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Neurocirculatory responses to muscle...

Greaney, Jody Leigh.

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Neurocirculatory responses to muscle contraction in aging and hypertension.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Neurocirculatory responses to muscle contraction in aging and hypertension./
Author:	Greaney, Jody Leigh.
Description:	176 p.
Notes:	Source: Dissertation Abstracts International, Volume: 75-01(E), Section: B.
Contained By:	Dissertation Abstracts International75-01B(E).
Subject:	Biology, Physiology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3594918
ISBN:	9781303398049

Neurocirculatory responses to muscle contraction in aging and hypertension.
Greaney, Jody Leigh.

Neurocirculatory responses to muscle contraction in aging and hypertension. - 176 p.

Source: Dissertation Abstracts International, Volume: 75-01(E), Section: B.

Thesis (Ph.D.)--University of Delaware, 2013.

Our goal, was to further investigate the mechanisms underlying altered neural cardiovascular control during muscle contraction in aging and in hypertension, utilizing a detailed assessment of the neurocirculatory responses to exercise.

ISBN: 9781303398049Subjects--Topical Terms:

1017816
Biology, Physiology.

Neurocirculatory responses to muscle contraction in aging and hypertension.
LDR:05371nam a2200313 4500 001 1965936
005 20141124082814.5
008 150210s2013 ||||||||||||||||| ||eng d
020 $a 9781303398049
035 $a (MiAaPQ)AAI3594918
035 $a AAI3594918
040 $a MiAaPQ $c MiAaPQ
100 1 $a Greaney, Jody Leigh. $3 2102687
245 1 0 $a Neurocirculatory responses to muscle contraction in aging and hypertension.
300 $a 176 p.
500 $a Source: Dissertation Abstracts International, Volume: 75-01(E), Section: B.
500 $a Adviser: William B. Farquhar.
502 $a Thesis (Ph.D.)--University of Delaware, 2013.
520 $a Our goal, was to further investigate the mechanisms underlying altered neural cardiovascular control during muscle contraction in aging and in hypertension, utilizing a detailed assessment of the neurocirculatory responses to exercise.
520 $a The first series of studies examined the neurocirculatory responses to exercise in 13 older normotensive adults [normal BP group (NBP)] and 17 older adults with elevated systolic BP [i.e. systolic BP > 130 mmHg; high BP group (HBP)]. We assessed arterial BP and MSNA during a bout of static handgrip (HG) followed by a period of post-exercise ischemia (PEI), an technique to experimentally isolate the muscle metaboreflex. Compared to NBP adults, during static HG, HBP adults had greater increases in mean BP (Delta17+/-2 NBP v. Delta25+/-2 HBP mmHg; P<0.05) and MSNA burst frequency (Delta13+/-4 NBP. v. Delta22+/-2 HBP bursts/min; P<0.05). These exaggerated responses were maintained during isolated activation of the muscle metaboreflex in the HBP group (BP: Delta12+/-2 NBP v. Delta17+/-2 HBP mmHg, P=0.06; MSNA burst frequency: Delta7+/-2 NBP v. Delta17+/-2 HBP bursts/min, P<0.05). A secondary aim of this study was to examine the contribution of purinergic (P2) receptors to the exaggerated neurocirculatory responses to exercise in the HBP group. To this end, we assessed the pressor and sympathetic responses to EPR activation during a control trial (normal saline; NS) and during P2 receptor blockade (pyridoxine hydrochloride; Px). Px blunted the ATP-induced increase in intracellular calcium in isolated dorsal root ganglion cells (Delta73+/-15 NS v. Delta11+/-3 Px nM; P<0.05), indicating that Px is a viable P2 receptor antagonist in neuronal cells. Local P2 receptor blockade partially attenuated the exaggerated sympathetic response to isolated metaboreflex activation in HBP adults (40+/-4 NS v. 34+/-5 Px bursts/min; P<0.05), but had no effect in NBP adults. Collectively, these findings suggest a modest role of P2 receptors in evoking the exaggerated sympathetic responses to EPR activation in adults with HBP.
520 $a Given the evidence in animal models of hypertension suggesting that an overactive mechanoreflex contributes to altered neurocirculatory responses to muscle contraction, in the second investigation, we examined a potential role for the muscle mechanoreflex in contributing to the exaggerated pressor and sympathetic responses to exercise in adults with hypertension. We measured BP and MSNA at the immediate onset (i.e. <30 sec) of graded intensity static HG in 23 normotensive (NTN) and 15 hypertensive (HTN) adults. Compared to NTN adults, HTN demonstrated augmented increases in mean BP and MSNA burst frequency at the onset of both moderate- (BP: Delta7+/-1 NTN v. Delta14+/-3 HTN mmHg; MSNA burst frequency: Delta-2+/-1 NTN v. Delta5+/-3 HTN bursts/min; P<0.05 for both) and high-intensity static HG (BP: Delta8+/-1 NTN v. Delta18+/-3 HTN mmHg; MSNA burst frequency: Delta2+/-1 NTN v. Delta11+/-3 HTN bursts/min; P<0.05 for both). The neurocirculatory responses to the cold pressor test, a generalized sympathoexcitatory stimulus, were not different between groups. These data suggest that rapid onset sympathoexcitation in response to muscle contraction contributes, in part, to the exaggerated pressor responses to exercise characteristic of HTN humans.
520 $a Lastly, given the evidence in young adults demonstrating a neural interaction between the arterial baroreflex and the muscle metaboreflex, as a first step to understanding how this neural interaction may potentially contribute to altered neurocirculatory responses to exercise in cardiovascular pathology, we examined sympathetic baroreflex sensitivity during isolated metaboreflex activation in healthy older adults. We assessed this neural interaction by examining sympathetic baroreflex sensitivity (i.e., gain around the operating point) during isolated metaboreflex activation in 10 young men and 9 older men. There were no age-related differences in the pressor and sympathetic responses to metaboreflex activation. In addition, the magnitude of the increase in gain of arterial baroreflex control of total MSNA during PEI was not different between groups (Delta2.6+/-0.7 AU/beat/mmHg young v. Delta2.6+/-0.7 AU/beat/mmHg older; P>0.05). These data suggest that the neural interaction between the arterial baroreflex and the skeletal muscle metaboreflex is preserved in healthy aging. (Abstract shortened by UMI.).
590 $a School code: 0060.
650 4 $a Biology, Physiology. $3 1017816
650 4 $a Health Sciences, Aging. $3 1669845
690 $a 0719
690 $a 0493
710 2 $a University of Delaware. $b Biological Sciences. $3 2102688
773 0 $t Dissertation Abstracts International $g 75-01B(E).
790 $a 0060
791 $a Ph.D.
792 $a 2013
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3594918