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NADH supplementation decreases pinacidil-primed I K ATP in ventricular cardiomyocytes by increasing intracellular ATP
1 The aim of this study was to investigate the effect of nicotinamide-adenine dinucleotide (NADH) supplementation on the metabolic condition of isolated guinea-pig ventricular cardiomyocytes. The pinacidil-primed ATP-dependent potassium current I(K(ATP)) was used as an indicator of subsarcolemmal AT...
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| Published in: | British journal of pharmacology 2003-06, Vol.139 (4), p.749-754 |
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| container_end_page | 754 |
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| container_title | British journal of pharmacology |
| container_volume | 139 |
| creator | Pelzmann, Brigitte Hallström, Seth Schaffer, Peter Lang, Petra Nadlinger, Karl Birkmayer, George D Vrecko, Karoline Reibnegger, Gilbert Koidl, Bernd |
| description | 1 The aim of this study was to investigate the effect of nicotinamide-adenine dinucleotide (NADH) supplementation on the metabolic condition of isolated guinea-pig ventricular cardiomyocytes. The pinacidil-primed ATP-dependent potassium current I(K(ATP)) was used as an indicator of subsarcolemmal ATP concentration and intracellular adenine nucleotide contents were measured. 2 Membrane currents were studied using the patch-clamp technique in the whole-cell recording mode at 36-37 degrees C. Adenine nucleotides were determined by HPLC. 3 Under physiological conditions (4.3 mM ATP in the pipette solution, ATP(i)) I(K(ATP)) did not contribute to basal electrical activity. 4 The ATP-dependent potassium (K((ATP))) channel opener pinacidil activated I(K(ATP)) dependent on [ATP](i) showing a significantly more pronounced activation at lower (1 mM) [ATP](i). 5 Supplementation of cardiomyocytes with 300 micro g ml(-1) NADH (4-6 h) resulted in a significantly reduced I(K(ATP)) activation by pinacidil compared to control cells. The current density was 13.8+/-3.78 (n=6) versus 28.9+/-3.38 pA pF(-1) (n=19; P |
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The pinacidil-primed ATP-dependent potassium current I(K(ATP)) was used as an indicator of subsarcolemmal ATP concentration and intracellular adenine nucleotide contents were measured. 2 Membrane currents were studied using the patch-clamp technique in the whole-cell recording mode at 36-37 degrees C. Adenine nucleotides were determined by HPLC. 3 Under physiological conditions (4.3 mM ATP in the pipette solution, ATP(i)) I(K(ATP)) did not contribute to basal electrical activity. 4 The ATP-dependent potassium (K((ATP))) channel opener pinacidil activated I(K(ATP)) dependent on [ATP](i) showing a significantly more pronounced activation at lower (1 mM) [ATP](i). 5 Supplementation of cardiomyocytes with 300 micro g ml(-1) NADH (4-6 h) resulted in a significantly reduced I(K(ATP)) activation by pinacidil compared to control cells. The current density was 13.8+/-3.78 (n=6) versus 28.9+/-3.38 pA pF(-1) (n=19; P<0.05). 6 Equimolar amounts of the related compounds nicotinamide and NAD(+) did not achieve a similar effect like NADH. 7 Measurement of adenine nucleotides by HPLC revealed a significant increase in intracellular ATP (NADH supplementation: 45.6+/-1.88 nmol mg(-1) protein versus control: 35.4+/-2.57 nmol mg(-1) protein, P<0.000005). 8 These data show that supplementation of guinea-pig ventricular cardiomyocytes with NADH results in a decreased activation of I(K(ATP)) by pinacidil compared to control myocytes, indicating a higher subsarcolemmal ATP concentration. 9 Analysis of intracellular adenine nucleotides by HPLC confirmed the significant increase in ATP.</description><identifier>ISSN: 0007-1188</identifier><identifier>PMID: 12812998</identifier><language>eng</language><publisher>England</publisher><subject>Action Potentials ; Adenosine Triphosphate - physiology ; Animals ; Dose-Response Relationship, Drug ; Glyburide - pharmacokinetics ; Guinea Pigs ; Heart Ventricles ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; NAD - pharmacokinetics ; NAD - physiology ; Patch-Clamp Techniques ; Pinacidil - administration & dosage ; Pinacidil - antagonists & inhibitors ; Pinacidil - pharmacokinetics ; Potassium Channels - drug effects ; Potassium Channels - physiology ; Sarcolemma - chemistry ; Sarcolemma - drug effects ; Sarcolemma - enzymology</subject><ispartof>British journal of pharmacology, 2003-06, Vol.139 (4), p.749-754</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12812998$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pelzmann, Brigitte</creatorcontrib><creatorcontrib>Hallström, Seth</creatorcontrib><creatorcontrib>Schaffer, Peter</creatorcontrib><creatorcontrib>Lang, Petra</creatorcontrib><creatorcontrib>Nadlinger, Karl</creatorcontrib><creatorcontrib>Birkmayer, George D</creatorcontrib><creatorcontrib>Vrecko, Karoline</creatorcontrib><creatorcontrib>Reibnegger, Gilbert</creatorcontrib><creatorcontrib>Koidl, Bernd</creatorcontrib><title>NADH supplementation decreases pinacidil-primed I K ATP in ventricular cardiomyocytes by increasing intracellular ATP</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>1 The aim of this study was to investigate the effect of nicotinamide-adenine dinucleotide (NADH) supplementation on the metabolic condition of isolated guinea-pig ventricular cardiomyocytes. The pinacidil-primed ATP-dependent potassium current I(K(ATP)) was used as an indicator of subsarcolemmal ATP concentration and intracellular adenine nucleotide contents were measured. 2 Membrane currents were studied using the patch-clamp technique in the whole-cell recording mode at 36-37 degrees C. Adenine nucleotides were determined by HPLC. 3 Under physiological conditions (4.3 mM ATP in the pipette solution, ATP(i)) I(K(ATP)) did not contribute to basal electrical activity. 4 The ATP-dependent potassium (K((ATP))) channel opener pinacidil activated I(K(ATP)) dependent on [ATP](i) showing a significantly more pronounced activation at lower (1 mM) [ATP](i). 5 Supplementation of cardiomyocytes with 300 micro g ml(-1) NADH (4-6 h) resulted in a significantly reduced I(K(ATP)) activation by pinacidil compared to control cells. The current density was 13.8+/-3.78 (n=6) versus 28.9+/-3.38 pA pF(-1) (n=19; P<0.05). 6 Equimolar amounts of the related compounds nicotinamide and NAD(+) did not achieve a similar effect like NADH. 7 Measurement of adenine nucleotides by HPLC revealed a significant increase in intracellular ATP (NADH supplementation: 45.6+/-1.88 nmol mg(-1) protein versus control: 35.4+/-2.57 nmol mg(-1) protein, P<0.000005). 8 These data show that supplementation of guinea-pig ventricular cardiomyocytes with NADH results in a decreased activation of I(K(ATP)) by pinacidil compared to control myocytes, indicating a higher subsarcolemmal ATP concentration. 9 Analysis of intracellular adenine nucleotides by HPLC confirmed the significant increase in ATP.</description><subject>Action Potentials</subject><subject>Adenosine Triphosphate - physiology</subject><subject>Animals</subject><subject>Dose-Response Relationship, Drug</subject><subject>Glyburide - pharmacokinetics</subject><subject>Guinea Pigs</subject><subject>Heart Ventricles</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>NAD - pharmacokinetics</subject><subject>NAD - physiology</subject><subject>Patch-Clamp Techniques</subject><subject>Pinacidil - administration & dosage</subject><subject>Pinacidil - antagonists & inhibitors</subject><subject>Pinacidil - pharmacokinetics</subject><subject>Potassium Channels - drug effects</subject><subject>Potassium Channels - physiology</subject><subject>Sarcolemma - chemistry</subject><subject>Sarcolemma - drug effects</subject><subject>Sarcolemma - enzymology</subject><issn>0007-1188</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><recordid>eNo1kDlPxDAUhF2A2GXhLyBXdJHs2I7tMlqOXbECivSRryCjXNgJUv493oNqXvHNaOZdgTVCiGcYC7ECtzF-I4Qp5-wGrHAucC6lWIP5vXzawTiPY-s6109q8kMPrTPBqegiHH2vjLe-zcbgO2fhHr7BsvqEvoe_iQ_ezK0K0Khg_dAtg1mmZNNLAk4Zvv9K5xSUcW17QpP7Dlw3qo3u_qIbUL08V9tddvh43W_LQzYyKjKsGKGmEEgQjLmlWmOkcGO41aTRVBbacskbiWguqWVMYKFErh0vBDXMabIBj-fYMQw_s4tT3fl47KF6N8yx5oRIQRhK4MMFnHUaWR-3qrDU_38if_GPZGk</recordid><startdate>200306</startdate><enddate>200306</enddate><creator>Pelzmann, Brigitte</creator><creator>Hallström, Seth</creator><creator>Schaffer, Peter</creator><creator>Lang, Petra</creator><creator>Nadlinger, Karl</creator><creator>Birkmayer, George D</creator><creator>Vrecko, Karoline</creator><creator>Reibnegger, Gilbert</creator><creator>Koidl, Bernd</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>200306</creationdate><title>NADH supplementation decreases pinacidil-primed I K ATP in ventricular cardiomyocytes by increasing intracellular ATP</title><author>Pelzmann, Brigitte ; Hallström, Seth ; Schaffer, Peter ; Lang, Petra ; Nadlinger, Karl ; Birkmayer, George D ; Vrecko, Karoline ; Reibnegger, Gilbert ; Koidl, Bernd</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p548-1a534c68083117d4bb10a1fc7db3fb496bd797f904294d55818a82be7684c5eb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Action