The Exercise Pressor Reflex Evoked by Static Contraction is influenced by the Active Skeletal Muscle Mass in Decerebrated Rats

The periaqueductal gray (PAG) of the midbrain is involved in the autonomic regulation of the cardiovascular system. The purpose of this study was to determine if static contraction of the skeletal muscle, which increases arterial blood pressure and heart rate, activates neuronal cells in the PAG by examining Fos-like immunoreactivity (FLI). Muscle contraction was induced by electrical stimulation of the L7 and S1 ventral roots of the spinal cord in anesthetized cats. An intravenous infusion of phenylephrine (PE) was used to selectively activate arterial baroreceptors. Extensive FLI was observed within the ventromedial region (VM) of the rostral PAG, the dorsolateral (DL), lateral (L), and ventrolateral (VL) regions of the middle and caudal PAG in barointact animals with muscle contractions, and in barointact animals with PE infusion. However, muscle contraction caused a lesser number of FLI in the VM region of the rostral PAG, the DL, L, and VL regions of the middle PAG and the L and VL regions of the caudal PAG after barodenervation compared with barointact animals. Additionally, the number of FLI in the DL and L regions of the middle PAG was greater in barodenervated animals with muscle contraction than in barodenervated control animals. Thus these results indicated that both muscle receptor and baroreceptor afferent inputs activate neuronal cells in regions of the PAG during muscle contraction. Furthermore, afferents from skeletal muscle activate neurons in specific regions of the PAG independent of arterial baroreceptor input. Therefore, neuronal cells in the PAG may play a role in determining the cardiovascular responses during the exercise pressor reflex.

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Exercise pressor reflex function in female rats fluctuates with the estrous cycle

Journal of Applied Physiology ◽

10.1152/japplphysiol.00396.2012 ◽

2012 ◽

Vol 113 (5) ◽

pp. 719-726 ◽

Cited By ~ 2

Author(s):

Satoshi Koba ◽

Kenshi Yoshinaga ◽

Sayaka Fujita ◽

Michio Miyoshi ◽

Tatsuo Watanabe

Keyword(s):

Skeletal Muscle ◽

Muscle Contraction ◽

Estrous Cycle ◽

Plasma Concentrations ◽

Female Rats ◽

Lumbar Spinal Cord ◽

Exercise Pressor Reflex ◽

Skeletal Muscle Contraction ◽

Static Contraction ◽

Pressor Reflex

In women, sympathoexcitation during static handgrip exercise is reduced during the follicular phase of the ovarian cycle compared with the menstrual phase. Previous animal studies have demonstrated that estrogen modulates the exercise pressor reflex, a sympathoexcitatory mechanism originating in contracting skeletal muscle. The present study was conducted in female rats to determine whether skeletal muscle contraction-evoked reflex sympathoexcitation fluctuates with the estrous cycle. The estrous cycle was judged by vaginal smear. Plasma concentrations of estrogen were significantly ( P < 0.05) higher in rats during the proestrus phase of the estrus cycle than those during the diestrus phase. In decerebrate rats, either electrically induced 30-s continuous static contraction of the hindlimb muscle or 30-s passive stretch of Achilles tendon (a maneuver that selectively stimulates mechanically sensitive muscle afferents) evoked less renal sympathoexcitatory and pressor responses in the proestrus animals than in the diestrus animals. Renal sympathoexcitatory response to 1-min intermittent (1- to 4-s stimulation to relaxation) bouts of static contraction was also significantly less in the proestrus rats than that in the diestrus rats. In ovariectomized female rats, 17β-estradiol applied into a well covering the dorsal surface of the lumbar spinal cord significantly reduced skeletal muscle contraction-evoked responses. These observations demonstrate that the exercise pressor reflex function and its mechanical component fluctuate with the estrous cycle in rats. Estrogen may cause these fluctuations through its attenuating effects on the spinal component of the reflex arc.

