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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

[3H]Nisoxetine (NIS) binding density is increased in brown adipose tissue, but not in left ventricle from angiotensin II (AngII)-infused rats. Rats were administered saline- or AngII (200–600 ng/kg per minute) for 14 days. ISBAT (A) and LV (B) were removed and membranes prepared for saturation isotherm binding using [3H] NIS as a ligand for the norepinephrine (NE) uptake transporter as described in methods. Data are mean ± SEM from n = 8 rats/dose of AngII; “*” denotes significantly different from saline-infused rats (P < 0.05).
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fig03: [3H]Nisoxetine (NIS) binding density is increased in brown adipose tissue, but not in left ventricle from angiotensin II (AngII)-infused rats. Rats were administered saline- or AngII (200–600 ng/kg per minute) for 14 days. ISBAT (A) and LV (B) were removed and membranes prepared for saturation isotherm binding using [3H] NIS as a ligand for the norepinephrine (NE) uptake transporter as described in methods. Data are mean ± SEM from n = 8 rats/dose of AngII; “*” denotes significantly different from saline-infused rats (P < 0.05).

Mentions: Saturation isotherms for [3H]NIS binding were performed in ISBAT and LV from saline or AngII-infused rats. In ISBAT membranes from all rats, [3H]NIS binding was saturable, of high affinity (nmol/L) and to a single class of sites. There was no effect of AngII infusion on the affinity of [3H]NIS binding (data not shown). Infusion of AngII resulted in a dose-dependent significant increase in the density of [3H]NIS binding sites in ISBAT membranes (Fig. 3A; P < 0.05). At 400 ng/kg per minute of AngII, [3H]NIS binding density in ISBAT was increased by 77%. At 600 ng/kg per minute of AngII infusion, [3H]NIS binding density in ISBAT was significantly increased (by 63%) compared to control, but was not increased compared to 400 ng/kg per minute. In LV, [3H]NIS bound to a single class of sites (data not shown). Moreover, in tissues from saline rats, the density of [3H]NIS binding sites was 9.5-fold lower in LV than ISBAT (Fig. 3A and B). Chronic infusion of AngII at any dose did not significantly alter [3H]NIS binding density (Fig. 3B) or affinity (data not shown) in LV compared to saline.


Angiotensin II Stimulates Sympathetic Neurotransmission to Adipose Tissue.

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

[3H]Nisoxetine (NIS) binding density is increased in brown adipose tissue, but not in left ventricle from angiotensin II (AngII)-infused rats. Rats were administered saline- or AngII (200–600 ng/kg per minute) for 14 days. ISBAT (A) and LV (B) were removed and membranes prepared for saturation isotherm binding using [3H] NIS as a ligand for the norepinephrine (NE) uptake transporter as described in methods. Data are mean ± SEM from n = 8 rats/dose of AngII; “*” denotes significantly different from saline-infused rats (P < 0.05).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig03: [3H]Nisoxetine (NIS) binding density is increased in brown adipose tissue, but not in left ventricle from angiotensin II (AngII)-infused rats. Rats were administered saline- or AngII (200–600 ng/kg per minute) for 14 days. ISBAT (A) and LV (B) were removed and membranes prepared for saturation isotherm binding using [3H] NIS as a ligand for the norepinephrine (NE) uptake transporter as described in methods. Data are mean ± SEM from n = 8 rats/dose of AngII; “*” denotes significantly different from saline-infused rats (P < 0.05).
Mentions: Saturation isotherms for [3H]NIS binding were performed in ISBAT and LV from saline or AngII-infused rats. In ISBAT membranes from all rats, [3H]NIS binding was saturable, of high affinity (nmol/L) and to a single class of sites. There was no effect of AngII infusion on the affinity of [3H]NIS binding (data not shown). Infusion of AngII resulted in a dose-dependent significant increase in the density of [3H]NIS binding sites in ISBAT membranes (Fig. 3A; P < 0.05). At 400 ng/kg per minute of AngII, [3H]NIS binding density in ISBAT was increased by 77%. At 600 ng/kg per minute of AngII infusion, [3H]NIS binding density in ISBAT was significantly increased (by 63%) compared to control, but was not increased compared to 400 ng/kg per minute. In LV, [3H]NIS bound to a single class of sites (data not shown). Moreover, in tissues from saline rats, the density of [3H]NIS binding sites was 9.5-fold lower in LV than ISBAT (Fig. 3A and B). Chronic infusion of AngII at any dose did not significantly alter [3H]NIS binding density (Fig. 3B) or affinity (data not shown) in LV compared to saline.

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