title: Obesity-induced increases in sympathetic nerve activity: sex matters.
abstract: Abundant evidence obtained largely from male human and animal subjects indicates that obesity increases sympathetic nerve activity (SNA), which contributes to hypertension development. However, recent studies that included women reported that the strong relationships between muscle SNA and waist circumference or body mass index (BMI) found in men are not present in overweight and obese women. A similar sex difference in the association between adiposity and hypertension development has been identified in animal models of obesity. In this brief review, we consider two possible mechanisms for this sex difference. First, visceral adiposity, leptin, insulin, and angiotensin II have been identified as potential culprits in obesity-induced sympathoexcitation in males. We explore if these factors wield the same impact in females. Second, we consider if sex differences in vascular reactivity to sympathetic activation contribute. Our survey of the literature suggests that premenopausal females may be able to resist obesity-induced sympathoexcitation and hypertension in part due to differences in adipose disposition as well as its muted inflammatory response and reduced production of pressor versus depressor components of the renin-angiotensin system. In addition, vascular responsiveness to increased SNA may be reduced. However, more importantly, we identify the urgent need for further study, not only of sex differences per se, but also of the mechanisms that may mediate these differences. This information is required not only to refine treatment options for obese premenopausal women but also to potentially reveal new therapeutic avenues in obese men and women.
authors.affiliation: Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, OR 97239, United States. Electronic address: brooksv@ohsu.edu.
authors.forename: Virginia L
authors.initials: VL
authors.lastname: Brooks
authors.affiliation: Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, OR 97239, United States.
authors.forename: Zhigang
authors.initials: Z
authors.lastname: Shi
authors.affiliation: Department of Medical Pharmacology and Physiology, Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO 65212, United States.
authors.forename: Seth W
authors.initials: SW
authors.lastname: Holwerda
authors.affiliation: Department of Medical Pharmacology and Physiology, Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO 65212, United States.
authors.forename: Paul J
authors.initials: PJ
authors.lastname: Fadel
mesh_terms: D001794:Blood Pressure / Q000502:physiology; D005260:Female; D006801:Humans; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000378:metabolism; D008297:Male; D009765:Obesity / Q000473:pathology*; D012727:Sex Characteristics; D013564:Sympathetic Nervous System / Q000378:metabolism / Q000503:physiopathology*; D014661:Vasoconstriction / Q000502:physiology
chemical_list: D007328:Insulin; D020738:Leptin
keywords: Blood pressure; Insulin; Leptin; Sex differences; Vasoconstriction; Visceral obesity