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  1. Article: Optimizing combination therapy in the management of hypertension: the role of the aliskiren, amlodipine, and hydrochlorothiazide fixed combination.

    Hovater, Michael B / Jaimes, Edgar A

    Integrated blood pressure control

    2013  Volume 6, Page(s) 59–67

    Abstract: High blood pressure is the leading risk factor for death and disability worldwide, and the prevalence is increasing. Effective treatment decreases the risk of adverse events in proportion to blood pressure reduction. Combination antihypertensive therapy ... ...

    Abstract High blood pressure is the leading risk factor for death and disability worldwide, and the prevalence is increasing. Effective treatment decreases the risk of adverse events in proportion to blood pressure reduction. Combination antihypertensive therapy reduces blood pressure promptly and effectively. Single-pill combinations reduce the pill burden and improve adherence, efficacy, and tolerability of treatment compared with single drug pills. A significant portion of the hypertensive population will require three drugs for adequate control. The single-pill combination of aliskiren, amlodipine, and hydrochlorothiazide is based on complementary mechanisms of action. Clinical trials have shown it to be a safe and effective treatment for hypertension. This combination is a reasonable choice in clinical practice for patients with hypertension that requires three drugs for effective treatment.
    Language English
    Publishing date 2013-06-14
    Publishing country New Zealand
    Document type Journal Article
    ZDB-ID 2520711-8
    ISSN 1178-7104
    ISSN 1178-7104
    DOI 10.2147/IBPC.S32649
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Effect of dietary salt on regulation of TGF-β in the kidney.

    Hovater, Michael B / Sanders, Paul W

    Seminars in nephrology

    2012  Volume 32, Issue 3, Page(s) 269–276

    Abstract: ... through proline-rich tyrosine kinase-2, cellular-sarcoma (c-Src), Akt (also known as protein kinase B), and ...

    Abstract Dietary sodium chloride (salt) has long been considered injurious to the kidney by promoting the development of glomerular and tubulointerstitial fibrosis. Endothelial cells throughout the vasculature and glomeruli respond to increased dietary salt intake with increased production of transforming growth factor-β (TGF-β) and nitric oxide. High-salt intake activates large-conductance, voltage- and calcium-activated potassium (BK(Ca)) channels in endothelial cells. Activation of BK(Ca) channels promotes signaling through proline-rich tyrosine kinase-2, cellular-sarcoma (c-Src), Akt (also known as protein kinase B), and mitogen-activated protein kinase pathways that lead to endothelial production of TGF-β and nitric oxide. TGF-β signaling is broadly accepted as a strong stimulator of renal fibrosis. The classic description of TGF-β signaling pathology in renal disease involves signaling through Smad proteins resulting in extracellular matrix deposition and fibrosis. Active TGF-β1 also causes fibrosis by inducing epithelial-mesenchymal transition and apoptosis. By enhancing TGF-β signaling, increased dietary salt intake leads to progressive renal failure from nephron loss and glomerular and tubulointerstitial fibrosis.
    MeSH term(s) Animals ; Endothelial Cells/metabolism ; Epithelial-Mesenchymal Transition ; Fibrosis ; Focal Adhesion Kinase 2/metabolism ; Humans ; Kidney/metabolism ; Kidney/pathology ; Kidney Failure, Chronic/metabolism ; Large-Conductance Calcium-Activated Potassium Channels/metabolism ; Mice ; Mitogen-Activated Protein Kinases/metabolism ; Nitric Oxide/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Rats ; Renal Insufficiency, Chronic/metabolism ; Signal Transduction ; Smad Proteins/metabolism ; Sodium Chloride, Dietary/metabolism ; Transforming Growth Factor beta/metabolism ; Transforming Growth Factor beta1/metabolism ; src-Family Kinases/metabolism
    Chemical Substances Large-Conductance Calcium-Activated Potassium Channels ; Smad Proteins ; Sodium Chloride, Dietary ; Transforming Growth Factor beta ; Transforming Growth Factor beta1 ; Nitric Oxide (31C4KY9ESH) ; Focal Adhesion Kinase 2 (EC 2.7.10.2) ; src-Family Kinases (EC 2.7.10.2) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2012-07-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 604652-6
    ISSN 1558-4488 ; 0270-9295
    ISSN (online) 1558-4488
    ISSN 0270-9295
    DOI 10.1016/j.semnephrol.2012.04.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  3. Article ; Online: Nitric oxide and carbon monoxide antagonize TGF-β through ligand-independent internalization of TβR1/ALK5.

