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Angiotensin II‐ mediated vasoconstriction of the visceral adipose tissue vasculature is linked to systemic hypertension in obesity
Author(s) -
Park SongYoung,
Karki Shakun,
Saggese Samantha M.,
Zuriaga Maria A.,
Carmine Brian,
Hess Donald,
Apovian Caroline,
Gokce Noyan
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.684.6
Subject(s) - adipose tissue , vasoconstriction , medicine , endocrinology , angiotensin ii , phenylephrine , renin–angiotensin system , obesity , pathophysiology of hypertension , blood pressure
Objectives Central adiposity, in particular the accumulation of intra‐abdominal visceral fat, has been linked to adipose tissue dysfunction and obesity‐related diseases including hypertension and atherosclerosis, however regulatory mechanisms are poorly understood. We hypothesized that increased micro‐vascular tone specifically in visceral fat may contribute to abnormal peripheral vascular resistance. Methods In 30 obese subjects(age 42±10 yr, BMI 42±3 kg/m 2 ) undergoing elective bariatric surgery, we characterized vaso‐contractile responses of isolated subcutaneous (SC) and visceral (VIS) adipose tissue arterioles using videomicroscopy, and examined relevant depot‐specific gene expression using qPCR. Results Visceral arterioles exhibited significantly greater angiotensin II‐mediated vasoconstriction by 20% in obese hypertensives (OH, SBP 146±8 mmHg) compared to obese normotensives (O, SBP 118±5 mmHg) (p<0.05). Additionally, VIS arterioles showed greater vasoconstriction in response to angiotensin II compared to SC in OH (by 25%, p<0.05) but not in O. Angiotensin converting enzyme (ACE) mRNA expression was significantly increased in VIS compared to SC (2‐fold, p<0.05) in OH but not O. In contrast, vasopressor responses to other agonists including endothelin‐1 and phenylephrine were not different between fat depots or subjects with or without hypertension. Conclusion The findings demonstrate differential activation of the renin‐angiotensin system (RAS) in the visceral adipose tissue microvasculature that may contribute to mechanisms of systemic hypertension in obesity. RAS targeting, in particular, may provide incremental clinical benefit in treating obesity‐related hypertension. Support or Funding Information NIH grants P01HL081587 and RO1 HL1145675