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Vasoconstrictor-mediated control of thermogenesis


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Ye, Jiming 1995 , 'Vasoconstrictor-mediated control of thermogenesis', PhD thesis, University of Tasmania.

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Vasoconstrictors either stimulate or inhibit oxygen consumption (V02) in
perfused, but not in incubated or perifused, skeletal muscle. The mechanism of this
phenomenon is not fully understood. This thesis attempted to investigate the
implication of vasoconstrictor-mediated control of V02 (thus thermogenesis) in
perfused muscle as well as other tissue beds, and the mechanism involved.
Effects of vasoconstrictors on V02 were examined in the perfused hindlimbs
of rats, Tasmanian bettongs (Bettongia gaimardi) and toads (Bufo marinus) as well as
in the perfused rat kidney, intestine and mesenteric artery. In line with in vitro
experiments, the effects of adrenergic agonists on thermogenesis were further studied
in conscious adult bettongs, an endothermic animal without detectable brown adipose
Norepinephrine (NE) and vasopressin (VP) stimulated, but serotonin (5-HT)
inhibited V02 in both constant-flow and constant-pressure perfiised hindlimbs when
causing vasoconstriction. In the constant-flow (once-through) perfusion, these
changes were blocked by vasodilators (ie. nitroprusside) but not by tubocurarine.
Vasoconstrictor-mediated changes in muscle metabolism were observed in the
hindlimbs of all the three species. a-Adrenoceptors were shown to be responsible for
NE-stimulated increase in V02 . Increasing the perfusion flow by resetting at different
rates also stimulated changes in V02 in the constant-flow perfused rat hindlimb, which
could be augmented by NE but inhibited by nitroprusside.
Similarly, a vasoconstriction-associated increase or decrease in V02 was
observed in the constant-flow perfused rat kidney and intestine although the effect of
a given vasoconstrictor to stimulate or inhibit V02 was not necessarily the same as
that in the perfused hindlimb. In the perfused rat mesenteric artery all vasoconstrictors
stimulated increases in V02 in parallel with the increased perfusion pressure.
By contrast, in the constant-pressure (recirculated) perfused rat hindlimb, ß-
adrenergic agonists, isoproterenol and BRL3 5135A were also found to stimulate V02
in addition to a-adrenergic agonists and VP.
During the induced vasoconstriction or vasodilation, creatine phosphate
(CrP), AMP, ADP, ATP and lactate remained normal in all the perfused mammalian
tissues. In skeletal muscle, the energy status, as indicated by energy charge, was not
significantly different among the normal (both in vivo and control perfusion), perfused
(high flow plus NE) and ischemic (for 60 min) muscles. In contrast, CrP and Cr
differed in the three oxygenation states.
Consistent with the observations in the perfused hindlimbs in vitro, NE and
isoproterenol elicited an increase in heat production in the intact bettong.
a-Adrenergic agonists, phenylephrine and naphazoline were also found to stimulate heat
production which was not blocked by propranolol.
These results taken together suggest that skeletal muscle is a potentially
thermogenic tissue under the control Of vascular functioning. Vasoconstrictor-mediated
V02 seems to be widespread across species and tissues. This control may
play an important role in the regulation of non-shivering thermogenesis.
The results support the notion that working blood vessels may partially
account for vasoconstrictor-stimulated changes in V02. However, the data do not
exclude the hypothesis that vasoconstrictors act on site-specific receptors on
arterioles to redistribute flow to areas or cells that are metabolically more active. The
results of this thesis can not definitively distinguish between these two hypotheses.
They may not be mutually exclusive.

Item Type: Thesis - PhD
Authors/Creators:Ye, Jiming
Keywords: Vasoconstrictors, Muscles, Oxygen
Copyright Holders: The Author
Copyright Information:

Copyright 1995 the Author - The University is continuing to endeavour to trace the copyright owner(s) and in the meantime this item has been reproduced here in good faith. We would be pleased to hear from the copyright owner(s).

Additional Information:

Thesis (Ph.D.)--University of Tasmania, 1995. Includes bibliographical references (leaves 152-177)

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