Potentials</topic><topic>Adenosine Triphosphate - physiology</topic><topic>Animals</topic><topic>Dose-Response Relationship, Drug</topic><topic>Glyburide - pharmacokinetics</topic><topic>Guinea Pigs</topic><topic>Heart Ventricles</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>NAD - pharmacokinetics</topic><topic>NAD - physiology</topic><topic>Patch-Clamp Techniques</topic><topic>Pinacidil - administration & dosage</topic><topic>Pinacidil - antagonists & inhibitors</topic><topic>Pinacidil - pharmacokinetics</topic><topic>Potassium Channels - drug effects</topic><topic>Potassium Channels - physiology</topic><topic>Sarcolemma - chemistry</topic><topic>Sarcolemma - drug effects</topic><topic>Sarcolemma - enzymology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pelzmann, Brigitte</creatorcontrib><creatorcontrib>Hallström, Seth</creatorcontrib><creatorcontrib>Schaffer, Peter</creatorcontrib><creatorcontrib>Lang, Petra</creatorcontrib><creatorcontrib>Nadlinger, Karl</creatorcontrib><creatorcontrib>Birkmayer, George D</creatorcontrib><creatorcontrib>Vrecko, Karoline</creatorcontrib><creatorcontrib>Reibnegger, Gilbert</creatorcontrib><creatorcontrib>Koidl, Bernd</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pelzmann, Brigitte</au><au>Hallström, Seth</au><au>Schaffer, Peter</au><au>Lang, Petra</au><au>Nadlinger, Karl</au><au>Birkmayer, George D</au><au>Vrecko, Karoline</au><au>Reibnegger, Gilbert</au><au>Koidl, Bernd</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>NADH supplementation decreases pinacidil-primed I K ATP in ventricular cardiomyocytes by increasing intracellular ATP</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2003-06</date><risdate>2003</risdate><volume>139</volume><issue>4</issue><spage>749</spage><epage>754</epage><pages>749-754</pages><issn>0007-1188</issn><abstract>1 The aim of this study was to investigate the effect of nicotinamide-adenine dinucleotide (NADH) supplementation on the metabolic condition of isolated guinea-pig ventricular cardiomyocytes. The pinacidil-primed ATP-dependent potassium current I(K(ATP)) was used as an indicator of subsarcolemmal ATP concentration and intracellular adenine nucleotide contents were measured. 2 Membrane currents were studied using the patch-clamp technique in the whole-cell recording mode at 36-37 degrees C. Adenine nucleotides were determined by HPLC. 3 Under physiological conditions (4.3 mM ATP in the pipette solution, ATP(i)) I(K(ATP)) did not contribute to basal electrical activity. 4 The ATP-dependent potassium (K((ATP))) channel opener pinacidil activated I(K(ATP)) dependent on [ATP](i) showing a significantly more pronounced activation at lower (1 mM) [ATP](i). 5 Supplementation of cardiomyocytes with 300 micro g ml(-1) NADH (4-6 h) resulted in a significantly reduced I(K(ATP)) activation by pinacidil compared to control cells. The current density was 13.8+/-3.78 (n=6) versus 28.9+/-3.38 pA pF(-1) (n=19; P<0.05). 6 Equimolar amounts of the related compounds nicotinamide and NAD(+) did not achieve a similar effect like NADH. 7 Measurement of adenine nucleotides by HPLC revealed a significant increase in intracellular ATP (NADH supplementation: 45.6+/-1.88 nmol mg(-1) protein versus control: 35.4+/-2.57 nmol mg(-1) protein, P<0.000005). 8 These data show that supplementation of guinea-pig ventricular cardiomyocytes with NADH results in a decreased activation of I(K(ATP)) by pinacidil compared to control myocytes, indicating a higher subsarcolemmal ATP concentration. 9 Analysis of intracellular adenine nucleotides by HPLC confirmed the significant increase in ATP.</abstract><cop>England</cop><pmid>12812998</pmid><tpages>6</tpages></addata></record> |
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| subjects | Action Potentials Adenosine Triphosphate - physiology Animals Dose-Response Relationship, Drug Glyburide - pharmacokinetics Guinea Pigs Heart Ventricles Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism NAD - pharmacokinetics NAD - physiology Patch-Clamp Techniques Pinacidil - administration & dosage Pinacidil - antagonists & inhibitors Pinacidil - pharmacokinetics Potassium Channels - drug effects Potassium Channels - physiology Sarcolemma - chemistry Sarcolemma - drug effects Sarcolemma - enzymology |
| title | NADH supplementation decreases pinacidil-primed I K ATP in ventricular cardiomyocytes by increasing intracellular ATP |
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