Identification and characterization of angiotensin II receptors in rat epididymal adipocyte membranes

Crandall, David L.; Herzlinger, H.; Saunders, Brian; Zolotor, R. C.; Feliciano, Lillybeth; Cervoni, Peter

doi:10.1016/0026-0495(93)90111-z

Cited by 37 publications

(11 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In rat adipocyte membranes, glucagon-like peptide-1 (1-36) amide did not stimulate [ 35 S]GTP␥S binding (not shown), which excludes the possibility that nicotinic acid might act on receptors for glucagonlike peptide-1. Membrane receptors for angiotensin II (subtype 1) have been characterized previously in rat epididymal adipocyte membranes (Crandall et al, 1993). However, angiotensin II did not mimic the stimulatory effect of nicotinic acid in G protein activation, and the angiotensin receptor antagonist [Sar 1 ,Ile 8 ]angiotensin II did not affect the stimulation by nicotinic acid (data not shown).…”

Section: Discussionmentioning

confidence: 72%

Characterization of a G Protein-Coupled Receptor for Nicotinic Acid

et al. 2001

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 72%

Characterization of a G Protein-Coupled Receptor for Nicotinic Acid

et al. 2001

View full text Add to dashboard Cite

show abstract

“…The exact nature of this metabolic effect is currently unknown and will be the subject of investigation in our laboratory. In view of the high density of AT 1 receptors on human and rat adipocytes (48,49), one can speculate that ang II may have a lipolytic effect. Our studies with the Dahl rats strongly support the hypothesis that the anorexigenic effect of ang II is not pressor related.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II causes weight loss and decreases circulating insulin-like growth factor I in rats through a pressor-independent mechanism.

Brink¹,

Wellen²,

1996

View full text Add to dashboard Cite

The renin-angiotensin system regulates normal cardiovascular homeostasis and is activated in certain forms of hypertension and in heart failure. Angiotensin II has multiple physiological effects and we have shown recently that its growth-promoting effects on vascular smooth muscle require autocrine activation of the IGF I receptor. To study the effect of angiotensin II on circulating IGF I, we infused rats with 500 ng/kg/min angiotensin II for up to 14 d. Angiotensin II markedly reduced plasma IGF I levels (56 and 41% decrease at 1 and 2 wk, respectively) and IGF binding protein-3 levels, and increased IGF binding protein-2 levels, a pattern suggestive of dietary restriction. Compared with sham, angiotensin II-infused hypertensive rats lost 18-26% of body weight by 1 wk, and pair-feeding experiments indicated that 74% of this loss was attributable to a reduction in food intake. The vasodilator hydralazine and the AT 1 receptor antagonist losartan had comparable effects to reverse angiotensin II-induced hypertension, but only losartan blocked the changes in body weight and in circulating IGF I and its binding proteins produced by angiotensin II. Moreover, in Dahl rats that were hypertensive in response to a high-salt diet, none of these changes occurred. Thus, angiotensin II produces weight loss through a pressor-independent mechanism that includes a marked anorexigenic effect and an additional (likely metabolic) effect. These findings have profound implications for understanding the pathophysiology of conditions, such as congestive heart failure, in which the renin-angiotensin system is activated. ( J. Clin. Invest. 1996. 97:2509-2516.)

show abstract

“…We previously demonstrated that rat brown and white adipose tissues exhibit a high level mRNA expression of angiotensinogen, the only known precursor to ANG II (6). Further studies demonstrated that rat and human adipose tissue possess all of the components necessary for production of ANG II, including angiotensinogen (7,15,19), renin-like activity (41), ANG-converting enzyme (ACE) (7,34,38), and the ANG type 1 (AT 1 ) receptor (4,9,10). Importantly, nutritional regulation of the angiotensinogen gene in adipose tissue has been demonstrated, with elevations in obesity and reductions with starvation (19,43).…”

mentioning

confidence: 99%

Activation of the systemic and adipose renin-angiotensin system in rats with diet-induced obesity and hypertension

Boustany

Bharadwaj

Daugherty

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

295

254

View full text Add to dashboard Cite

In obesity-related hypertension, activation of the renin-angiotensin system (RAS) has been reported despite marked fluid volume expansion. Adipose tissue expresses components of the RAS and is markedly expanded in obesity. This study evaluated changes in components of the adipose and systemic RAS in diet-induced obese hypertensive rats. RAS was quantified in adipose tissue and compared with primary sources for the circulating RAS. Male Sprague-Dawley rats were fed either a low-fat (LF; 11% kcal as fat) or moderately high-fat (32% kcal as fat) diet for 11 wk. After 8 wk, rats fed the moderately high-fat diet segregated into obesity-prone (OP) and obesity-resistant (OR) groups based on their body weight gain (body weight: OR, 566 +/- 10; OP, 702 +/- 20 g; P < 0.05). Mean arterial blood pressure was increased in OP rats (LF: 97 +/- 2; OR: 97 +/- 2; OP: 105 +/- 1 mmHg; P < 0.05). Quantification of mRNA expression by real-time PCR demonstrated a selective increase (2-fold) in angiotensinogen gene expression in retroperitoneal adipose tissue from OP vs. OR and LF rats. Similarly, plasma angiotensinogen concentration was increased in OP rats (LF: 390 +/- 48; OR: 355 +/- 24; OP: 530 +/- 22 ng/ml; P < 0.05). In contrast, other components of the RAS were not altered in OP rats. Marked increases in the plasma concentrations of angiotensin peptides were observed in OP rats (angiotensin II: LF: 95 +/- 31; OR: 59 +/- 20; OP: 295 +/- 118 pg/ml; P < 0.05). These results demonstrate increased activity of the adipose and systemic RAS in obesity-related hypertension.

show abstract

Identification and characterization of angiotensin II receptors in rat epididymal adipocyte membranes

Cited by 37 publications

References 25 publications

Characterization of a G Protein-Coupled Receptor for Nicotinic Acid

Characterization of a G Protein-Coupled Receptor for Nicotinic Acid

Angiotensin II causes weight loss and decreases circulating insulin-like growth factor I in rats through a pressor-independent mechanism.

Activation of the systemic and adipose renin-angiotensin system in rats with diet-induced obesity and hypertension

Contact Info

Product

Resources

About