K+‐Induced Dilation of Hamster Cremasteric Arterioles Involves Both the Na+/K+‐ATPase and Inward‐Rectifier K+ Channels

Burns, Wendy; Cohen, Kenneth D.; Jackson, William F.

doi:10.1080/10739680490425985

Cited by 88 publications

(123 citation statements)

References 37 publications

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“…We have shown previously that K ϩ is involved in the dilation in response to a single contraction over a range of stimulus frequencies (2) in the absence of a contraction frequency, and our data here indicate that there may be a role for K ϩ within the first 10 s of contraction, but its role is minimized over time and its role changes depending on contraction frequency. The role for K ϩ involvement is a complex one; K ϩ dilations have been shown to be transient, and whether K ϩ acts as a dilator or constrictor is dependent on its concentration; 15 mM will produce dilation while 40 mM will cause constriction (11,48,57). The concentrations of K ϩ measured from contracting muscle range from 4 to 5 mM for a single action potential (25) to 52.4 mM (17) depending on skeletal muscle type and stimulation parameters.…”

Section: How Stimulation Parameters May Affect the Vasodilator Complementioning

confidence: 99%

Skeletal muscle contraction-induced vasodilator complement production is dependent on stimulus and contraction frequency

Dua¹,

Dua²,

Murrant³

2009

American Journal of Physiology-Heart and Circulatory Physiology

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Dua AK, Dua N, Murrant CL. Skeletal muscle contraction-induced vasodilator complement production is dependent on stimulus and contraction frequency. Am J Physiol Heart Circ Physiol 297: H433-H442, 2009. First published May 22, 2009 doi:10.1152/ajpheart.00216.2009.-To test the hypothesis that the vasodilator complement that produces arteriolar vasodilation during muscle contraction depends on both stimulus and contraction frequency, we stimulated four to five skeletal muscle fibers in the anesthetized hamster cremaster preparation in situ and measured the change in diameter of arterioles at a site of overlap with the stimulated muscle fibers. Diameter was measured before, during, and after 2 min of skeletal muscle contraction stimulated over a range of stimulus frequencies [4,20, and 40 Hz;15 . L-NAME inhibited the dilations at all stimulus frequencies and contraction frequencies except 60 cpm. XAC inhibited the dilations at all contraction frequencies and stimulus frequencies except 40 Hz. Glibenclamide inhibited all dilations at all stimulus and contraction frequencies, and DAP did not inhibit dilations at any stimulus frequencies while attenuating dilation at a contraction frequency of 60 cpm only. Our data show that the complement of dilators responsible for the vasodilations induced by skeletal muscle contraction differed depending on the stimulus and contraction frequency; therefore, both are important determinants of the dilators involved in the processes of arteriolar vasodilation associated with active hyperemia. stimulus frequency; contraction frequency; arteriole; skeletal muscle contraction; active hyperemia BLOOD FLOW TO ACTIVE SKELETAL muscle increases during contraction. It is hypothesized that active skeletal muscle cell metabolites are a source of vasodilators that cause active hyperemia during contraction, but there is little consensus as to the identity of the vasodilators involved. A host of potential metabolic vasodilators such as adenosine (ADO), hydrogen ions, decreased oxygen tension, carbon dioxide, phosphate, etc., as well as a host of endothelial-derived products and products of muscle activation such as nitric oxide (NO), potassium (K ϩ ), prostaglandins, ACh, ATP-dependent K ϩ (K ATP ) channels, etc. (for review, see Refs. 6,18,28,36), have been implicated in the processes of active hyperemia, but there is a general lack of agreement as to the relative importance of each. We have been investigating the impact of stimulation parameters in the processes of arteriolar vasodilation during active hyperemia to understand this general lack of agreement. We surmised that if the dilators are proposed to be products of skeletal muscle activation or metabolism then it stands to reason that if activation or metabolism is changed through different stimulation parameters then the dilators being produced may also change. Thus, to understand the impact that stimulation parameters have on the production of different vasodilators in active hyperemia, we have investigated the effects of stimulation par...

