Renal vascular responses to static handgrip: role of muscle  mechanoreflex

Momen, Afsana; Leuenberger, Urs A.; Ray, Chester A.; Cha, Susan; Handly, Brian; Sinoway, Lawrence I.

doi:10.1152/ajpheart.00214.2003

Cited by 82 publications

(124 citation statements)

References 39 publications

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“…The results of the present study indicate that, in humans, heating the forearm muscles elicits a similar influence on mechanoreceptor-mediated renal vasoconstriction, because the differences in renal vasoconstriction occurred only during exercise but not when the muscle metaboreceptors were engaged in isolation during postexercise muscle ischemia. These findings are in agreement with other studies that have found that mechanoreceptors contribute to decreases in renal conductance in humans (14,15) and decreases in renal conductance and sympathetic nerve activity in animals (9,10,29). The greater decrease in calf vascular conductance with heating corresponds to greater increases in muscle sympathetic nerve activity, which we observed previously using the same protocol (19).…”

Section: Discussionsupporting

confidence: 93%

“…During exercise, renal vasoconstriction appears to be mediated by activation of the exercise pressor reflex (4,15,29). This reflex is controlled by mechanically and metabolically sensitive afferents in the working muscle.…”

mentioning

confidence: 99%

“…Because, in humans, activation of the exercise pressor reflex can alter renal vascular conductance (14,15) and because muscle heating and cooling augment and attenuate muscle sympathetic nerve activity, respectively (20,21), the following two hypotheses were tested in the present study: 1) forearm heating would augment renal and calf vasoconstriction during ischemic IHG via sensitization of mechanically sensitive afferents, and 2) forearm cooling would delay renal and calf vasoconstriction during ischemic IHG via delayed activation of metabolically active muscle afferents.…”

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confidence: 99%

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Changes in forearm muscle temperature alter renal vascular responses to isometric handgrip

Kuipers

Sauder²,

Kearney³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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The purpose of the present study was to examine the effect of heating and cooling the forearm muscles on renal vascular responses to ischemic isometric handgrip (IHG). It was hypothesized that heating and cooling the forearm would augment and attenuate, respectively, renal vascular responses to IHG. Renal vascular responses to IHG were studied during forearm heating at 39°C ( n = 15, 26 ± 1 yr) and cooling at 26°C ( n = 12, 26 ± 1 yr). For a control trial, subjects performed the experimental protocol while the forearm was normothermic (∼34°C). Muscle temperature (measured by intramuscular probe) was controlled by changing the temperature of water cycling through a water-perfused sleeve. The experimental protocol was as follows: 3 min at baseline, 1 min of ischemia, ischemic IHG to fatigue, and 2 min of postexercise muscle ischemia. At rest, renal artery blood velocity (RBV; Doppler ultrasound) and renal vascular conductance (RVC = RBV/mean arterial blood pressure) were not different between normothermia and the two thermal conditions. During ischemic IHG, there were greater decreases in RBV and RVC in the heating trial. However, RBV and RVC were similar during postexercise muscle ischemia during heating and normothermia. RVC decreased less during cooling than in normothermia while the subjects performed the ischemic IHG protocol. During postexercise muscle ischemia, RVC was greater during cooling than in normothermia. These results indicate that heating augments mechanoreceptor-mediated renal vasoconstriction whereas cooling blunts metaboreceptor-mediated renal vasoconstriction.

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Section: Discussionsupporting

confidence: 93%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Changes in forearm muscle temperature alter renal vascular responses to isometric handgrip

Kuipers

Sauder²,

Kearney³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…The rapid sympathetic nerve responses are hardly explained by the muscle mechanoreflex. Momen et al (31,32) recently reported that a 15-s bout of evoked static muscle contraction by percutaneous electrical stimulation increased renal vascular resistance in humans, suggesting that muscle mechanoreflex engagement was responsible for the increase in renal vascular resistance. Taken together, the muscle mechanoreflex may not work on the whole vascular system but may affect the renal vascular bed particularly.…”

Section: Central Command But Not the Muscle Mechanoreflex Is Responmentioning

confidence: 99%

Gadolinium does not blunt the cardiovascular responses at the onset of voluntary static exercise in cats: a predominant role of central command

