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Coronary perivascular adipose tissue...

Noblet, Jillian Nicole.

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Coronary perivascular adipose tissue and vascular smooth muscle function: Influence of obesity.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Coronary perivascular adipose tissue and vascular smooth muscle function: Influence of obesity./
作者:	Noblet, Jillian Nicole.
面頁冊數:	211 p.
附註:	Source: Dissertation Abstracts International, Volume: 77-09(E), Section: B.
Contained By:	Dissertation Abstracts International77-09B(E).
標題:	Physiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10107419
ISBN:	9781339708201

Coronary perivascular adipose tissue and vascular smooth muscle function: Influence of obesity.
Noblet, Jillian Nicole.

Coronary perivascular adipose tissue and vascular smooth muscle function: Influence of obesity. - 211 p.

Source: Dissertation Abstracts International, Volume: 77-09(E), Section: B.

Thesis (Ph.D.)--Indiana University - Purdue University Indianapolis, 2016.

Factors released from coronary perivascular adipose tissue (PVAT), which surrounds large coronary arteries, have been implicated in the development of coronary disease. However, the precise contribution of coronary PVAT-derived factors to the initiation and progression of coronary vascular dysfunction remains ill defined. Accordingly, this investigation was designed to delineate the mechanisms by which PVAT-derived factors influence obesity-induced coronary smooth muscle dysfunction. Isometric tension studies of coronary arteries from lean and obese swine demonstrated that both lean and obese coronary PVAT attenuate vasodilation via inhibitory effects on smooth muscle K+ channels. Specifically, lean coronary PVAT attenuated KCa and K V7 channel-mediated dilation, whereas obese coronary PVAT impaired K ATP channel-mediated dilation. Importantly, these effects were independent of alterations in underlying smooth muscle function in obese arteries. The PVAT-derived factor calpastatin impaired adenosine dilation in lean but not obese arteries, suggesting that alterations in specific factors may contribute to the development of smooth muscle dysfunction. Further studies tested the hypothesis that leptin, which is expressed in coronary PVAT and is upregulated in obesity, acts as an upstream mediator of coronary smooth muscle dysfunction. Long-term administration (3 day culture) of obese concentrations of leptin markedly altered the coronary artery proteome, favoring pathways associated with calcium signaling and cellular proliferation. Isometric tension studies demonstrated that short-term (30 min) exposure to leptin potentiated depolarization-induced contraction of coronary arteries and that this effect was augmented following longer-term leptin administration (3 days). Inhibition of Rho kinase reduced leptin-mediated increases in coronary artery contractions. Acute treatment was associated with increased Rho kinase activity, whereas longer-term exposure was associated with increases in Rho kinase protein abundance. Alterations in Rho kinase signaling were also associated with leptin-mediated increases in coronary vascular smooth muscle proliferation. These findings provide novel mechanistic evidence linking coronary PVAT with vascular dysfunction and further support a role for coronary PVAT in the pathogenesis of coronary disease.

ISBN: 9781339708201Subjects--Topical Terms:

518431
Physiology.

Coronary perivascular adipose tissue and vascular smooth muscle function: Influence of obesity.
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