title: Novel Pathophysiological Mechanisms in Hypertension.
abstract: Hypertension is the most common disease affecting humans and imparts a significant cardiovascular and renal risk to patients. Extensive research over the past few decades has enhanced our understanding of the underlying mechanisms in hypertension. However, in most instances, the cause of hypertension in a given patient continues to remain elusive. Nevertheless, achieving aggressive blood pressure goals significantly reduces cardiovascular morbidity and mortality, as demonstrated in the recently concluded SPRINT trial. Since a large proportion of patients still fail to achieve blood pressure goals, knowledge of novel pathophysiologic mechanisms and mechanism based treatment strategies is crucial. The following chapter will review the novel pathophysiological mechanisms in hypertension, with a focus on role of immunity, inflammation and vascular endothelial homeostasis. The therapeutic implications of these mechanisms will be discussed where applicable.
authors.affiliation: Tulane University Heart and Vascular Institute, Tulane School of Medicine, 1430 Tulane Avenue, SL-48, New Orleans, LA, 70112, USA. rsamson@tulane.edu.
authors.forename: Rohan
authors.initials: R
authors.lastname: Samson
authors.affiliation: Tulane University Heart and Vascular Institute, Tulane School of Medicine, 1430 Tulane Avenue, SL-48, New Orleans, LA, 70112, USA.
authors.forename: Andrew
authors.initials: A
authors.lastname: Lee
authors.affiliation: Tulane University Heart and Vascular Institute, Tulane School of Medicine, 1430 Tulane Avenue, SL-48, New Orleans, LA, 70112, USA.
authors.forename: Sean
authors.initials: S
authors.lastname: Lawless
authors.affiliation: Tulane University Heart and Vascular Institute, Tulane School of Medicine, 1430 Tulane Avenue, SL-48, New Orleans, LA, 70112, USA.
authors.forename: Robert
authors.initials: R
authors.lastname: Hsu
authors.affiliation: Tulane University Heart and Vascular Institute, Tulane School of Medicine, 1430 Tulane Avenue, SL-48, New Orleans, LA, 70112, USA.
authors.forename: Gary
authors.initials: G
authors.lastname: Sander
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001120:Arginine / Q000031:analogs & derivatives / Q000378:metabolism; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000187:drug effects; D016207:Cytokines / Q000276:immunology / Q000378:metabolism; D004351:Drug Resistance; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology*; D007113:Immunity, Innate; D018836:Inflammation Mediators / Q000276:immunology / Q000378:metabolism; D012084:Renin-Angiotensin System; D015398:Signal Transduction
chemical_list: D000959:Antihypertensive Agents; D015415:Biomarkers; D016207:Cytokines; D018836:Inflammation Mediators; C018524:N,N-dimethylarginine; D001120:Arginine
keywords: ADMA; AT2 receptor; Angiotensin- (1–7); Bone marrow; Hypertension; Immune system; Mineralocorticoid receptor; Neuro-inflammation; Pathophysiology; RAAS; VEGF