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Acid-sensing ion channels contribute to the metaboreceptor component of the exercise pressor reflex

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00328.2009 ◽

2009 ◽

Vol 297 (1) ◽

pp. H443-H449 ◽

Cited By ~ 31

Author(s):

Jennifer L. McCord ◽

Hirotsugu Tsuchimochi ◽

Marc P. Kaufman

Keyword(s):

Skeletal Muscle ◽

Ion Channels ◽

Pressor Response ◽

Triceps Surae ◽

Exercise Pressor Reflex ◽

Acid Sensing Ion Channels ◽

Pressor Responses ◽

Static Contraction ◽

Pressor Reflex ◽

Triceps Surae Muscles

The exercise pressor reflex is evoked by both mechanical and metabolic stimuli arising in contracting skeletal muscle. Recently, the blockade of acid-sensing ion channels (ASICs) with amiloride and A-316567 attenuated the reflex. Moreover, amiloride had no effect on the mechanoreceptor component of the reflex, prompting us to determine whether ASICs contributed to the metaboreceptor component of the exercise pressor reflex. The metaboreceptor component can be assessed by measuring mean arterial pressure during postcontraction circulatory occlusion when only the metaboreceptors are stimulated. We examined the effects of amiloride (0.5 μg/kg), A-317567 (10 mM, 0.5 ml), and saline (0.5 ml) on the pressor response to and after static contraction while the circulation was occluded in 30 decerebrated cats. Amiloride ( n = 11) and A-317567 ( n = 7), injected into the arterial supply of the triceps surae muscles, attenuated the pressor responses both to contraction while the circulation was occluded and to postcontraction circulatory occlusion (all, P < 0.05). Saline ( n = 11), however, had no effect on the pressor responses to contraction while the circulation was occluded or to postcontraction circulatory occlusion (both, P > 0.79). Our findings led us to conclude that ASICs contribute to the metaboreceptor component of the exercise pressor reflex.

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Bradykinin release from contracting skeletal muscle of the cat

Journal of Applied Physiology ◽

10.1152/jappl.1990.69.4.1225 ◽

1990 ◽

Vol 69 (4) ◽

pp. 1225-1230 ◽

Cited By ~ 62

Author(s):

C. L. Stebbins ◽

O. A. Carretero ◽

T. Mindroiu ◽

J. C. Longhurst

Keyword(s):

Skeletal Muscle ◽

Arterial Occlusion ◽

Triceps Surae ◽

Strongly Correlated ◽

Exercise Pressor Reflex ◽

Static Contraction ◽

Before And After ◽

Pressor Reflex ◽

Triceps Surae Muscles ◽

Induced Changes

Results of previous studies from our laboratory suggest that bradykinin has a role in the exercise pressor reflex elicited by static muscle contraction. The purpose of this study was to quantify the release of bradykinin from contracting skeletal muscle. In 18 cats, blood samples were withdrawn directly from the venous effluent of the triceps surae muscles immediately before and after 30 s of static contraction producing peak muscle tensions of 33, 50, and 100% of maximum electrically stimulated contraction. Contractions producing muscle tensions of 50 and 100% of maximum increased muscle venous bradykinin levels by 27 +/- 9 and 19 +/- 10 pg/ml, respectively. Conversely, 33% maximum contraction did not alter muscle venous bradykinin concentrations. However, when captopril was administered to slow the degradation of bradykinin, muscle venous bradykinin increased from 68 +/- 15 pg/ml at rest to 106 +/- 18 after contractions of 33% of maximum. When muscle ischemia was induced by 2 min of arterial occlusion before and during 30 s of 33% of maximum contraction, muscle venous bradykinin increased by 15 +/- 5 pg/ml. In addition, contraction-induced changes in muscle venous pH and lactate strongly correlated with bradykinin concentrations (r = 0.80 and 0.83, respectively). These data demonstrate that static contraction of relatively high intensity evokes the release of bradykinin from skeletal muscle and that ischemia, decreased pH, and increased lactate are strongly correlated with this release.

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