion Rats Rats, Sprague-Dawley Receptors Receptors and Transporters Solute Carrier Family 12, Member 2 - metabolism Zinc Sulfate - metabolism |
| title | Secretagogue-dependent and -independent transport of zinc hydration forms in rat parietal cells |
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