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The effects of chronic activation of...

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The effects of chronic activation of endothelin ETB receptors on blood pressure, venomotor tone, neurohumoral activity, and oxidative stress.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	The effects of chronic activation of endothelin ETB receptors on blood pressure, venomotor tone, neurohumoral activity, and oxidative stress./
Author:	Li, Melissa Wei.
Description:	214 p.
Notes:	Adviser: Gregory D. Fink.
Contained By:	Dissertation Abstracts International69-09B.
Subject:	Biology, Neuroscience. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3331962
ISBN:	9780549837510

The effects of chronic activation of endothelin ETB receptors on blood pressure, venomotor tone, neurohumoral activity, and oxidative stress.
Li, Melissa Wei.

The effects of chronic activation of endothelin ETB receptors on blood pressure, venomotor tone, neurohumoral activity, and oxidative stress. - 214 p.

Adviser: Gregory D. Fink.

Thesis (Ph.D.)--Michigan State University, 2008.

Activation of endothelin ETB receptors (ETBRs) modulates blood pressure by affecting several different physiological systems. The stimulation of ETBRs is known to cause transient arterial relaxation, a marked increase in renal excretion of sodium and water, and a clearance of endogenous endothelin-1 (ET-1). It is reasonable to speculate that the depressor and natriuretic effects induced by ETBR activation would cause blood pressure to decrease. Our lab, however, revealed for the first time that chronic activation (5 days) of ETBRs using intravenous infusion of the ETBR selective agonist sarafotoxin 6c (S6c) in rats caused a seemingly paradoxical increase in arterial pressure ( S6c-induced hypertension).

ISBN: 9780549837510Subjects--Topical Terms:

1017680
Biology, Neuroscience.

The effects of chronic activation of endothelin ETB receptors on blood pressure, venomotor tone, neurohumoral activity, and oxidative stress.
LDR:03789nam 2200313 a 45 001 855230
005 20100708
008 100708s2008 ||||||||||||||||| ||eng d
020 $a 9780549837510
035 $a (UMI)AAI3331962
035 $a AAI3331962
040 $a UMI $c UMI
100 1 $a Li, Melissa Wei. $3 1021785
245 1 4 $a The effects of chronic activation of endothelin ETB receptors on blood pressure, venomotor tone, neurohumoral activity, and oxidative stress.
300 $a 214 p.
500 $a Adviser: Gregory D. Fink.
500 $a Source: Dissertation Abstracts International, Volume: 69-09, Section: B, page: 5339.
502 $a Thesis (Ph.D.)--Michigan State University, 2008.
520 $a Activation of endothelin ETB receptors (ETBRs) modulates blood pressure by affecting several different physiological systems. The stimulation of ETBRs is known to cause transient arterial relaxation, a marked increase in renal excretion of sodium and water, and a clearance of endogenous endothelin-1 (ET-1). It is reasonable to speculate that the depressor and natriuretic effects induced by ETBR activation would cause blood pressure to decrease. Our lab, however, revealed for the first time that chronic activation (5 days) of ETBRs using intravenous infusion of the ETBR selective agonist sarafotoxin 6c (S6c) in rats caused a seemingly paradoxical increase in arterial pressure ( S6c-induced hypertension).
520 $a I proposed the hypothesis that S6c-induced hypertension is mediated by direct venoconstriction, increased sympathetic activity to the splanchnic region mediated by elevated reactive oxygen species levels in sympathetic ganglia, and increased release of vasodilating neurotransmitters from sensory nerves.
520 $a Most studies of hypertension have focused on altered regulation of the arterial vasculature. It is true that arterial resistance is elevated in hypertension. However, there is also a decrease in venous capacitance. Unfortunately, there have been few studies of the mechanisms causing constriction of veins in hypertension. Since S6c is a selective venoconstrictor, venoconstriction may mediate S6c-induced hypertension. Since the splanchnic veins are the main capacitance region of the circulation, I focused on the effects of ETBR activation in the splanchnic bed in my thesis project. In addition, celiac ganglionectomy (CGX) attenuated S6c-induced hypertension, indicating that sympathetic innervation participates in this hypertension model as well. My data also show that there was an increased neuronal, but not vascular, superoxide level in S6c-induced hypertension. Systemic treatment of antioxidant (tempol) lowered neuronal oxidative stress and blood pressure, suggesting that S6c-induced hypertension is partially mediated by sympathoexcitation to the splanchnic organs driven by increased oxidative stress in sympathetic ganglia. In ETBR-deficient transgenic (Tg) rats, ETBRs are not functional in endothelium, smooth muscle, or renal tubules. The only place where ETBRs are functional is where dopamine-beta-hydroxylase is expressed. When CGX Tg wildtype (+/+) received S6c, the increase in blood pressure was attenuated.
520 $a The results of my work provide strong evidence that S6c-induced hypertension is mediated by increased splanchnic sympathetic activity at least partially driven by increased neuronal superoxide level. Therefore, my studies provide more information on how oxidative stress and sympathetic innervation contribute to blood pressure regulation.
590 $a School code: 0128.
650 4 $a Biology, Neuroscience. $3 1017680
650 4 $a Health Sciences, Pharmacology. $3 1017717
690 $a 0317
690 $a 0419
710 2 $a Michigan State University. $3 676168
773 0 $t Dissertation Abstracts International $g 69-09B.
790 $a 0128
790 1 0 $a Fink, Gregory D., $e advisor
791 $a Ph.D.
792 $a 2008
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3331962