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Article ; Online: The sympathetic nervous system as a target for the treatment of hypertension and cardiometabolic diseases.

Sorota, Steve

2014 Volume 63, Issue 5, Page(s) 466–476

Abstract: The regulation of blood pressure by the sympathetic nervous system is reviewed with an emphasis on the role of the sympathetic nervous system in the development and maintenance of hypertension. Evidence from patients and animal models is summarized. ... ...

Abstract	The regulation of blood pressure by the sympathetic nervous system is reviewed with an emphasis on the role of the sympathetic nervous system in the development and maintenance of hypertension. Evidence from patients and animal models is summarized. Because it is clear that there is a neural contribution to many types of human hypertension and other cardiometabolic diseases, the case is presented for a renewed emphasis on the development of sympatholytic approaches for the treatment of hypertension and other conditions associated with hyperactivity of the sympathetic nervous system.
MeSH term(s)	Animals ; Heart Diseases/drug therapy ; Heart Diseases/metabolism ; Heart Diseases/physiopathology ; Humans ; Hypertension/drug therapy ; Hypertension/physiopathology ; Sympathetic Nervous System/drug effects ; Sympathetic Nervous System/pathology ; Sympathetic Nervous System/physiopathology ; Sympatholytics/therapeutic use
Chemical Substances	Sympatholytics
Language	English
Publishing date	2014-05
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	391970-5
ISSN	1533-4023 ; 0160-2446
ISSN (online)	1533-4023
ISSN	0160-2446
DOI	10.1097/FJC.0000000000000064
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Article ; Online: C-type natriuretic peptide induces inotropic and lusitropic effects in human 3D-engineered cardiac tissue: Implications for the regulation of cardiac function in humans.

Bachmann, Julian C / Kirchhoff, Jeppe E / Napolitano, Julia E / Sorota, Steve / Gordon, William M / Feric, Nicole / Aschar-Sobbi, Roozbeh / Lv, Juan / Cao, Zhiyou / Coppieters, Ken / Borghetti, Giulia / Nyberg, Michael

Experimental physiology

2023 Volume 108, Issue 9, Page(s) 1172–1188

Abstract: The role of C-type natriuretic peptide (CNP) in the regulation of cardiac function in humans remains to be established as previous investigations have been confined to animal model systems. Here, we used well-characterized engineered cardiac tissues ( ... ...

Abstract	The role of C-type natriuretic peptide (CNP) in the regulation of cardiac function in humans remains to be established as previous investigations have been confined to animal model systems. Here, we used well-characterized engineered cardiac tissues (ECTs) generated from human stem cell-derived cardiomyocytes and fibroblasts to study the acute effects of CNP on contractility. Application of CNP elicited a positive inotropic response as evidenced by increases in maximum twitch amplitude, maximum contraction slope and maximum calcium amplitude. This inotropic response was accompanied by a positive lusitropic response as demonstrated by reductions in time from peak contraction to 90% of relaxation and time from peak calcium transient to 90% of decay that paralleled increases in maximum contraction decay slope and maximum calcium decay slope. To establish translatability, CNP-induced changes in contractility were also assessed in rat ex vivo (isolated heart) and in vivo models. Here, the effects on force kinetics observed in ECTs mirrored those observed in both the ex vivo and in vivo model systems, whereas the increase in maximal force generation with CNP application was only detected in ECTs. In conclusion, CNP induces a positive inotropic and lusitropic response in ECTs, thus supporting an important role for CNP in the regulation of human cardiac function. The high degree of translatability between ECTs, ex vivo and in vivo models further supports a regulatory role for CNP and expands the current understanding of the translational value of human ECTs. NEW FINDINGS: What is the central question of this study? What are the acute responses to C-type natriuretic peptide (CNP) in human-engineered cardiac tissues (ECTs) on cardiac function and how well do they translate to matched concentrations in animal ex vivo and in vivo models? What is the main finding and its importance? Acute stimulation of ECTs with CNP induced positive lusitropic and inotropic effects on cardiac contractility, which closely reflected the changes observed in rat ex vivo and in vivo cardiac models. These findings support an important role for CNP in the regulation of human cardiac function and highlight the translational value of ECTs.
MeSH term(s)	Animals ; Humans ; Rats ; Calcium ; Myocardial Contraction/physiology ; Myocytes, Cardiac ; Natriuretic Peptide, C-Type/pharmacology
Chemical Substances	Calcium (SY7Q814VUP) ; Natriuretic Peptide, C-Type (127869-51-6)
Language	English
Publishing date	2023-07-26
Publishing country	England
Document type	Journal Article
ZDB-ID	1016295-1
ISSN	1469-445X ; 0958-0670
ISSN (online)	1469-445X
ISSN	0958-0670
DOI	10.1113/EP091303
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Article: Insights into the structure, distribution and function of the cardiac chloride channels.