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Section: How Stimulation Parameters May Affect the Vasodilator Complementioning

confidence: 99%

Skeletal muscle contraction-induced vasodilator complement production is dependent on stimulus and contraction frequency

Dua¹,

Dua²,

Murrant³

2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…Protocol 1. Muscle fiber bundles were stimulated to contract with a 250-ms train duration for either one, two, three, or four contractions at 4-s intervals (15 CPM) for up to 12 s, at stimulus frequencies of 4,10,20,30,40,60, and 80 Hz. Fused tetanus and maximal force generation for hamster cremaster muscle occurs at ϳ30 Hz (31).…”

Section: Experimental Protocolsmentioning

confidence: 99%

“…Changes in smooth muscle reactivity could also be the result of saturation of receptor-mediated processes or dilators whose effect on vascular smooth muscle or endothelial cells is transient. Some of the proposed "metabolic dilators" act through receptor-mediated processes (such as acetylcholine and adenosine), and there are some dilators whose effect on vascular smooth muscle is very transient [i.e., potassium (10)]. Further understanding of the vasodilatory plateaus will be aided by the identity of the vasodilators themselves.…”

Section: Implications For Vasodilator Release and Flow Controlmentioning

confidence: 99%

“…We tested the hypothesis that the vasodilation in response to muscle contraction would be rapid and the pattern of dilation would be dependent on both stimulus frequency and contraction frequency. We directly stimulated a small bundle of skeletal muscle fibers (four to five) in an anesthetized hamster cremaster muscle in situ overlying an arteriole (maximum diameter ϳ40 m) for one, two, three, or four contractions (train duration 250 ms) at 4-s intervals [therefore, a maximum 12-s contraction bout at a contraction frequency of 15 contractions per minute (CPM)] over a range of stimulus frequencies (4,10,20,30,40,60, and 80 Hz). Only one train duration was used, as our laboratory has previously observed that short, physiological train durations do not significantly alter the dilatory pattern, only the magnitude (30).…”

mentioning

confidence: 99%

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Time course of vasodilation at the onset of repetitive skeletal muscle contractions

Armstrong¹,

Dua²,

Murrant³

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Armstrong ML, Dua AK, Murrant CL. Time course of vasodilation at the onset of repetitive skeletal muscle contractions. Am J Physiol Regul Integr Comp Physiol 292: R505-R515, 2007. First published August 24, 2006; doi:10.1152/ajpregu.00381.2006.-To characterize the vasodilatory response in the transition from a single skeletal contraction to a series of contractions, we measured the response of hamster cremaster muscle arterioles associated with four to five skeletal muscle fibers stimulated to contract for one, two, three, or four contractions (250-ms train duration) at 4-s intervals [15 contractions per minute (CPM)] for up to 12 s, at stimulus frequencies of 4, 10, 20, 30, 40, 60, and 80 Hz. To investigate the contribution of contraction frequency, we stimulated muscle fiber bundles at 30 or 60 CPM for 12 s at stimulus frequencies of 4, 20, and 60 Hz. Arteriolar diameters at the site of overlap with the stimulated muscle fibers were measured before and after each contraction. At 15 CPM at 4, 20, and 60 Hz, we observed a peak change in diameter following the first contraction of 1.1 Ϯ 0.1, 1.6 Ϯ 0.2, and 2.1 Ϯ 0.2 m that almost doubled in response to the second contraction (2.0 Ϯ 0.1, 3.0 Ϯ 0.1, and 3.8 Ϯ 0.1 m, respectively), but there was no further dilation following the third or fourth contraction. A similar response occurred at all stimulus and contraction frequencies tested. At 30 and 60 CPM at 60 Hz, the plateau after two contractions was followed by a further increase in diameter to a second plateau at 7-8 s. Therefore, the vasodilatory response in the transition from single to multiple contractions had components that were stimulation parameter dependent and independent and showed a plateauing behavior indicative of rapid changes in either the nature and/or concentration of vasodilators released or changes in vascular reactivity. stimulus frequency; arteriole; muscle contraction; contraction frequency THE PATTERN OF CHANGE IN BLOOD flow in response to skeletal muscle contractions is a multiphase process with an initial, rapid increase at the onset of contractions, followed by a slower change to a steady state over time (for example, Refs. 4,9,35,40,47,54,59). While vascular compression was thought to be the major process in developing the initial, rapid hyperemia (for review, see Ref. 55), rapid vasodilation has been conclusively identified as an important component of this response (21,30,33,41,57). The identity of the dilators responsible for the rapid dilation remain unclear. Since Gaskell (19), it has been hypothesized that the vasodilation responsible for the changes in blood flow in response to skeletal muscle contraction is due, in part, to dilatory products released from the active skeletal muscle cells themselves. Potential vasodilators released as a result of skeletal muscle activation and metabolism have been identified (for review, see Refs. 12, 27), but no single vasoactive substance has emerged as having a consistent, predominantly large contribution, especially at the onset of exercis...

