Reflex stimulation of cardiac sympathetic nerve activity during static muscle contraction in cats

Abstract

Reflex response of cardiac sympathetic nerve activity (CSNA) during static contraction of the triceps surae muscle was studied using anesthetized cats. A 1-min contraction was evoked by stimulating the peripheral ends of the cut L7 and S1 ventral roots. CSNA increased 48 +/- 13% immediately after the onset of contraction, which was abolished by cutting the L4-S1 dorsal roots. This rapid increase in CSNA preceded rises in heart rate (13 +/- 1 beats/min) and arterial blood pressure (33 +/- 6 mmHg). When tension development was altered by changing the frequency of ventral root stimulation or the initial muscle length, the CSNA increase depended on the tension developed. Passive stretch of the muscle, which primarily activates mechanoreceptors, increased CSNA by 41 +/- 22%. When the contraction was sustained for 5 min, CSNA remained elevated throughout the contraction despite a fall in tension, suggesting that the later increase in CSNA is caused by factors other than a mechanical event of contraction (e.g., metabolic products). Thus it is suggested that cardiac sympathetic outflow is stimulated due to a reflex arising from the contracting muscle. The increase in CSNA at the initiation of contraction is likely to be caused by a reflex from muscle mechanoreceptors, which is followed by a subsequent increase due to a reflex from muscle metaboreceptors.

Reflex Responses in Plasma Catecholamines Caused by Static Contraction of Skeletal Muscle.

“…With respect to the reflex adjustment of the sympathetic nervous system arising from the contracting muscles, static muscle contraction reflexly augments postganglionic sympathetic nerve activities to the heart, kidney, and skeletal muscle within 10 s from the onset of static muscle contraction evoked in anesthetized animals [1][2][3][4]10]. The rapid increase in cardiac sympathetic nerve activity contributes to an acceleration of cardiac rhythm [4], and the increase in renal sympathetic nerve activity contributes to renal vasoconstriction and a reduction in renal blood flow [3].…”

“…The rapid increase in cardiac sympathetic nerve activity contributes to an acceleration of cardiac rhythm [4], and the increase in renal sympathetic nerve activity contributes to renal vasoconstriction and a reduction in renal blood flow [3]. The initial cardiovascular responses can be explained by the reflex responses of postganglionic sympathetic nerve activities to the heart and blood vessels as well as a withdrawal of cardiac parasympathetic nerve activity [11], but not by a humoral effect of circulating catecholamines.…”

“…It was demonstrated that sympathetic outflows to the heart and the kidneys increase during static muscle contraction induced by electrical stimulation of the ventral roots in anesthetized cats [1][2][3][4]. The increase in cardiac sympathetic nerve activity correlates with an increase in heart rate [3], and the increase in renal sympathetic nerve activity correlates with reduced renal blood flow [2], suggesting that the reflex changes in postganglionic sympathetic nerve activities caused by skeletal muscle contraction contribute to cardiovascular adjustments, such as increases in cardiac output and arterial blood pressure and a redistribution of car-…”

Exercise pressor reflex in health and diseases: Animal studies

“…Sympathetic nerve activities (SNA) directed toward blood vessels in a variety of organs including kidney 36,37) , skeletal muscle 38) , and heart 39) , were increased when hindlimb skeletal muscle was continuously and statically contracted in anesthetized or unanesthetized decerebrate cats. Moreover, the roles played by the EPR-evoked sympathoexcitation in mediating renal vasoconstriction 40) and tachycardia 39) have been demonstrated. Of note, skin SNA was not reflexly increased by skeletal muscle contraction 41) , suggesting that the EPR-elicited sympathetic outflows are organ-specific.…”

“…It was demonstrated in anesthetized cats that the blood pressure was reflexly elevated by passively stretching the triceps surae muscles, which did not generate any muscle metabolites 42) . Subsequent electrophysiological studies demonstrated stimulation of mechanically sensitive group III muscle afferents 43) , cardiac 39) and renal 40) SNA increases, as well as vagal withdrawal 44) , in response to muscle stretch in anesthetized or decerebrate cats. Human subjects also exhibited reflexly increased muscle SNA during passive muscle stretch 45) .…”