Sorota, S

Cardiovascular research

1999 Volume 42, Issue 2, Page(s) 361–376

Abstract: This review describes the properties and distribution of the three major types of chloride currents that have been studied in cardiac tissue. These include a cAMP- and protein kinase A-dependent current, a calcium-activated current and a swelling-induced ...

Abstract	This review describes the properties and distribution of the three major types of chloride currents that have been studied in cardiac tissue. These include a cAMP- and protein kinase A-dependent current, a calcium-activated current and a swelling-induced current. The study of cardiac anion currents is a less mature field than the study of cardiac cation currents. Consequently, less is known regarding the structure, molecular identity and physiological role of anion currents in comparison to cardiac cation currents. Where known, the available molecular and structural information is also discussed. Although there is no proven physiological role for cardiac chloride currents, the possible clinical electrophysiological roles of cardiac chloride currents are discussed.
MeSH term(s)	Animals ; Arrhythmias, Cardiac/physiopathology ; Biological Transport, Active ; Chloride Channels/genetics ; Chloride Channels/metabolism ; Electrophysiology ; Gene Expression Regulation ; Heart/physiology ; Heart/physiopathology ; Humans ; Ion Channel Gating/physiology ; Ion Transport ; Myocardial Contraction/physiology ; Signal Transduction ; Structure-Activity Relationship
Chemical Substances	Chloride Channels
Language	English
Publishing date	1999-05
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1016/s0008-6363(99)00039-5
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Zs.A 565: Show issues

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Article: Tyrosine protein kinase inhibitors prevent activation of cardiac swelling-induced chloride current.

Sorota, S

Pflugers Archiv : European journal of physiology

1995 Volume 431, Issue 2, Page(s) 178–185

Abstract: ... adenosine 5'-O-(3-thiotriphosphate (ATP[gamma S]) was used, genistein did not prevent the reactivation ... of ICl-swelling. Intracellular ATP[gamma S] did not result in a persistent activation of ICl-swelling ...

