AJP - Heart Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Heart Circ Physiol 248: H678-H687, 1985;
0363-6135/85 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Beaty, O.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Beaty, O., 3rd

AJP - Heart and Circulatory Physiology, Vol 248, Issue 5 678-H687, Copyright © 1985 by American Physiological Society


ARTICLES

Arterial blood pressure control during hindlimb and forelimb contraction in the dog

O. Beaty 3rd

This study examined the differential reflex cardiovascular responses evoked by separate contractions of the right hindlimb and forelimb and established the mechanism of a regional reflex vasodilation associated with hindlimb skeletal muscle contraction. The two groups of skeletal muscle were contracted separately by electrical stimulation (2-48 Hz) of the peripheral motor nerves. The left nonexercising hindlimb was perfused at constant flow. All blood pressure-regulating mechanisms were intact. Arterial blood pressure (ABP), left nonexercising hindlimb perfusion pressure (HLPP), and heart rate (HR) were recorded. HR was increased by skeletal muscle contraction. This response was independent of muscle group and contraction frequency. Increases in both ABP and HLPP were produced by high-frequency contractions (greater than 16 Hz) of either the hindlimb or forelimb. Decreases were evoked only by hindlimb contractions (greater than 8 Hz). The nonexercising skeletal muscle vascular bed contributed to this systemic depressor response by vasodilating. The mechanism involved a contraction-induced withdrawal of sympathetic nerve activity to that vascular bed. Concomitant with this response was an increase in heart rate that was blocked with propranolol. Similar heart rate changes evoked by forelimb contractions also were blocked with propranolol. These data indicate that sympathetic outflow to resting skeletal muscle depends on the origin and magnitude of the afferent signal from the contracting skeletal muscle.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online