AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 248: H688-H694, 1985;
0363-6135/85 $5.00
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AJP - Heart and Circulatory Physiology, Vol 248, Issue 5 688-H694, Copyright © 1985 by American Physiological Society


ARTICLES

Carotid sinus and blood pressure control during hindlimb and forelimb contractions

O. Beaty 3rd

Arterial blood pressure (ABP) regulation during exercise involves in part medullary interaction of afferent information from contracting skeletal muscles and the major baroreceptors. This study examined in chloralose-anesthetized dogs the role of the carotid sinus baroreceptors in modulating reflex changes in ABP, nonexercising hindlimb skeletal muscle vascular resistance, and heart rate (HR) evoked by two separately contracting (4, 16, and 48 Hz) groups of skeletal muscle, the right hindlimb and forelimb. When arterial and cardiopulmonary baroreceptor afferent information was interrupted, hindlimb contractions evoked a greater augmentation of ABP (16 and 48 Hz) and no further increase in nonexercising hindlimb perfusion pressure (HLPP). Forelimb contractions, which in the presence of baroreceptors had not affected ABP (4 and 16 Hz), now reduced it profoundly. Nonexercising HLPP, which increased independently of contraction frequency, now was decreased by 4 Hz, not affected by 16 Hz, and increased by 48 Hz. The increase in HR was abolished. Increasing carotid sinus pressure to 220 mmHg in vagotomized dogs abolished the reflex changes evoked by hindlimb skeletal muscle contractions. However, forelimb contractions continued to decrease ABP. Nonexercising HLPP and HR did not change from the precontraction values. These data indicate that the carotid sinus baroreceptor could buffer completely those changes in the selected cardiovascular variables evoked by hindlimb but not forelimb skeletal muscle contractions. Thus the role of the carotid sinus baroreceptors in controlling ABP during exercise depends on the group of skeletal muscle initiating the somatic afferent signal and its influence on the contraction-induced distribution of the efferent signals.





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