Abstract	The effect of tyrosine protein kinase inhibitors on the swelling-induced chloride current (ICl-swelling) of dog atrial myocytes was studied using the whole-cell patch-clamp recording technique. Currents were measured during hyperpolarizing voltage ramps with potassium currents blocked by cesium. Osmolarity was varied using mannitol. Exposure to hypotonic solution (approximately 249 mosmol/kg) activated ICl-swelling. Hypertonic solution (approximately 363 mosmol/kg) was used to shrink swollen cells and turn off ICl-swelling. In studies on the acute effect of tyrosine protein kinase inhibitors each cell was swollen three separate times. Control, treatment, and washout ICl-swelling were compared. Genistein (50-80 microM) prevented reactivation of ICl-swelling without affecting cell size. The effect of genistein partially subsided upon washout. The effect of genistein on ICl-swelling was not mimicked by 80 microM daidzein, a related compound that does not inhibit tyrosine protein kinases. When intracellular adenosine 5'-O-(3-thiotriphosphate (ATP[gamma S]) was used, genistein did not prevent the reactivation of ICl-swelling. Intracellular ATP[gamma S] did not result in a persistent activation of ICl-swelling when cell size was returned to control. Acute exposure to 1 microM herbimycin A or 100 microM tyrphostin 51 did not prohibit the activation of ICl-swelling. A 24-h exposure to 1 microM herbimycin A did inhibit ICl-swelling. The results provide important clues regarding the activation mechanism for ICl-swelling and suggest that a tyrosine protein phosphorylation may be necessary, but not sufficient, for activation of ICl-swelling.
MeSH term(s)	Adenosine Triphosphate/analogs & derivatives ; Adenosine Triphosphate/pharmacology ; Animals ; Benzoquinones ; Cell Size/physiology ; Chloride Channels/drug effects ; Chloride Channels/metabolism ; Dogs ; Electrophysiology ; Enzyme Inhibitors/pharmacology ; Genistein ; Heart/drug effects ; Hypotonic Solutions ; In Vitro Techniques ; Isoflavones/pharmacology ; Lactams, Macrocyclic ; Membrane Potentials/physiology ; Myocardium/cytology ; Myocardium/metabolism ; Patch-Clamp Techniques ; Phosphorylation/drug effects ; Protein-Tyrosine Kinases/antagonists & inhibitors ; Quinones/pharmacology ; Rifabutin/analogs & derivatives
Chemical Substances	Benzoquinones ; Chloride Channels ; Enzyme Inhibitors ; Hypotonic Solutions ; Isoflavones ; Lactams, Macrocyclic ; Quinones ; Rifabutin (1W306TDA6S) ; adenosine 5'-O-(3-thiotriphosphate) (35094-46-3) ; herbimycin (70563-58-5) ; Adenosine Triphosphate (8L70Q75FXE) ; Genistein (DH2M523P0H) ; Protein-Tyrosine Kinases (EC 2.7.10.1)
Language	English
Publishing date	1995-12
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	6380-0
ISSN	1432-2013 ; 0031-6768
ISSN (online)	1432-2013
ISSN	0031-6768
DOI	10.1007/bf00410189
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Article: Pharmacologic properties of the swelling-induced chloride current of dog atrial myocytes.

Sorota, S

Journal of cardiovascular electrophysiology

1994 Volume 5, Issue 12, Page(s) 1006–1016

Abstract: ... contribution(s) of this current.: Methods and results: Dog atrial cells were used to investigate ...

Abstract	Introduction: Swelling-induced chloride currents may contribute to cardiac electrical activity and cell volume regulation. Identification of selective blockers would aid in understanding the functional contribution(s) of this current. Methods and results: Dog atrial cells were used to investigate the pharmacologic properties of the swelling-induced chloride current. Whole cell patch clamp was used. Swelling-induced chloride current was activated by osmotic stress. Initially, the chloride selectivity and calcium independence of the swelling-induced current in dog atrial cells was demonstrated. Subsequently, a number of putative chloride channel blockers were examined. Anthracene-9-carboxylic acid (1 mM) and dideoxyforskolin (100 microM) and extracellular cAMP (5 mM) were found to partially inhibit the swelling-induced chloride current (approximately 50%, 80%, and 10% inhibition, respectively). Niflumic acid (100 microM), nitrophenylpropylamino benzoate (NPPB; 10 to 40 microM), and (+) 2-[(2-cyclopentyl-6,7-dichloro-2,3-dihydro-2-methyl-1-oxy-1H-inden -5-yl)oxy d acetic acid (indanyloxyacetic acid; IAA-94; 100 microM) could fully inhibit the swelling-induced chloride current without decreasing cell size. DIDS (100 microM) and dinitrostilbene disulfonic acid (DNDS; 5 mM) fully inhibited outward currents but only partially inhibited inward current. Conclusions: Niflumic acid, IAA-94, and NPPB were identified as full blockers of cardiac swelling-induced chloride current. Nonspecific effects were identified for each of the full blockers. Experiments that use these agents as functional antagonists should be carefully designed and interpreted with caution.
MeSH term(s)	Animals ; Anthracenes/pharmacology ; Atrial Function ; Calcium/metabolism ; Chloride Channels/antagonists & inhibitors ; Chloride Channels/metabolism ; Colforsin/analogs & derivatives ; Colforsin/pharmacology ; Dogs ; Electrophysiology ; Glycolates/pharmacology ; Heart Atria/cytology ; Heart Atria/drug effects ; Niflumic Acid/pharmacology ; Nitrobenzoates/pharmacology ; Patch-Clamp Techniques ; Stilbenes/pharmacology
Chemical Substances	Anthracenes ; Chloride Channels ; Glycolates ; Nitrobenzoates ; Stilbenes ; Colforsin (1F7A44V6OU) ; 5-nitro-2-(3-phenylpropylamino)benzoic acid (3A35O9G3YZ) ; Niflumic Acid (4U5MP5IUD8) ; MK 473 (54197-05-6) ; 4,4'-dinitro-2,2'-stilbenedisulfonic acid (6ND7PC82E2) ; 9-anthroic acid (723-62-6) ; 1,9-dideoxyforskolin (OAW710HWIX) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	1994-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1025989-2
ISSN	1540-8167 ; 1045-3873
ISSN (online)	1540-8167
ISSN	1045-3873
DOI	10.1111/j.1540-8167.1994.tb01143.x
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Zs.A 2863: Show issues

