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Angiotensin II Stimulates Sympathetic Neurotransmission to Adipose Tissue.

King VL, English VL, Bharadwaj K, Cassis LA - Physiol Rep (2013)

Bottom Line: These effects of AngII contribute to cardiovascular control.At doses that lowered body weight, AngII significantly increased ISBAT [(3)H]NIS binding density.AngII significantly increased the rate of NE decline in all tissues compared to saline.

View Article: PubMed Central - PubMed

Affiliation: Division of Cardiology, University of Kentucky, Lexington, KY 40536.

ABSTRACT
Angiotensin II (AngII) facilitates sympathetic neurotransmission by regulating norepinephrine (NE) synthesis, release and uptake. These effects of AngII contribute to cardiovascular control. Previous studies in our laboratory demonstrated that chronic AngII infusion decreased body weight of rats. We hypothesized that AngII facilitates sympathetic neurotransmission to adipose tissue and may thereby decrease body weight. The effect of chronic AngII infusion on the NE uptake transporter and NE turnover was examined in metabolic (interscapular brown adipose tissue, ISBAT; epididymal fat, EF) and cardiovascular tissues (left ventricle, LV; kidney) of rats. To examine the uptake transporter saturation isotherms were performed using [(3)H]nisoxetine (NIS). At doses that lowered body weight, AngII significantly increased ISBAT [(3)H]NIS binding density. To quantify NE turnover, alpha-methyl-para-tyrosine (AMPT) was injected in saline-infused, AngII-infused, or saline-infused rats that were pair-fed to food intake of AngII-infused rats. AngII significantly increased the rate of NE decline in all tissues compared to saline. The rate of NE decline in EF was increased to a similar extent by AngII and by pair-feeding. In rats administered AngII and propranolol, reductions in food and water intake and body weight were eliminated. These data support the hypothesis that AngII facilitates sympathetic neurotransmission to adipose tissue. Increased sympathetic neurotransmission to adipose tissue following AngII exposure is suggested to contribute to reductions in body weight.

No MeSH data available.


Related in: MedlinePlus

Propranolol administration prevents angiotensin II (AngII) regulation of body weight (A), food intake (B), and water intake (C). Rats were administered saline, saline + propranolol, AngII or AngII + propranolol. Arrow denotes the start of drug treatment by osmotic minipump. Data are mean ± SEM from n = 6 rats/group; “*” denotes significantly different from saline (P < 0.05).
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fig07: Propranolol administration prevents angiotensin II (AngII) regulation of body weight (A), food intake (B), and water intake (C). Rats were administered saline, saline + propranolol, AngII or AngII + propranolol. Arrow denotes the start of drug treatment by osmotic minipump. Data are mean ± SEM from n = 6 rats/group; “*” denotes significantly different from saline (P < 0.05).

Mentions: To determine if AngII-induced increases in sympathetic neurotransmission contribute to AngII-mediated reductions in body weight, the nonselective β-receptor antagonist, propranolol, was administered to rats receiving saline- and/or AngII- (400 ng/kg per minute) for 14 days. Propranolol had no effect on blood pressure in saline-infused rats (data not shown); however, propranolol administration significantly decreased the hypertensive response to AngII (AngII: 125 ± 10; AngII + prop: 102 ± 5 mmHg, P < 0.05). AngII infusion decreased body weight beginning on day 3 of infusion (Fig. 7A). Administration of propranolol to saline-infused rats resulted in a modest increase in body weight compared to saline. In rats coadministered AngII + propranolol, AngII-mediated reductions in body weight were eliminated. Moreover, propranolol administration eliminated AngII-induced reductions in food (Fig. 7B) and water intake (Fig. 7C). Propranolol administration abolished AngII-induced increases in plasma concentrations of free fatty acids (saline: 0.13 ± 0.02; AngII: 0.21 ± 0.03; saline/propranolol: 0.11 ± 0.02; AngII/propranolol: 0.08 ± 0.01 mEq/L).


