Arteriolar network responses to opposing dilator and constrictor stimuli: Mechanism of sympathetic attenuation during muscle contraction.

Persistent Link:
http://hdl.handle.net/10150/184572
Title:
Arteriolar network responses to opposing dilator and constrictor stimuli: Mechanism of sympathetic attenuation during muscle contraction.
Author:
Dodd, Laurie Rose.
Issue Date:
1988
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
Evidence suggests different sections of the arteriolar network supplying muscle can respond independently and this may provide a mechanism for the localized distribution of blood flow. This hypothesis was tested in the microcirculation of the cat sartorius muscle by measurement of arteriolar diameter changes during muscle contraction and sympathetic nerve stimulation in each consecutive section of the network. The diameter changes were referenced to the initial distribution of resistance across the network, as determined from arteriolar pressure measurements and morphometric data. This led to an estimate of the change in network resistance. Unlike previous reports, the most distal arterioles dilated little during muscle contraction and our resistance estimate indicates these vessels play an insignificant role in functional hyperemia. The more proximal, third order arterioles dilated proportionately more than other arteriolar orders and made the largest single contribution to resting resistance. Similarly, these vessels were the largest single site of resistance change during sympathetic stimulation. Together, these findings suggest the third order arterioles play a dominant role in regulating flow to the capillaries that each supplies. Antagonism of sympathetic control during muscle contraction has been attributed to direct inhibition of vascular smooth muscle contraction and to inhibition of sympathetic neurotransmission. Evidence to support the latter mechanism comes from the observation that functional dilation is reduced with exogenous norepinephrine as compared to sympathetic stimulation. However, exogenous norepinephrine may bind to both alpha-1 and alpha-2 adrenergic receptors, whereas that released by sympathetic stimulation may bind primarily to alpha-1 receptors. Since this difference could be significant, functional dilation after systemic injection of norepinephrine or phenylephrine, a selective alpha-1 agonist, was compared to that during sympathetic stimulation. In contrast to the findings with norepinephrine, functional dilation after phenylephrine did not differ from that observed during sympathetic stimulation. This indicates the dilator substance(s) released during exercise may selectively inhibit alpha-1 mediated vasoconstriction but less effectively inhibit vasoconstriction mediated by alpha-2 receptors. Furthermore, these findings suggest that the vasodilator mechanism may act primarily at the level of the vascular smooth muscle, without appreciable pre-junctional inhibition of sympathetic nerves.
Type:
text; Dissertation-Reproduction (electronic)
Keywords:
Regional blood flow -- Measurement.; Microcirculation -- Measurement.; Muscle contraction.
Degree Name:
Ph.D.
Degree Level:
doctoral
Degree Program:
Physiology; Graduate College
Degree Grantor:
University of Arizona
Advisor:
Johnson, Paul C.

Full metadata record

DC FieldValue Language
dc.language.isoenen_US
dc.titleArteriolar network responses to opposing dilator and constrictor stimuli: Mechanism of sympathetic attenuation during muscle contraction.en_US
dc.creatorDodd, Laurie Rose.en_US
dc.contributor.authorDodd, Laurie Rose.en_US
dc.date.issued1988en_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractEvidence suggests different sections of the arteriolar network supplying muscle can respond independently and this may provide a mechanism for the localized distribution of blood flow. This hypothesis was tested in the microcirculation of the cat sartorius muscle by measurement of arteriolar diameter changes during muscle contraction and sympathetic nerve stimulation in each consecutive section of the network. The diameter changes were referenced to the initial distribution of resistance across the network, as determined from arteriolar pressure measurements and morphometric data. This led to an estimate of the change in network resistance. Unlike previous reports, the most distal arterioles dilated little during muscle contraction and our resistance estimate indicates these vessels play an insignificant role in functional hyperemia. The more proximal, third order arterioles dilated proportionately more than other arteriolar orders and made the largest single contribution to resting resistance. Similarly, these vessels were the largest single site of resistance change during sympathetic stimulation. Together, these findings suggest the third order arterioles play a dominant role in regulating flow to the capillaries that each supplies. Antagonism of sympathetic control during muscle contraction has been attributed to direct inhibition of vascular smooth muscle contraction and to inhibition of sympathetic neurotransmission. Evidence to support the latter mechanism comes from the observation that functional dilation is reduced with exogenous norepinephrine as compared to sympathetic stimulation. However, exogenous norepinephrine may bind to both alpha-1 and alpha-2 adrenergic receptors, whereas that released by sympathetic stimulation may bind primarily to alpha-1 receptors. Since this difference could be significant, functional dilation after systemic injection of norepinephrine or phenylephrine, a selective alpha-1 agonist, was compared to that during sympathetic stimulation. In contrast to the findings with norepinephrine, functional dilation after phenylephrine did not differ from that observed during sympathetic stimulation. This indicates the dilator substance(s) released during exercise may selectively inhibit alpha-1 mediated vasoconstriction but less effectively inhibit vasoconstriction mediated by alpha-2 receptors. Furthermore, these findings suggest that the vasodilator mechanism may act primarily at the level of the vascular smooth muscle, without appreciable pre-junctional inhibition of sympathetic nerves.en_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
dc.subjectRegional blood flow -- Measurement.en_US
dc.subjectMicrocirculation -- Measurement.en_US
dc.subjectMuscle contraction.en_US
thesis.degree.namePh.D.en_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplinePhysiologyen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorJohnson, Paul C.en_US
dc.contributor.committeememberSeals, Douglas R.en_US
dc.contributor.committeememberKreulen, David L.en_US
dc.contributor.committeememberSecomb, Timothy W.en_US
dc.contributor.committeememberHasan, Ziaulen_US
dc.identifier.proquest8906383en_US
dc.identifier.oclc701552650en_US
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