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Article ; Online: Additive effects of combined application of multiple hERG blockers.

Margulis, Michael / Sorota, Steve

Journal of cardiovascular pharmacology

2008 Volume 51, Issue 6, Page(s) 549–552

Abstract: Pro-arrhythmia by noncardiac drugs has become an important safety concern in the pharmaceutical industry. The most common underlying mechanism for induction of arrhythmias by noncardiac drugs is off-target block of the native cardiac repolarizing current, ...

Abstract	Pro-arrhythmia by noncardiac drugs has become an important safety concern in the pharmaceutical industry. The most common underlying mechanism for induction of arrhythmias by noncardiac drugs is off-target block of the native cardiac repolarizing current, I Kr. The pore-forming subunit of I Kr is encoded by the human ether-a-go-go related gene (hERG), and in vitro measurements of hERG activity has become a standard component of drug safety evaluations. hERG/I Kr channels are blocked by a wide array of different chemical series; therefore, patients could be exposed to multiple blockers. There are few published studies addressing whether multiple blockers will exert independent actions on hERG channels. Whole cell patch clamp was used to evaluate the potential for cooperative effects when 2 hERG blocking agents were applied simultaneously. Cisapride, quinidine, fluvoxamine, and BeKm-1 were selected as representative agents binding to: (1) hydrophobic residues in the inner vestibule (cisapride and quinidine, the most frequent sites of interaction), (2) an extracellular segment near the pore (BeKm-1) or, (3) an unknown site (fluvoxamine). No synergistic blocking actions were seen. In some cases block was slightly less than additive. On balance, the results are consistent with additive and independent actions with simultaneous application of 2 hERG blockers.
MeSH term(s)	Animals ; Cell Culture Techniques ; Cisapride/pharmacology ; Drug Synergism ; ERG1 Potassium Channel ; Ether-A-Go-Go Potassium Channels/antagonists & inhibitors ; Fluvoxamine/pharmacology ; Humans ; Mice ; Patch-Clamp Techniques ; Quinidine/pharmacology ; Scorpion Venoms/pharmacology
Chemical Substances	BeKm-1 toxin ; ERG1 Potassium Channel ; Ether-A-Go-Go Potassium Channels ; KCNH2 protein, human ; Scorpion Venoms ; Quinidine (ITX08688JL) ; Fluvoxamine (O4L1XPO44W) ; Cisapride (UVL329170W)
Language	English
Publishing date	2008-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	391970-5
ISSN	1533-4023 ; 0160-2446
ISSN (online)	1533-4023
ISSN	0160-2446
DOI	10.1097/FJC.0b013e31817532ee
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Article: Swelling-induced chloride-sensitive current in canine atrial cells revealed by whole-cell patch-clamp method.

Sorota, S

Circulation research

1992 Volume 70, Issue 4, Page(s) 679–687

Abstract: An isoproterenol-induced chloride current has been detected in ventricular myocytes from guinea pig and rabbit but has not been found in canine ventricular cells. This investigation was undertaken to determine whether canine atrial cells possessed such a ...

