title: Obesity-induced hypertension: interaction of neurohumoral and renal mechanisms.
abstract: Excess weight gain, especially when associated with increased visceral adiposity, is a major cause of hypertension, accounting for 65% to 75% of the risk for human primary (essential) hypertension. Increased renal tubular sodium reabsorption impairs pressure natriuresis and plays an important role in initiating obesity hypertension. The mediators of abnormal kidney function and increased blood pressure during development of obesity hypertension include (1) physical compression of the kidneys by fat in and around the kidneys, (2) activation of the renin-angiotensin-aldosterone system, and (3) increased sympathetic nervous system activity. Activation of the renin-angiotensin-aldosterone system is likely due, in part, to renal compression, as well as sympathetic nervous system activation. However, obesity also causes mineralocorticoid receptor activation independent of aldosterone or angiotensin II. The mechanisms for sympathetic nervous system activation in obesity have not been fully elucidated but may require leptin and activation of the brain melanocortin system. With prolonged obesity and development of target organ injury, especially renal injury, obesity-associated hypertension becomes more difficult to control, often requiring multiple antihypertensive drugs and treatment of other risk factors, including dyslipidemia, insulin resistance and diabetes mellitus, and inflammation. Unless effective antiobesity drugs are developed, the effect of obesity on hypertension and related cardiovascular, renal and metabolic disorders is likely to become even more important in the future as the prevalence of obesity continues to increase.
authors.affiliation: From the Departments of Physiology and Biophysics (J.E.H., J.M.d.C., A.A.d.S., Z.W., M.E.H.), Medicine (M.E.H.), Mississippi Center for Obesity Research (J.E.H., J.M.d.C., A.A.d.S., Z.W., M.E.H.), and Cardiovascular-Renal Research Center (J.E.H., J.M.d.C., A.A.d.S., Z.W., M.E.H.), University of Mississippi Medical Center, Jackson. jehall@umc.edu.
authors.forename: John E
authors.initials: JE
authors.lastname: Hall
authors.affiliation: From the Departments of Physiology and Biophysics (J.E.H., J.M.d.C., A.A.d.S., Z.W., M.E.H.), Medicine (M.E.H.), Mississippi Center for Obesity Research (J.E.H., J.M.d.C., A.A.d.S., Z.W., M.E.H.), and Cardiovascular-Renal Research Center (J.E.H., J.M.d.C., A.A.d.S., Z.W., M.E.H.), University of Mississippi Medical Center, Jackson.
authors.forename: Jussara M
authors.initials: JM
authors.lastname: do Carmo
authors.affiliation: From the Departments of Physiology and Biophysics (J.E.H., J.M.d.C., A.A.d.S., Z.W., M.E.H.), Medicine (M.E.H.), Mississippi Center for Obesity Research (J.E.H., J.M.d.C., A.A.d.S., Z.W., M.E.H.), and Cardiovascular-Renal Research Center (J.E.H., J.M.d.C., A.A.d.S., Z.W., M.E.H.), University of Mississippi Medical Center, Jackson.
authors.forename: Alexandre A
authors.initials: AA
authors.lastname: da Silva
authors.affiliation: From the Departments of Physiology and Biophysics (J.E.H., J.M.d.C., A.A.d.S., Z.W., M.E.H.), Medicine (M.E.H.), Mississippi Center for Obesity Research (J.E.H., J.M.d.C., A.A.d.S., Z.W., M.E.H.), and Cardiovascular-Renal Research Center (J.E.H., J.M.d.C., A.A.d.S., Z.W., M.E.H.), University of Mississippi Medical Center, Jackson.
authors.forename: Zhen
authors.initials: Z
authors.lastname: Wang
authors.affiliation: From the Departments of Physiology and Biophysics (J.E.H., J.M.d.C., A.A.d.S., Z.W., M.E.H.), Medicine (M.E.H.), Mississippi Center for Obesity Research (J.E.H., J.M.d.C., A.A.d.S., Z.W., M.E.H.), and Cardiovascular-Renal Research Center (J.E.H., J.M.d.C., A.A.d.S., Z.W., M.E.H.), University of Mississippi Medical Center, Jackson.
authors.forename: Michael E
authors.initials: ME
authors.lastname: Hall
mesh_terms: D000450:Aldosterone / Q000502:physiology; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology / Q000627:therapeutic use; D050171:Dyslipidemias / Q000150:complications / Q000503:physiopathology; D006329:Heart Conduction System / Q000503:physiopathology; D006439:Hemodynamics; D006801:Humans; D006973:Hypertension / Q000453:epidemiology / Q000209:etiology* / Q000503:physiopathology; D007333:Insulin Resistance / Q000502:physiology; D050152:Intra-Abdominal Fat / Q000503:physiopathology; D007668:Kidney / Q000503:physiopathology; D020738:Leptin / Q000502:physiology; D024821:Metabolic Syndrome / Q000150:complications / Q000503:physiopathology; D023421:Models, Animal; D008955:Models, Cardiovascular; D009318:Natriuresis / Q000502:physiology; D009765:Obesity / Q000150:complications* / Q000453:epidemiology / Q000503:physiopathology; D009928:Organ Specificity; D010275:Parasympathetic Nervous System / Q000503:physiopathology; D011312:Pressure; D015995:Prevalence; D011333:Pro-Opiomelanocortin / Q000502:physiology; D054411:Receptors, Leptin / Q000502:physiology; D051436:Renal Insufficiency, Chronic / Q000503:physiopathology; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology; D012964:Sodium / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000503:physiopathology
chemical_list: D000959:Antihypertensive Agents; C515448:LEPR protein, human; D020738:Leptin; D054411:Receptors, Leptin; D000450:Aldosterone; D011333:Pro-Opiomelanocortin; D012964:Sodium
keywords: blood pressure; chronic renal insufficiency; kidney; leptin; melanocortins; mineralocorticoids