New targets for the treatment of hypertension and associate diseases

Detalles Bibliográficos
Clasificación:Libro Electrónico
Otros Autores: Campbell, William B., Imig, John D.
Formato: Electrónico eBook
Idioma:Inglés
Publicado: Cambridge, MA : Academic Press, 2022.
Colección:Advances in pharmacology (San Diego, Calif.) ; 94.
Temas:
Hypertension > Treatment.
Pharmacology.
Acceso en línea:Texto completo
Tabla de Contenidos:
  • 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.
  • 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.
  • 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.
  • 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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