Cardiovascular Reflex Control by Afferent Fibers from Skeletal Muscle Receptors

2011 ◽  
Author(s):  
Jere H. Mitchell ◽  
Robert F. Schmidt
Keyword(s):  
Skeletal Muscle ◽  
Cardiovascular Reflex ◽  
Afferent Fibers ◽  
Muscle Receptors ◽  
Reflex Control

Rapid resetting of carotid baroreceptor reflex by afferent input from skeletal muscle receptors

1998 ◽  
Vol 275 (6) ◽  
pp. H2000-H2008 ◽  
Author(s):  
Jeffrey T. Potts ◽  
Jere H. Mitchell
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Afferent Input ◽  
Baroreceptor Reflex ◽  
Central Command ◽  
Carotid Baroreceptor ◽  
Afferent Fibers ◽  
Carotid Baroreflex ◽  
Muscle Receptors ◽  
Muscle Afferent

Resetting of the arterial baroreflex is mediated by central (central command) or peripheral (exercise pressor reflex) mechanisms. The purpose of this study was to determine the effect of somatosensory input from skeletal muscle receptors on resetting of the carotid baroreceptor reflex. Resetting of the baroreflex was determined by measuring carotid sinus threshold pressure (Pth) during a ramp protocol that consisted of a linear increase in sinus pressure from 50 to 250 mmHg at ∼3 mmHg/s. Experiments were performed in seven α-chloralose-anesthetized and vagotomized dogs. To determine the effect of skeletal muscle afferent input on resetting, electrically induced muscle contraction was used to activate mechanically and metabolically senstive afferent fibers, whereas passive stretch of the hindlimb was used to activate predominantly mechanically sensitive afferent fibers. Pth for heart rate (HR) and arterial blood pressure (BP) during the control ramp protocol was 110 ± 4 and 118 ± 7 mmHg, respectively. Electrically induced muscle contraction increased hindlimb tension (5.7 ± 0.4 kg) and significantly increased Pth-HR and Pth-BP above control (135 ± 6 and 141 ± 5 mmHg, respectively; P< 0.05). Muscle paralysis prevented the increase in Pth-HR and Pth-BP during ventral root stimulation (104 ± 7 and 116 ± 5 mmHg, respectively; P = not significant). Passive muscle stretch ( n = 3) increased hindlimb tension (5.9 ± 0.9 kg) and significantly increased Pth-BP (125 ± 21 vs. 159 ± 16 mmHg, control vs. contraction; P< 0.05). There was no difference in the magnitude of Pth resetting between muscle contraction or stretch. The present study demonstrates that activation of skeletal muscle afferent fibers, by either muscle contraction or stretch, increases Pth of the carotid baroreflex. Therefore, neural input from skeletal muscle receptors resets the carotid baroreflex in a manner similar to that ascribed by central command.

scholarly journals Astrocytes in the Rat Nucleus Tractus Solitarii Are Critical for Cardiovascular Reflex Control

2013 ◽  
Vol 33 (47) ◽  
pp. 18608-18617 ◽  
Author(s):  
L.-H. Lin ◽  
S. A. Moore ◽  
S. Y. Jones ◽  
J. McGlashon ◽  
W. T. Talman
Keyword(s):  
Nucleus Tractus Solitarii ◽  
Cardiovascular Reflex ◽  
Reflex Control

Glutamate release in midbrain periaqueductal gray by activation of skeletal muscle receptors and arterial baroreceptors

2003 ◽  
Vol 285 (1) ◽  
pp. H137-H144 ◽  
Author(s):  
Jianhua Li ◽  
Jere H. Mitchell
Keyword(s):  
Skeletal Muscle ◽  
Arterial Pressure ◽  
Glutamate Release ◽  
Periaqueductal Gray ◽  
Triceps Surae ◽  
Muscle Receptor ◽  
Arterial Baroreceptors ◽  
Muscle Receptors ◽  
Afferent Inputs ◽  
Arterial Baroreceptor

We have previously reported that both skeletal muscle receptor and arterial baroreceptor afferent inputs activate neurons in the dorsolateral (DL) and lateral regions of the midbrain periaqueductal gray (PAG). In this study, we determined whether the excitatory amino acid glutamate (Glu) is released to mediate the increased activity in these regions. Static contraction of the triceps surae muscle for 4 min was evoked by electrical stimulation of the L7 and S1 ventral roots in cats. Activation of arterial baroreceptor was induced by intravenous injection of phenylephrine. The endogenous release of Glu from the PAG was recovered with the use of a microdialysis probe. Glu concentration was measured by the HPLC method. Muscle contraction increased mean arterial pressure (MAP) from 98 ± 10 to 149 ± 12 mmHg ( P < 0.05) and increased Glu release in the DL and lateral regions of the middle PAG from 0.39 ± 0.10 to 0.73 ± 0.12 μM (87%, P < 0.05) in intact cats. After sinoaortic denervation and vagotomy were performed, contraction increased MAP from 95 ± 12 to 158 ± 15 mmHg, and Glu from 0.34 ± 0.08 to 0.54 ± 0.10 μM (59%, P < 0.05). The increases in arterial pressure and Glu were abolished by muscle paralysis. Phenylephrine increased MAP from 100 ± 13 to 162 ± 22 mmHg and increased Glu from 0.36 ± 0.10 to 0.59 ± 0.18 μM (64%, P < 0.05) in intact animals. Denervation abolished this Glu increase. Summation of the changes in Glu evoked by muscle receptor and arterial baroreceptor afferent inputs was greater than the increase in Glu produced when both reflexes were activated simultaneously in intact state (123% vs. 87%). These data demonstrate that activation of skeletal muscle receptors evokes release of Glu in the DL and lateral regions of the middle PAG, and convergence of afferent inputs from muscle receptors and arterial baroreceptors in these regions inhibits the release of Glu. These results suggest that the PAG is a neural integrating site for the interaction between the exercise pressor reflex and the arterial baroreceptor reflex.