    Hovater, Michael B / Ying, Wei-Zhong / Agarwal, Anupam / Sanders, Paul W

    American journal of physiology. Renal physiology

    2014  Volume 307, Issue 6, Page(s) F727–35

    Abstract: Transforming growth factor (TGF)-β plays a central role in vascular homeostasis and in the pathology of vascular disease. There is a growing appreciation for the role of nitric oxide (NO) and carbon monoxide (CO) as highly diffusible, bioactive signaling ...

    Abstract Transforming growth factor (TGF)-β plays a central role in vascular homeostasis and in the pathology of vascular disease. There is a growing appreciation for the role of nitric oxide (NO) and carbon monoxide (CO) as highly diffusible, bioactive signaling molecules in the vasculature. We hypothesized that both NO and CO increase endocytosis of TGF-β receptor type 1 (TβR1) in vascular smooth muscle cells (VSMCs) through activation of dynamin-2, shielding cells from the effects of circulating TGF-β. In this study, primary cultures of VSMCs from Sprague-Dawley rats were treated with NO-releasing molecule 3 (a NO chemical donor), CO-releasing molecule 2 (a CO chemical donor), or control. NO and CO stimulated dynamin-2 activation in VSMCs. NO and CO promoted time- and dose-dependent endocytosis of TβR1. By decreasing TβR1 surface expression through this dynamin-2-dependent process, NO and CO diminished the effects of TGF-β on VSMCs. These findings help explain an important mechanism by which NO and CO signal in the vasculature by decreasing surface expression of TβR1 and the cellular response to TGF-β.
    MeSH term(s) Animals ; Carbon Monoxide/metabolism ; Dynamin II/metabolism ; Male ; Muscle, Smooth, Vascular/metabolism ; Myocytes, Smooth Muscle/metabolism ; Nerve Tissue Proteins/metabolism ; Nitric Oxide/metabolism ; Polymerization ; Protein-Serine-Threonine Kinases/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptor, Transforming Growth Factor-beta Type I ; Receptors, Transforming Growth Factor beta/metabolism ; T-Box Domain Proteins/metabolism ; Transforming Growth Factor beta/metabolism
    Chemical Substances Nerve Tissue Proteins ; Receptors, Transforming Growth Factor beta ; T-Box Domain Proteins ; Tbr1 protein, rat ; Transforming Growth Factor beta ; Nitric Oxide (31C4KY9ESH) ; Carbon Monoxide (7U1EE4V452) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Receptor, Transforming Growth Factor-beta Type I (EC 2.7.11.30) ; Tgfbr1 protein, rat (EC 2.7.11.30) ; Dynamin II (EC 3.6.5.5)
    Language English
    Publishing date 2014-08-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00353.2014
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  4. Article ; Online: Optimizing combination therapy in the management of hypertension

    Hovater MB / Jaimes EA

    Integrated Blood Pressure Control, Vol 2013, Iss default, Pp 59-

    the role of the aliskiren, amlodipine, and hydrochlorothiazide fixed combination

    2013  Volume 67

    Abstract: Michael B Hovater,1 Edgar A Jaimes1,2 1Division of Nephrology, Department of Medicine, University ...