Abstract	An isoproterenol-induced chloride current has been detected in ventricular myocytes from guinea pig and rabbit but has not been found in canine ventricular cells. This investigation was undertaken to determine whether canine atrial cells possessed such a current. Steady-state currents were examined with potassium currents blocked by cesium. In whole-cell patch-clamp experiments, an isoproterenol-induced chloride current could not be detected shortly after patch rupture. However, whole-cell current in the absence of isoproterenol increased over time after patch rupture. The spontaneously activating steady-state current was outwardly rectifying with a reversal potential of approximately -25 mV. The current that developed over time was sensitive to variation in extracellular chloride concentration and was partially blocked by anthracene-9-carboxylic acid. Isoproterenol could enhance the amplitude of this current once it developed. Although isosmotic pipette filling and extracellular solutions were used, cell swelling was found to be the cause of the increase in whole-cell conductance that was observed during whole-cell patch-clamp experiments. The development of the current and the associated cell swelling could be prevented with the addition of 50-75 mM mannitol to the extracellular solution. The current could be observed in perforated patch recordings with nystatin when extracellular osmolarity was low (221 mosm/kg) but not when the extracellular solution was isosmotic (293 mosm/kg). Cardiac chloride currents have the potential to depolarize the resting membrane potential and cause abnormal automaticity. Chloride currents can also decrease the refractory period through a reduction in action potential duration.(ABSTRACT TRUNCATED AT 250 WORDS)
MeSH term(s)	Animals ; Atrial Function ; Chlorides/physiology ; Cytological Techniques ; Dogs ; Electrophysiology ; Heart Atria/cytology ; Heart Atria/drug effects ; In Vitro Techniques ; Inflammation ; Isoproterenol/pharmacology ; Mannitol/pharmacology ; Membrane Potentials ; Myocarditis/physiopathology ; Nystatin/pharmacology ; Osmolar Concentration
Chemical Substances	Chlorides ; Nystatin (1400-61-9) ; Mannitol (3OWL53L36A) ; Isoproterenol (L628TT009W)
Language	English
Publishing date	1992-04
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/01.res.70.4.679
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Ui IV Zs.60: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Cyp1 Inhibition Prevents Doxorubicin-Induced Cardiomyopathy in a Zebrafish Heart-Failure Model.

Lam, Pui-Ying / Kutchukian, Peter / Anand, Rajan / Imbriglio, Jason / Andrews, Christine / Padilla, Hugo / Vohra, Anita / Lane, Sarah / Parker, Dann L / Cornella Taracido, Ivan / Johns, Douglas G / Beerens, Manu / MacRae, Calum A / Caldwell, John P / Sorota, Steve / Asnani, Aarti / Peterson, Randall T

Chembiochem : a European journal of chemical biology

2020 Volume 21, Issue 13, Page(s) 1905–1910

Abstract: Doxorubicin is a highly effective chemotherapy agent used to treat many common malignancies. However, its use is limited by cardiotoxicity, and cumulative doses exponentially increase the risk of heart failure. To identify novel heart failure treatment ... ...

