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SCIDIR_on1323453856 |
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OCoLC |
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20231120010648.0 |
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220605s2022 mau o 000 0 eng d |
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|b eng
|c YDX
|d OPELS
|d SFB
|d OCLCF
|d N$T
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| 020 |
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|a 9780323910880
|q (electronic bk.)
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|a 0323910882
|q (electronic bk.)
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|z 9780323910873
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|z 0323910874
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|a RC685.H8
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|a 616.13206
|2 23
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|a New targets for the treatment of hypertension and associate diseases
|h [electronic resource] /
|c Edited by William B. Campbell, John D. Imig.
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|a Cambridge, MA :
|b Academic Press,
|c 2022.
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|a 1 online resource.
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1 |
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|a Advances in pharmacology ;
|v v. 94
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|a Print version record.
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|a Intro -- New Targets for the Treatment of Hypertension and Associated Diseases -- Copyright -- Contents -- Contributors -- Chapter One: The CYP/20-HETE/GPR75 axis in hypertension -- 1. Introduction -- 2. 20-HETE biosynthesis, regulation, and metabolism -- 3. Human CYP polymorphisms associated with hypertension -- 4. The 20-HETE receptors -- 5. 20-HETE and the kidney in hypertension -- 6. 20-HETE, vascular smooth muscle cells (VSMCs) and hypertension -- 7. 20-HETE, endothelial cell dysfunction and activation -- 8. 20-HETE and the renin angiotensin system (RAS) -- 9. 20-HETE and vascular remodeling -- 10. 20-HETE and cardio-metabolic disease -- 11. 20-HETE synthesis inhibitors and 20-HETE receptor blockers (20HRBs) -- 12. Conclusion -- Conflict of interest statement -- References -- Chapter Two: Orally active epoxyeicosatrienoic acid analogs in hypertension and renal injury -- 1. Introduction -- 2. CYP Epoxygenase, sEH, and EET regulation in human hypertension -- 3. EET contribution to experimental hypertension and kidney disease -- 4. Therapeutic development of EET mimics/analogs -- 5. EET analogs in preclinical hypertension and kidney disease -- 6. Advances toward clinical trials -- 7. Conclusion -- Acknowledgments -- Conflict of interest statement -- References -- Further reading -- Chapter Three: Pharmacological developments in antihypertensive treatment through nitric oxide-cGMP modulation -- 1. Introduction -- 1.1. Hypertension, a risk factor that is not optimally treated -- 1.2. The NO-cGMP signaling cascade -- 1.3. Mechanisms that disturb NO-cGMP signaling -- 2. Strategies to improve eNOS activity -- 2.1. General aspects of eNOS -- 2.2. Uncoupling of eNOS -- 2.3. Assymetric dimethylarginine -- 2.4. Improvement of aging-related eNOS inactivation: Sirtuins and resveratrol -- 3. (Re)Activation of sGC -- 3.1. Structure and activation of sGC.
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|a 3.2. Supplementation of NO to activate sGC -- 3.3. Activation of sGC with sGC stimulators -- 3.4. Deactivation of sGC -- 3.5. Reactivation of sGC: sGC activators -- 4. PKG activation as a drug target -- 4.1. PKG structure and activation by cGMP -- 4.2. PKG activation by oxidation: Deviation to hyperpolarization -- 4.3. PKG oxidation: Relation to nitrate tolerance, PDE5 and reactivation -- 4.4. PKG as a drug target in hypertension -- 5. PDE inhibitors -- 5.1. General aspects, structure and regulation of activity -- 5.2. Involvement of PDE1 in BP regulation -- 5.3. PDE5 inhibition in blood pressure -- 6. Interventions targeted at reduction of ROS -- 6.1. General aspects -- 6.2. XO and Lox -- 6.3. Nox inhibition -- 6.4. Administration of exogenous and upgrade of endogenous antioxidants -- 6.5. Attenuation of mitochondrial ROS -- 7. Conclusion -- Conflict of interest -- References -- Chapter Four: Sphingosine-1-phosphate and Sphingosine-1-phosphate receptors in the cardiovascular system: pharmacology an ... -- 1. Introduction -- 2. S1P synthesis, kinetics and general function -- 3. Receptor-mediated S1P signaling -- 4. S1P function at the endothelium -- 5. S1P at vascular level -- 6. S1P effects at the kidney -- 7. The hazy link between the immune system and hypertension and the role of S1P -- 8. A role for S1P also in pulmonary arterial hypertension -- 9. Indirect effects of S1P on cardiovascular events that may impact the control of blood pressure -- 9.1. The dual role of S1P receptors in atherosclerosis lesion development -- 9.2. S1P and cardiac physiology -- 9.3. S1P, cardiac hypertrophy and fibrosis -- 9.4. S1P and myocardial infarction -- 9.5. A role for S1P and its receptors in cerebral ischemia -- 10. Conclusion -- Acknowledgments -- Conflict of interest -- References.