scholarly journals Evidence for functional alterations in the skeletal muscle mechanoreflex and metaboreflex in hypertensive rats

2008 ◽  
Vol 295 (4) ◽  
pp. H1429-H1438 ◽  
Author(s):  
Anna K. Leal ◽  
Maurice A. Williams ◽  
Mary G. Garry ◽  
Jere H. Mitchell ◽  
Scott A. Smith
Keyword(s):  
Skeletal Muscle ◽  
Cardiovascular Response ◽  
Cardiac Events ◽  
Spontaneously Hypertensive ◽  
Afferent Fibers ◽  
Hindlimb Muscle ◽  
Wide Range ◽  
Muscle Mechanoreflex ◽  
Wistar Kyoto ◽  
Stimulation Of

Exercise in hypertensive individuals elicits exaggerated increases in mean arterial pressure (MAP) and heart rate (HR) that potentially enhance the risk for adverse cardiac events or stroke. Evidence suggests that exercise pressor reflex function (EPR; a reflex originating in skeletal muscle) is exaggerated in this disease and contributes significantly to the potentiated cardiovascular responsiveness. However, the mechanism of EPR overactivity in hypertension remains unclear. EPR function is mediated by the muscle mechanoreflex (activated by stimulation of mechanically sensitive afferent fibers) and metaboreflex (activated by stimulation of chemically sensitive afferent fibers). Therefore, we hypothesized the enhanced cardiovascular response mediated by the EPR in hypertension is due to functional alterations in the muscle mechanoreflex and metaboreflex. To test this hypothesis, mechanically and chemically sensitive afferent fibers were selectively activated in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) decerebrate rats. Activation of mechanically sensitive fibers by passively stretching hindlimb muscle induced significantly greater increases in MAP and HR in SHR than WKY over a wide range of stimulus intensities. Activation of chemically sensitive fibers by administering capsaicin (0.01–1.00 μg/100 μl) into the hindlimb arterial supply induced increases in MAP that were significantly greater in SHR compared with WKY. However, HR responses to capsaicin were not different between the two groups at any dose. This data is consistent with the concept that the abnormal EPR control of MAP described previously in hypertension is mediated by both mechanoreflex and metaboreflex overactivity. In contrast, the previously reported alterations in the EPR control of HR in hypertension may be principally due to overactivity of the mechanically sensitive component of the reflex.

Differential reflex control of forearm and calf resistance vessels by chemosensitive cardiac afferent activation

1994 ◽  
Vol 76 (3) ◽  
pp. 1123-1129 ◽  
Author(s):  
T. N. Jacobsen ◽  
R. A. Lange ◽  
M. T. Olivari ◽  
C. W. Yancy ◽  
V. P. Horn ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Heart Transplantation ◽  
Reflex Response ◽  
Vasomotor Tone ◽  
Vascular Responses ◽  
Vascular Bed ◽  
Afferent Activation ◽  
Resistance Vessels ◽  
Reflex Control ◽  
Muscle Circulation

The aim of this study was to determine whether chemosensitive ventricular afferent activation in humans evokes a diffuse pattern of reflex vasodilation involving the skeletal muscle circulation of all the extremities or a highly specified pattern of vasodilation that is limited to the rather small vascular bed of the forearm. In 10 patients with innervated ventricles and 7 patients with denervated ventricles resulting from heart transplantation, we performed simultaneous plethysmographic recordings of blood flow in the forearm and calf during chemosensitive ventricular afferent activation with intracoronary Renografin. In patients with innervated ventricles, intracoronary Renografin evoked directionally opposite vascular responses in the forearm and calf: forearm resistance decreased from 50 +/- 11 to 31 +/- 8 units, whereas calf resistance increased from 42 +/- 7 to 59 +/- 9 units (P < 0.05, calf vs. forearm). Forearm vasodilation was eliminated after heart transplantation, indicating that this is a reflex response caused by ventricular afferents. In contrast, calf vasoconstriction was well preserved despite ventricular deafferentation, indicating that this response is caused by mechanisms other than ventricular afferent activation, possibly the sinoaortic baroreceptors. Taken together, these findings document a remarkable degree of specificity in the effects of cardiac afferent activation on the reflex regulation of regional vasomotor tone in humans.

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