Systemic beta-adrenergic stimulation resulted in higher plasma Ang II concentrations in obese compared with lean subjects (12.6 vs 8.1 pmol/L; P=0.04), alongside AGT release from adipose tissue.
Observational (n=23)
Does systemic beta-adrenergic stimulation affect the release of renin-angiotensin system components from adipose tissue and skeletal muscle in lean and obese subjects?
Angiotensinogen is released from adipose tissue and muscle during beta-adrenergic stimulation in obese subjects, providing a mechanistic link to obesity-related hypertension.
Absolute Event Rate: 12.6% vs 8.1%
p-value: p=0.04
The renin-angiotensin system has been implicated in obesity-related hypertension and insulin resistance. We examined whether locally produced components of the renin-angiotensin system in adipose tissue and skeletal muscle play an endocrine role in vivo in humans. Furthermore, the effects of beta-adrenergic stimulation on plasma concentrations and tissue release of renin-angiotensin system components were investigated. Systemic renin-angiotensin system components and arteriovenous differences of angiotensin II (Ang II) and angiotensinogen (AGT) across abdominal subcutaneous adipose tissue and skeletal muscle were assessed in combination with measurements of tissue blood flow before and during systemic beta-adrenergic stimulation in 13 lean and 10 obese subjects. Basal plasma Ang II and AGT concentrations were not significantly different between lean and obese subjects. Ang II concentrations were increased in obese compared with lean subjects during beta-adrenergic stimulation (12.6+/-1.5 versus 8.1+/-1.0 pmol/L; P=0.04), whereas AGT concentrations remained unchanged. Plasma renin activity increased to a similar extent in lean and obese subjects during beta-adrenergic stimulation (both P<0.01). No net Ang II release across adipose tissue and skeletal muscle could be detected in both groups of subjects. However, AGT was released from adipose tissue and muscle during beta-adrenergic stimulation in obese subjects (both P<0.05). In conclusion, locally produced Ang II in adipose tissue and skeletal muscle exerts no endocrine role in lean and obese subjects. In contrast, AGT is released from adipose tissue and muscle in obese subjects during beta-adrenergic stimulation, which may contribute to the increased plasma Ang II concentrations during beta-adrenergic stimulation in obese subjects.
Goossens et al. (Tue,) conducted a observational in Obesity (n=23). Systemic beta-adrenergic stimulation vs. Lean subjects was evaluated on Plasma Ang II concentrations during beta-adrenergic stimulation (p=0.04). Systemic beta-adrenergic stimulation resulted in higher plasma Ang II concentrations in obese compared with lean subjects (12.6 vs 8.1 pmol/L; P=0.04), alongside AGT release from adipose tissue.
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