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“…The resting membrane potential (RMP) of VSMC in most vascular beds during physiologic pressures ranges between ¡60 mV to ¡35 mV. [67][68][69][70] This range of RMP is a prerequisite for setting the basal tone upon which vasodilators can act. Increases in perfusion pressure further depolarize VSMC.…”

Section: Myogenic Responsementioning

confidence: 99%

T-type Ca²⁺channels and autoregulation of local blood flow

et al. 2017

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L-type voltage gated Ca2C channels are considered to be the primary source of calcium influx during the myogenic response. However, many vascular beds also express T-type voltage gated Ca 2C channels. Recent studies suggest that these channels may also play a role in autoregulation. At low pressures (40-80 mmHg) T-type channels affect myogenic responses in cerebral and mesenteric vascular beds. T-type channels also seem to be involved in skeletal muscle autoregulation. This review discusses the expression and role of T-type voltage gated Ca 2C channels in the autoregulation of several different vascular beds. Lack of specific pharmacological inhibitors has been a huge challenge in the field. Now the research has been strengthened by genetically modified models such as mice lacking expression of T-type voltage gated Ca 2C channels (Ca V 3.1 and Ca V 3.2). Hopefully, these new tools will help further elucidate the role of voltage gated T-type Ca 2C channels in autoregulation and vascular function.

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K⁺‐Induced Dilation of Hamster Cremasteric Arterioles Involves Both the Na⁺/K⁺‐ATPase and Inward‐Rectifier K⁺ Channels

Cited by 88 publications

References 37 publications

Skeletal muscle contraction-induced vasodilator complement production is dependent on stimulus and contraction frequency

Skeletal muscle contraction-induced vasodilator complement production is dependent on stimulus and contraction frequency

Time course of vasodilation at the onset of repetitive skeletal muscle contractions

T-type Ca²⁺channels and autoregulation of local blood flow

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K+‐Induced Dilation of Hamster Cremasteric Arterioles Involves Both the Na+/K+‐ATPase and Inward‐Rectifier K+ Channels

Cited by 88 publications

References 37 publications

Skeletal muscle contraction-induced vasodilator complement production is dependent on stimulus and contraction frequency

Skeletal muscle contraction-induced vasodilator complement production is dependent on stimulus and contraction frequency

Time course of vasodilation at the onset of repetitive skeletal muscle contractions

T-type Ca2+channels and autoregulation of local blood flow

Contact Info

Product

Resources

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K⁺‐Induced Dilation of Hamster Cremasteric Arterioles Involves Both the Na⁺/K⁺‐ATPase and Inward‐Rectifier K⁺ Channels

T-type Ca²⁺channels and autoregulation of local blood flow