title: Obesity-associated hypertension: new insights into mechanisms.
abstract: Obesity is strongly associated with hypertension and cardiovascular disease. Several central and peripheral abnormalities that can explain the development or maintenance of high arterial pressure in obesity have been identified. These include activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system. Obesity is also associated with endothelial dysfunction and renal functional abnormalities that may play a role in the development of hypertension. The continuing discovery of mechanisms regulating appetite and metabolism is likely to lead to new therapies for obesity-induced hypertension. Better understanding of leptin signaling in the hypothalamus and the mechanisms of leptin resistance should facilitate therapeutic approaches to reverse the phenomenon of selective leptin resistance. Other hunger and satiety signals such as ghrelin and peptide YY are potentially attractive therapeutic strategies for treatment of obesity and its complications. These recent discoveries should lead to novel strategies for treatment of obesity and hypertension.
authors.affiliation: Specialized Center of Research in Hypertension Genetics, Department of Internal Medicine, University of Iowa, Iowa City, IA 52242, USA. kamal-rahmouni@uiowa.edu
authors.forename: Kamal
authors.initials: K
authors.lastname: Rahmouni
authors.forename: Marcelo L G
authors.initials: ML
authors.lastname: Correia
authors.forename: William G
authors.initials: WG
authors.lastname: Haynes
authors.forename: Allyn L
authors.initials: AL
authors.lastname: Mark
mesh_terms: D052242:Adiponectin; D000450:Aldosterone / Q000502:physiology; D000818:Animals; D001066:Appetite / Q000502:physiology; D004730:Endothelium, Vascular / Q000503:physiopathology; D004734:Energy Metabolism / Q000502:physiology; D054439:Ghrelin; D006801:Humans; D006946:Hyperinsulinism / Q000503:physiopathology; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology; D036341:Intercellular Signaling Peptides and Proteins / Q000502:physiology; D007668:Kidney / Q000503:physiopathology; D020738:Leptin / Q000502:physiology; D051379:Mice; D008817:Mice, Mutant Strains; D000451:Mineralocorticoid Receptor Antagonists / Q000494:pharmacology; D009765:Obesity / Q000150:complications* / Q000503:physiopathology; D036361:Peptide Hormones / Q000502:physiology; D019894:Peptide YY / Q000502:physiology; D011956:Receptors, Cell Surface / Q000502:physiology; D054411:Receptors, Leptin; D012084:Renin-Angiotensin System / Q000502:physiology; D012097:Repressor Proteins / Q000502:physiology; D012527:Satiation / Q000502:physiology; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins; D013564:Sympathetic Nervous System / Q000503:physiopathology; D014157:Transcription Factors / Q000502:physiology
chemical_list: D052242:Adiponectin; D054439:Ghrelin; D036341:Intercellular Signaling Peptides and Proteins; D020738:Leptin; D000451:Mineralocorticoid Receptor Antagonists; D036361:Peptide Hormones; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; D012097:Repressor Proteins; C106644:SOCS3 protein, human; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins; D014157:Transcription Factors; D019894:Peptide YY; D000450:Aldosterone