Abstract	Doxorubicin is a highly effective chemotherapy agent used to treat many common malignancies. However, its use is limited by cardiotoxicity, and cumulative doses exponentially increase the risk of heart failure. To identify novel heart failure treatment targets, a zebrafish model of doxorubicin-induced cardiomyopathy was previously established for small-molecule screening. Using this model, several small molecules that prevent doxorubicin-induced cardiotoxicity both in zebrafish and in mouse models have previously been identified. In this study, exploration of doxorubicin cardiotoxicity is expanded by screening 2271 small molecules from a proprietary, target-annotated tool compound collection. It is found that 120 small molecules can prevent doxorubicin-induced cardiotoxicity, including 7 highly effective compounds. Of these, all seven exhibited inhibitory activity towards cytochrome P450 family 1 (CYP1). These results are consistent with previous findings, in which visnagin, a CYP1 inhibitor, also prevents doxorubicin-induced cardiotoxicity. Importantly, genetic mutation of cyp1a protected zebrafish against doxorubicin-induced cardiotoxicity phenotypes. Together, these results provide strong evidence that CYP1 is an important contributor to doxorubicin-induced cardiotoxicity and highlight the CYP1 pathway as a candidate therapeutic target for clinical cardioprotection.
MeSH term(s)	Animals ; Animals, Genetically Modified ; Cardiomyopathies/chemically induced ; Cardiomyopathies/pathology ; Cardiomyopathies/prevention & control ; Cytochrome P450 Family 1/antagonists & inhibitors ; Cytochrome P450 Family 1/genetics ; Cytochrome P450 Family 1/metabolism ; Disease Models, Animal ; Doxorubicin/toxicity ; Heart Failure ; Mutagenesis ; Phenotype ; Small Molecule Libraries/chemistry ; Small Molecule Libraries/metabolism ; Small Molecule Libraries/therapeutic use ; Structure-Activity Relationship ; Zebrafish ; Zebrafish Proteins/antagonists & inhibitors ; Zebrafish Proteins/genetics ; Zebrafish Proteins/metabolism
Chemical Substances	Small Molecule Libraries ; Zebrafish Proteins ; Doxorubicin (80168379AG) ; Cytochrome P450 Family 1 (EC 1.14.14.1)
Language	English
Publishing date	2020-03-06
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2020469-3
ISSN	1439-7633 ; 1439-4227
ISSN (online)	1439-7633
ISSN	1439-4227
DOI	10.1002/cbic.201900741
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Article: Cardiac swelling-induced chloride current is enhanced by endothelin.

Du, X Y / Sorota, S

Journal of cardiovascular pharmacology

2000 Volume 35, Issue 5, Page(s) 769–776

Abstract: Endothelins (ETs) are a family of peptide hormones that act on G protein-coupled ET(A) and ET(B) receptors. ETs exert inotropic and chronotropic actions in the heart. Myocardial ischemia is associated with increased plasma levels of ET and cell swelling. ...

Abstract	Endothelins (ETs) are a family of peptide hormones that act on G protein-coupled ET(A) and ET(B) receptors. ETs exert inotropic and chronotropic actions in the heart. Myocardial ischemia is associated with increased plasma levels of ET and cell swelling. We examined the effect of ETs on dog atrial swelling-induced chloride current (I(Cl,swell)). Whole-cell patch clamp was used; 10 nM ET-1 or ET-2 increased I(Cl,swell) by approximately twofold. ET-2 had no effect if I(Cl,swell) activation was prevented by hypertonic superfusate. Outward ET-2-induced current was blocked by 150 microM DIDS more effectively than inward current. Overnight pretreatment with phorbol 12-myristate 13-acetate (1.6 microM), pertussis toxin (100 ng/ml), or dialysis of the cell with 300 microM 2'-deoxyadenosine 3'-monophosphate, a P-site inhibitor of adenylyl cyclase, did not diminish the effect of ET-2. The effect of ET-2 was blocked by an ET(A1)- (BQ123), but not an ET(B)-selective (BQ788) antagonist. ET-2-induced currents were inhibited approximately 70% by PD 98059 (30 microM), a selective MAPK kinase (MEK) blocker. PD 98059 did not affect basal whole cell current or I(Cl,swell) before exposure to ET-2. The data suggest that MEK activity is not required for activation of atrial I(Cl,swell) but that ET-2 stimulates I(Cl,swell) by a MEK-dependent pathway.
MeSH term(s)	Adenylate Cyclase Toxin ; Adenylyl Cyclase Inhibitors ; Adenylyl Cyclases/metabolism ; Animals ; Calcium/metabolism ; Chloride Channels/metabolism ; Dogs ; Down-Regulation ; Endothelin-1/pharmacology ; Endothelin-2/antagonists & inhibitors ; Endothelin-2/pharmacology ; Heart/drug effects ; Heart Atria/cytology ; Heart Atria/metabolism ; In Vitro Techniques ; MAP Kinase Kinase Kinases/antagonists & inhibitors ; MAP Kinase Kinase Kinases/metabolism ; Myocardium/metabolism ; Pertussis Toxin ; Protein Kinase C/antagonists & inhibitors ; Protein Kinase C/metabolism ; Receptor, Endothelin A ; Receptors, Endothelin/metabolism ; Virulence Factors, Bordetella/pharmacology
Chemical Substances	Adenylate Cyclase Toxin ; Adenylyl Cyclase Inhibitors ; Chloride Channels ; Endothelin-1 ; Endothelin-2 ; Receptor, Endothelin A ; Receptors, Endothelin ; Virulence Factors, Bordetella ; Pertussis Toxin (EC 2.4.2.31) ; Protein Kinase C (EC 2.7.11.13) ; MAP Kinase Kinase Kinases (EC 2.7.11.25) ; Adenylyl Cyclases (EC 4.6.1.1) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2000-05
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	391970-5
ISSN	1533-4023 ; 0160-2446
ISSN (online)	1533-4023
ISSN	0160-2446
DOI	10.1097/00005344-200005000-00014
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Article: Protein kinase C stimulates swelling-induced chloride current in canine atrial cells.