Matsukawa¹,

Nakamoto²,

Inomoto³

2007

American Journal of Physiology-Heart and Circulatory Physiology

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The cardiovascular adaptation at the onset of voluntary static exercise is controlled by the autonomic nervous system. Two neural mechanisms are responsible for the cardiovascular adaptation: one is central command descending from higher brain centers, and the other is a muscle mechanosensitive reflex from activation of mechanoreceptors in the contracting muscles. To examine which mechanism played a major role in producing the initial cardiovascular adaptation during static exercise, we studied the effect of intravenous administration of gadolinium (55 mol/kg), a blocker of stretch-activated ion channels, on the increases in heart rate (HR) and mean arterial blood pressure (MAP) at the onset of voluntary static exercise (pressing a bar with a forelimb) in conscious cats. HR increased by 31 Ϯ 5 beats/min and MAP increased by 15 Ϯ 1 mmHg at the onset of voluntary static exercise. Gadolinium affected neither the baseline values nor the initial increases of HR and MAP at the onset of exercise, although the peak force applied to the bar tended to decrease to 65% of the control value before gadolinium. Furthermore, we examined the effect of gadolinium on the reflex responses in HR and MAP (18 Ϯ 7 beats/min and 30 Ϯ 6 mmHg, respectively) during passive mechanical stretch of a forelimb or hindlimb in anesthetized cats. Gadolinium significantly blunted the passive stretch-induced increases in HR and MAP, suggesting that gadolinium blocks the stretch-activated ion channels and thereby attenuates the reflex cardiovascular responses to passive mechanical stretch of a limb. We conclude that the initial cardiovascular adaptation at the onset of voluntary static exercise is predominantly induced by feedforward control of central command descending from higher brain centers but not by a muscle mechanoreflex. muscle mechanosensitive receptors; stretch-activated ion channels; mechanical stretch of skeletal muscle; exercise pressor reflex; conscious cats

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“…Immediately before exercise was stopped, posthandgrip circulatory arrest (PHG-CA) was initiated by inflation of a previously placed BP cuff around the arm at ϳ250 mmHg, which was kept inflated for 2 min. Vascular resistance responses during PHG-CA are thought to be due to 1) engagement of the muscle metaboreflex; and/or 2) myogenic vasoconstriction, if BP remains above baseline (13).…”

Section: Study Protocolsmentioning

confidence: 99%

Renal vascular response to static handgrip exercise: sympathetic vs. autoregulatory control

Momen

Bower

Leuenberger³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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Static exercise causes activation of the sympathetic nervous system, which results in increased blood pressure (BP) and renal vascular resistance (RVR). The question arises as to whether renal vasoconstriction that occurs during static exercise is due to sympathetic activation and/or related to a pressure-dependent renal autoregulatory mechanism. To address this issue, we monitored renal blood flow velocity (RBV) responses to two different handgrip (HG) exercise paradigms in 7 kidney transplant recipients (RTX) and 11 age-matched healthy control subjects. Transplanted kidneys are functionally denervated. Beat-by-beat analyses of changes in RBV (observed via duplex ultrasound), BP, and heart rate were performed during HG exercise in all subjects. An index of RVR was calculated as BP/RBV. In protocol 1, fatiguing HG exercise (40% of maximum voluntary contraction) led to significant increases in RVR in both groups. However, at the end of exercise, RVR was more than fourfold higher in control subjects than in the RTX group (88 vs. 20% increase over baseline; interaction, P Ͻ 0.001). In protocol 2, short bouts of HG exercise (15 s) led to significant increases in RVR at higher workloads (50 and 70% of maximum voluntary contraction) in the control subjects (P Ͻ 0.001). RVR did not increase in the RTX group. In conclusion, we observed grossly attenuated renal vasoconstrictor responses to exercise in RTX subjects, in whom transplanted kidneys were considered functionally denervated. Our results suggest that renal vasoconstrictor responses to exercise in conscious humans are mainly dependent on activation of a neural mechanism.kidney; blood flow; autoregulation; handgrip; vasoconstriction; transplant DURING EXERCISE, THE SYMPATHETIC nervous system is activated, and this results in increases in heart rate (HR), blood pressure (BP), and peripheral vasoconstriction. As part of this process, renal vasoconstriction occurs and serves to maintain BP as well as to redistribute blood flow to the contracting skeletal muscle bed.Of note, the observed increase in renal vascular resistance (RVR) is associated with an increase in arterial pressure. Thus the question arises as to whether renal vasoconstriction that occurs during static exercise is due to sympathetic activation and/or related to a pressure-dependent renal autoregulatory mechanism. To address this issue, we monitored renal hemodynamic responses during two different handgrip exercise paradigms in a group of kidney transplant recipients (RTX) and in age-matched healthy control subjects. Previous reports (7,8,16) suggest that transplanted kidneys remain functionally denervated for several months after transplantation. In studies measuring tissue norepinephrine in rat kidney grafts (7), researchers found grossly diminished norepinephrine levels compared with native kidneys 9 mo after transplantation. Similarly, necropsy specimens from human renal allografts demonstrate a reduction in sympathetic ganglia synaptic density 3 yr after transplantation (16). In addition, the resea...

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Renal vascular responses to static handgrip: role of muscle mechanoreflex

Cited by 82 publications

References 39 publications

Changes in forearm muscle temperature alter renal vascular responses to isometric handgrip

Changes in forearm muscle temperature alter renal vascular responses to isometric handgrip

Gadolinium does not blunt the cardiovascular responses at the onset of voluntary static exercise in cats: a predominant role of central command

Renal vascular response to static handgrip exercise: sympathetic vs. autoregulatory control

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