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|a 2.1. Discovery and characterization of GLP-1 -- 2.2. The GLP-1 receptor -- 2.3. Complexity of the signaling cascades and the concept of biased agonism -- 3. GLP-1 peptide agonists for use in type 2 diabetes -- 3.1. Marketed GLP-1RAs -- 3.2. GLP-1RAs: Future directions -- 4. Cardiovascular protection by GLP-1RA therapy in clinical trials -- 4.1. Cardiovascular outcomes trials -- 4.2. Meta-analyses of outcomes trials -- 5. Putative mechanisms underlying cardioprotection -- 5.1. Effects on cardiovascular hemodynamics -- 5.2. Direct effects on cardiac cells -- 5.3. Direct effects on vascular function -- 5.3.1. Vascular Wall -- 5.3.2. Direct effects on vascular endothelium -- 5.3.3. Direct effects on vascular smooth muscle -- 5.3.4. Stimulation of autophagy -- 6. Biased agonism and GLP-1RA action: Future directions -- 7. Conclusion -- Acknowledgment -- Conflict of interest statement -- References -- Chapter Eight: ADAM and ADAMTS disintegrin and metalloproteinases as major factors and molecular targets in vascular malf ... -- 1. Introduction -- 2. ADAMs and ADAMTS structure -- 3. Sources and tissue distribution of ADAM and ADAMTS family -- 4. ADAMs and ADAMTS activation -- 5. ADAMs targets, substrates, functions and mouse KO phenotype -- 6. ADAMTS targets, substrates, functions and mouse KO phenotype -- 7. ADAMs and ADAMTS inhibitors -- 8. ADAMs and ADAMTS in vascular processes and malfunction -- 8.1. ADAMs and ADAMTS in angiogenesis -- 8.2. ADAMs and ADAMTS in VSMC proliferation and migration -- 8.3. ADAMs and ADAMTS in neointimal hyperplasia and vascular restenosis -- 8.4. ADAMs and ADAMTS in vascular cell apoptosis -- 8.5. ADAMs and ADAMTS in endothelial permeability -- 8.6. ADAMs and ADAMTS in vascular inflammation -- 8.7. ADAMs and ADAMTS in tissue repair and wound healing -- 9. ADAMs and ADAMTS in cardiovascular disease.
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|a 9.1. ADAMs and ADAMTS in hypertension -- 9.2. ADAMs and ADAMTS in atherosclerosis -- 9.3. ADAMTS13 deficiency and thrombotic thrombocytopenic purpura (TTP) -- 9.4. ADAMs and ADAMTS in coronary artery disease -- 9.5. ADAMs and ADAMTS in myocardial infarction -- 9.6. ADAMs and ADAMTS in cardiac hypertrophy and heart failure -- 9.7. ADAMs and ADAMTS in ischemic stroke -- 9.8. ADAMs and ADAMTS in ischemia-reperfusion injury -- 9.9. ADAMs and ADAMTS in peripheral artery disease -- 9.10. ADAMs and ADAMTS in vascular aneurysm -- 9.11. ADAMs and ADAMTS in venous thromboembolism -- 9.12. ADAMs and ADAMTS in obesity and diabetes-related vascular disease -- 10. Conclusion -- Acknowledgments -- Conflict of interest -- References -- Chapter Nine: Beyond hypertension: Diastolic dysfunction associated with cancer treatment in the era of cardio-oncology -- 1. Introduction -- 2. Diastolic versus systolic dysfunction -- 3. Anthracyclines and the mechanisms of diastolic dysfunction -- 4. Anthracyclines and pathophysiologic trajectories of diastolic dysfunction -- 5. General considerations on anthracycline cardiotoxicity prevention -- 6. Pharmacologic interventions on cancer treatment-related diastolic dysfunction: Lessons from natriuretic peptide -- 6.1. Pathophysiology and role of B-type natriuretic peptide in diastolic dysfunction -- 6.2. BNP and cGMP to treat DD: Current status and perspectives -- 6.3. cGMP-independent lusitropic agents: Ranolazine -- 7. Novel potential pharmacologic opportunities -- 8. Conclusion -- Conflict of interest statement -- References.
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| 650 |
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|a Hypertension
|x Treatment.
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| 650 |
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0 |
|a Pharmacology.
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| 650 |
|
7 |
|a Hypertension
|x Treatment.
|2 fast
|0 (OCoLC)fst00965867
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| 650 |
|
7 |
|a Pharmacology.
|2 fast
|0 (OCoLC)fst01060259
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| 700 |
1 |
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|a Campbell, William B.
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| 700 |
1 |
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|a Imig, John D.
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| 776 |
0 |
8 |
|i Print version:
|z 9780323910880
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| 776 |
0 |
8 |
|i Print version:
|z 0323910874
|z 9780323910873
|w (OCoLC)1284287517
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| 830 |
|
0 |
|a Advances in pharmacology (San Diego, Calif.) ;
|v 94.
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| 856 |
4 |
0 |
|u https://sciencedirect.uam.elogim.com/science/bookseries/10543589/94
|z Texto completo
|