    Abstract Michael B Hovater,1 Edgar A Jaimes1,2 1Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA; 2Department of Veterans Affairs Medical Center, University of Alabama at Birmingham, Birmingham, AL, USA Abstract: High blood pressure is the leading risk factor for death and disability worldwide, and the prevalence is increasing. Effective treatment decreases the risk of adverse events in proportion to blood pressure reduction. Combination antihypertensive therapy reduces blood pressure promptly and effectively. Single-pill combinations reduce the pill burden and improve adherence, efficacy, and tolerability of treatment compared with single drug pills. A significant portion of the hypertensive population will require three drugs for adequate control. The single-pill combination of aliskiren, amlodipine, and hydrochlorothiazide is based on complementary mechanisms of action. Clinical trials have shown it to be a safe and effective treatment for hypertension. This combination is a reasonable choice in clinical practice for patients with hypertension that requires three drugs for effective treatment. Keywords: aliskiren, amlodipine, hydrochlorothiazide, Amturnide, hypertension, combination
    Keywords Internal medicine ; RC31-1245
    Subject code 610
    Language English
    Publishing date 2013-06-01T00:00:00Z
    Publisher Dove Medical Press
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article: Intraluminal autocrine purinergic signaling within cysts: implications for the progression of diseases that involve encapsulated cyst formation.

    Olteanu, Dragos / Hovater, Michael B / Schwiebert, Erik M

    American journal of physiology. Renal physiology

    2007  Volume 292, Issue 1, Page(s) F11–4

    MeSH term(s) Adenosine Triphosphate/physiology ; Animals ; Autocrine Communication/physiology ; Cysts/pathology ; Disease Progression ; Humans ; Kidney Tubules/pathology ; Ligands ; Paracrine Communication/physiology ; Receptors, Purinergic/physiology
    Chemical Substances Ligands ; Receptors, Purinergic ; Adenosine Triphosphate (8L70Q75FXE)
    Language English
    Publishing date 2007-01
    Publishing country United States
    Document type Comment ; Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 1931-857X ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 1931-857X ; 0363-6127
    DOI 10.1152/ajprenal.00291.2006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  6. Article: Purinergic signaling in the lumen of a normal nephron and in remodeled PKD encapsulated cysts.

    Hovater, Michael B / Olteanu, Dragos / Welty, Elisabeth A / Schwiebert, Erik M

    Purinergic signalling

    2008  Volume 4, Issue 2, Page(s) 109–124

    Abstract: The nephron is the functional unit of the kidney. Blood and plasma are continually filtered within the glomeruli that begin each nephron. Adenosine 5' triphosphate (ATP) and its metabolites are freely filtered by each glomerulus and enter the lumen of ... ...

    Abstract The nephron is the functional unit of the kidney. Blood and plasma are continually filtered within the glomeruli that begin each nephron. Adenosine 5' triphosphate (ATP) and its metabolites are freely filtered by each glomerulus and enter the lumen of each nephron beginning at the proximal convoluted tubule (PCT). Flow rate, osmolality, and other mechanical or chemical stimuli for ATP secretion are present in each nephron segment. These ATP-release stimuli are also different in each nephron segment due to water or salt permeability or impermeability along different luminal membranes of the cells that line each nephron segment. Each of the above stimuli can trigger additional ATP release into the lumen of a nephron segment. Each nephron-lining epithelial cell is a potential source of secreted ATP. Together with filtered ATP and its metabolites derived from the glomerulus, secreted ATP and adenosine derived from cells along the nephron are likely the principal two of several nucleotide and nucleoside candidates for renal autocrine and paracrine ligands within the tubular fluid of the nephron. This minireview discusses the first principles of purinergic signaling as they relate to the nephron and the urinary bladder. The review discusses how the lumen of a renal tubule presents an ideal purinergic signaling microenvironment. The review also illustrates how remodeled and encapsulated cysts in autosomal dominant polycystic kidney disease (ADPKD) and remodeled pseudocysts in autosomal recessive PKD (ARPKD) of the renal collecting duct likely create an even more ideal microenvironment for purinergic signaling. Once trapped in these closed microenvironments, purinergic signaling becomes chronic and likely plays a significant epigenetic and detrimental role in the secondary progression of PKD, once the remodeling of the renal tissue has begun. In PKD cystic microenvironments, we argue that normal purinergic signaling within the lumen of the nephron provides detrimental acceleration of ADPKD once remodeling is complete.
    Language English
    Publishing date 2008-04-26
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2172143-9
    ISSN 1573-9546 ; 1573-9538
    ISSN (online) 1573-9546
    ISSN 1573-9538
    DOI 10.1007/s11302-008-9102-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Loss of apical monocilia on collecting duct principal cells impairs ATP secretion across the apical cell surface and ATP-dependent and flow-induced calcium signals.