Du, X Y / Sorota, S

Pflugers Archiv : European journal of physiology

1999 Volume 437, Issue 2, Page(s) 227–234

Abstract: The whole-cell patch-clamp technique was used to study the effect of protein kinase C (PKC) stimulation and alpha-adrenergic agonists on the swelling-induced chloride current (ICl,swell) in canine atrial cells. ICl,swell was activated by positive- ... ...

Abstract	The whole-cell patch-clamp technique was used to study the effect of protein kinase C (PKC) stimulation and alpha-adrenergic agonists on the swelling-induced chloride current (ICl,swell) in canine atrial cells. ICl,swell was activated by positive-pressure inflation. 4beta-Phorbol 12, 13-dibutyrate (PDBu) concentration-dependently stimulated ICl,swell. PDBu (500 nM) increased the current density of ICl,swell from 9.1+/-1.3 to 24.2+/-4.8 pA/pF at +20 mV (n=4). This effect developed slowly, reaching a steady-state after more than 5 min of exposure. 4alpha-Phorbol 12, 13-dibutyrate (4alpha-PDBu, 500 nM), an inactive analogue of PDBu, did not affect ICl,swell. The effect of PDBu was inhibited by bisindolylmaleimide I. After down regulation of PKC by phorbol 12-myristate 13-acetate (PMA, 1.6 microM, 24 h), ICl,swell no longer responded to PDBu (n=4). Neither the basal whole-cell current (prior to cell inflation) nor inflation-induced ICl,swell were affected by PKC down regulation. Phenylephrine did not affect ICl,swell. We conclude that PKC activity stimulates and does not prevent the activation of dog atrial ICl,swell. These results contrast with reports of PKC-dependent inhibition of rabbit atrial ICl,swell and currents conducted by ClC-3, a putative clone for ICl,swell. The data suggest species-dependent variations in the modulation of cardiac ICl,swell by PKC.
MeSH term(s)	Adrenergic alpha-Agonists/pharmacology ; Animals ; Cell Size/drug effects ; Cell Size/physiology ; Chloride Channels/drug effects ; Chloride Channels/metabolism ; Dogs ; Down-Regulation/drug effects ; Electrophysiology ; Heart Atria/cytology ; Heart Atria/drug effects ; In Vitro Techniques ; Membrane Potentials/physiology ; Myocardium/cytology ; Myocardium/metabolism ; Patch-Clamp Techniques ; Phenylephrine/pharmacology ; Phorbol 12,13-Dibutyrate/pharmacology ; Protein Kinase C/pharmacology ; Stimulation, Chemical
Chemical Substances	Adrenergic alpha-Agonists ; Chloride Channels ; Phenylephrine (1WS297W6MV) ; Phorbol 12,13-Dibutyrate (37558-16-0) ; Protein Kinase C (EC 2.7.11.13)
Language	English
Publishing date	1999-01
Publishing country	Germany
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	6380-0
ISSN	1432-2013 ; 0031-6768
ISSN (online)	1432-2013
ISSN	0031-6768
DOI	10.1007/s004240050773
Database	MEDical Literature Analysis and Retrieval System OnLINE

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