Angiotensin II Stimulates Sympathetic Neurotransmission to Adipose Tissue.

King VL, English VL, Bharadwaj K, Cassis LA - Physiol Rep (2013)

Propranolol administration prevents angiotensin II (AngII) regulation of body weight (A), food intake (B), and water intake (C). Rats were administered saline, saline + propranolol, AngII or AngII + propranolol. Arrow denotes the start of drug treatment by osmotic minipump. Data are mean ± SEM from n = 6 rats/group; “*” denotes significantly different from saline (P < 0.05).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3818081&req=5

fig07: Propranolol administration prevents angiotensin II (AngII) regulation of body weight (A), food intake (B), and water intake (C). Rats were administered saline, saline + propranolol, AngII or AngII + propranolol. Arrow denotes the start of drug treatment by osmotic minipump. Data are mean ± SEM from n = 6 rats/group; “*” denotes significantly different from saline (P < 0.05).
Mentions: To determine if AngII-induced increases in sympathetic neurotransmission contribute to AngII-mediated reductions in body weight, the nonselective β-receptor antagonist, propranolol, was administered to rats receiving saline- and/or AngII- (400 ng/kg per minute) for 14 days. Propranolol had no effect on blood pressure in saline-infused rats (data not shown); however, propranolol administration significantly decreased the hypertensive response to AngII (AngII: 125 ± 10; AngII + prop: 102 ± 5 mmHg, P < 0.05). AngII infusion decreased body weight beginning on day 3 of infusion (Fig. 7A). Administration of propranolol to saline-infused rats resulted in a modest increase in body weight compared to saline. In rats coadministered AngII + propranolol, AngII-mediated reductions in body weight were eliminated. Moreover, propranolol administration eliminated AngII-induced reductions in food (Fig. 7B) and water intake (Fig. 7C). Propranolol administration abolished AngII-induced increases in plasma concentrations of free fatty acids (saline: 0.13 ± 0.02; AngII: 0.21 ± 0.03; saline/propranolol: 0.11 ± 0.02; AngII/propranolol: 0.08 ± 0.01 mEq/L).

Bottom Line: These effects of AngII contribute to cardiovascular control.At doses that lowered body weight, AngII significantly increased ISBAT [(3)H]NIS binding density.AngII significantly increased the rate of NE decline in all tissues compared to saline.

View Article: PubMed Central - PubMed

Affiliation: Division of Cardiology, University of Kentucky, Lexington, KY 40536.

ABSTRACT
Angiotensin II (AngII) facilitates sympathetic neurotransmission by regulating norepinephrine (NE) synthesis, release and uptake. These effects of AngII contribute to cardiovascular control. Previous studies in our laboratory demonstrated that chronic AngII infusion decreased body weight of rats. We hypothesized that AngII facilitates sympathetic neurotransmission to adipose tissue and may thereby decrease body weight. The effect of chronic AngII infusion on the NE uptake transporter and NE turnover was examined in metabolic (interscapular brown adipose tissue, ISBAT; epididymal fat, EF) and cardiovascular tissues (left ventricle, LV; kidney) of rats. To examine the uptake transporter saturation isotherms were performed using [(3)H]nisoxetine (NIS). At doses that lowered body weight, AngII significantly increased ISBAT [(3)H]NIS binding density. To quantify NE turnover, alpha-methyl-para-tyrosine (AMPT) was injected in saline-infused, AngII-infused, or saline-infused rats that were pair-fed to food intake of AngII-infused rats. AngII significantly increased the rate of NE decline in all tissues compared to saline. The rate of NE decline in EF was increased to a similar extent by AngII and by pair-feeding. In rats administered AngII and propranolol, reductions in food and water intake and body weight were eliminated. These data support the hypothesis that AngII facilitates sympathetic neurotransmission to adipose tissue. Increased sympathetic neurotransmission to adipose tissue following AngII exposure is suggested to contribute to reductions in body weight.

No MeSH data available.


Related in: MedlinePlus