    Hovater, Michael B / Olteanu, Dragos / Hanson, Elizabeth L / Cheng, Nai-Lin / Siroky, Brian / Fintha, Attila / Komlosi, Peter / Liu, Wen / Satlin, Lisa M / Bell, P Darwin / Yoder, Bradley K / Schwiebert, Erik M

    Purinergic signalling

    2007  Volume 4, Issue 2, Page(s) 155–170

    Abstract: Renal epithelial cells release ATP constitutively under basal conditions and release higher quantities of purine nucleotide in response to stimuli. ATP filtered at the glomerulus, secreted by epithelial cells along the nephron, and released serosally by ... ...

    Abstract Renal epithelial cells release ATP constitutively under basal conditions and release higher quantities of purine nucleotide in response to stimuli. ATP filtered at the glomerulus, secreted by epithelial cells along the nephron, and released serosally by macula densa cells for feedback signaling to afferent arterioles within the glomerulus has important physiological signaling roles within kidneys. In autosomal recessive polycystic kidney disease (ARPKD) mice and humans, collecting duct epithelial cells lack an apical central cilium or express dysfunctional proteins within that monocilium. Collecting duct principal cells derived from an Oak Ridge polycystic kidney (orpk ( Tg737 ) ) mouse model of ARPKD lack a well-formed apical central cilium, thought to be a sensory organelle. We compared these cells grown as polarized cell monolayers on permeable supports to the same cells where the apical monocilium was genetically rescued with the wild-type Tg737 gene that encodes Polaris, a protein essential to cilia formation. Constitutive ATP release under basal conditions was low and not different in mutant versus rescued monolayers. However, genetically rescued principal cell monolayers released ATP three- to fivefold more robustly in response to ionomycin. Principal cell monolayers with fully formed apical monocilia responded three- to fivefold greater to hypotonicity than mutant monolayers lacking monocilia. In support of the idea that monocilia are sensory organelles, intentionally harsh pipetting of medium directly onto the center of the monolayer induced ATP release in genetically rescued monolayers that possessed apical monocilia. Mechanical stimulation was much less effective, however, on mutant orpk collecting duct principal cell monolayers that lacked apical central monocilia. Our data also show that an increase in cytosolic free Ca(2+) primes the ATP pool that is released in response to mechanical stimuli. It also appears that hypotonic cell swelling and mechanical pipetting stimuli trigger release of a common ATP pool. Cilium-competent monolayers responded to flow with an increase in cell Ca(2+) derived from both extracellular and intracellular stores. This flow-induced Ca(2+) signal was less robust in cilium-deficient monolayers. Flow-induced Ca(2+) signals in both preparations were attenuated by extracellular gadolinium and by extracellular apyrase, an ATPase/ADPase. Taken together, these data suggest that apical monocilia are sensory organelles and that their presence in the apical membrane facilitates the formation of a mature ATP secretion apparatus responsive to chemical, osmotic, and mechanical stimuli. The cilium and autocrine ATP signaling appear to work in concert to control cell Ca(2+). Loss of a cilium-dedicated autocrine purinergic signaling system may be a critical underlying etiology for ARPKD and may lead to disinhibition and/or upregulation of multiple sodium (Na(+)) absorptive mechanisms and a resultant severe hypertensive phenotype in ARPKD and, possibly, other diseases.
    Language English
    Publishing date 2007-11-13
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2172143-9
    ISSN 1573-9546 ; 1573-9538
    ISSN (online) 1573-9546
    ISSN 1573-9538
    DOI 10.1007/s11302-007-9072-0
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