Neurally mediated renal vasoconstriction during isometric muscle contraction in cats

Abstract

The aim of this study was to determine if the reflex increase in renal sympathetic nerve activity (RSNA) during static (isometric) muscle contraction evokes renal vasoconstriction and decreases renal blood flow. RSNA, renal blood flow velocity, and arterial pressure were measured simultaneously during isometric contraction of the hindlimb triceps surae muscle in eight chloralose-anesthetized cats. A 1-min contraction was evoked by stimulating the peripheral ends of the cut L7 and S1 ventral roots. RSNA and mean arterial pressure (MAP) increased 41 +/- 14% (SE) and 50 +/- 10 mmHg during static contraction, whereas mean renal blood flow velocity (MRBV) decreased 14 +/- 5%. Calculated renal vascular resistance increased 73 +/- 20% during the contraction. The increase in RSNA preceded the decrease in MRBV by 20 s. Passive mechanical stretch of the muscle increased RSNA 21 +/- 12% but did not alter MRBV. Renal denervation abolished the decrease in MRBV during isometric contraction but only attenuated the rise in MAP. Cutting the L4-S1 dorsal roots or muscle paralysis abolished the MRBV and MAP responses. Thus reflex stimulation of RSNA from the contracting muscle can induce renal vasoconstriction and decrease renal blood flow.

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].…”

“…Since the passive mechanical stretch of muscle in a physiological range can stimulate myelinated group III afferents rather than unmyelinated group IV afferents, a comparison in the reflex responses of sympathetic efferent nerve activity between the contraction and the mechanical stretch of skeletal muscle should lead to an insight into the afferent mechanisms in the contracting muscle. The mechanical stretch of muscle increases cardiac and renal sympathetic nerve activities to 85 and 51% of their responses observed during static contraction with the same tension development [1,3]. Regarding AdSNA, it increased immediately after the onset of static muscle contraction in anesthetized rats [5].…”

“…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-591Japanese Journal of Physiology, 51, 591-597, 2001 Key words: norepinephrine, epinephrine, adrenal medulla, adrenal sympathetic nerve activity, mechanical stretch of muscle. …”

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) .…”