Exercise training increases inwardly rectifying K+ current and augments K+-mediated vasodilatation in deep femoral artery of rats

Jin, Chun‐Sil; Kim, Hyang Sun; Seo, Eun Yeong; Shin, Dong Hoon; Park, Kyung Sun; Chun, Yang Sook; Zhang, Yin Hua; Kim, Sung Joon

doi:10.1093/cvr/cvr050

Cited by 14 publications

(18 citation statements)

References 35 publications

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“…These mechanisms might fulfill the general criteria that their concentration is linked to contractile activity in a graded way, but experiments over many years have cast doubt over their role as major contributors to ongoing exercise hyperemia. In the case of K ϩ , it is clear that the concentration can rise sufficiently (Ͼ10 mM) to evoke marked dilation via activation of K IR channels and Na ϩ -K ϩ -ATPase with hyperpolarization of affected cells (64,232). However, exogenous administration of potassium does not cause marked dilation, and it is painful in humans.…”

Section: Potassium and Osmolaritymentioning

confidence: 99%

Regulation of Increased Blood Flow (Hyperemia) to Muscles During Exercise: A Hierarchy of Competing Physiological Needs

Joyner

Casey

2015

Physiological Reviews

582

513

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LJoyner MJ, Casey DP. Regulation of Increased Blood Flow (Hyperemia) to Muscles During Exercise: A Hierarchy of Competing Physiological Needs. Physiol Rev 95: 549 -601, 2015; doi:10.1152/physrev.00035.2013.-This review focuses on how blood flow to contracting skeletal muscles is regulated during exercise in humans. The idea is that blood flow to the contracting muscles links oxygen in the atmosphere with the contracting muscles where it is consumed. In this context, we take a top down approach and review the basics of oxygen consumption at rest and during exercise in humans, how these values change with training, and the systemic hemodynamic adaptations that support them. We highlight the very high muscle blood flow responses to exercise discovered in the 1980s. We also discuss the vasodilating factors in the contracting muscles responsible for these very high flows. Finally, the competition between demand for blood flow by contracting muscles and maximum systemic cardiac output is discussed as a potential challenge to blood pressure regulation during heavy large muscle mass or whole body exercise in humans. At this time, no one dominant dilator mechanism accounts for exercise hyperemia. Additionally, complex interactions between the sympathetic nervous system and the microcirculation facilitate high levels of systemic oxygen extraction and permit just enough sympathetic control of blood flow to contracting muscles to regulate blood pressure during large muscle mass exercise in humans.

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Section: Potassium and Osmolaritymentioning

confidence: 99%

Regulation of Increased Blood Flow (Hyperemia) to Muscles During Exercise: A Hierarchy of Competing Physiological Needs

Joyner

Casey

2015

Physiological Reviews

582

513

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“…Thus, there appears to be species or model-dependent differences in the participation of K V channels in the local regulation of blood flow in the heart. In skeletal muscle, exercise training is accompanied by an increase in the functional expression of K V channels in resistance arteries (709), but their function in the local regulation of blood flow was not studied.…”

Section: Kv Channelsmentioning

confidence: 99%

Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles

Tykocki

Boerman

Jackson

2017

Comprehensive Physiology

283

347

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Vascular tone of resistance arteries and arterioles determines peripheral vascular resistance, contributing to the regulation of blood pressure and blood flow to, and within the body’s tissues and organs. Ion channels in the plasma membrane and endoplasmic reticulum of vascular smooth muscle cells (SMCs) in these blood vessels importantly contribute to the regulation of intracellular Ca2+ concentration, the primary determinant of SMC contractile activity and vascular tone. Ion channels provide the main source of activator Ca2+ that determines vascular tone, and strongly contribute to setting and regulating membrane potential, which, in turn, regulates the open-state-probability of voltage gated Ca2+ channels (VGCCs), the primary source of Ca2+ in resistance artery and arteriolar SMCs. Ion channel function is also modulated by vasoconstrictors and vasodilators, contributing to all aspects of the regulation of vascular tone. This review will focus on the physiology of VGCCs, voltage-gated K+ (KV) channels, large-conductance Ca2+-activated K+ (BKCa) channels, strong-inward-rectifier K+ (KIR) channels, ATP-sensitive K+ (KATP) channels, ryanodine receptors (RyRs), inositol 1,4,5-trisphosphate receptors (IP3Rs), and a variety of transient receptor potential (TRP) channels that contribute to pressure-induced myogenic tone in resistance arteries and arterioles, the modulation of the function of these ion channels by vasoconstrictors and vasodilators, their role in the functional regulation of tissue blood flow and their dysfunction in diseases such as hypertension, obesity, and diabetes.

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“…After full anesthesia was confirmed, rats were quickly killed by cervical dislocation, and their proximal hindlimbs were dissected in ice-cold normal Tyrode's (NT) solution for the isolation of DFA. The DFA used in this study was a segment of skeletal artery located between the adductor magnus and gastrocnemius (15). In some rats, coronary arteries, middle cerebral arteries, and renal arteries were also dissected to be compared with DFA.…”

Section: Preparation Of Dfas and Isometric Tension Measurementmentioning

confidence: 99%

“…DFA myocytes were isolated and applied for patch-clamp study as described previously (15). Briefly, DFAs were incubated in Ca 2ϩ -free NT with 1 mg/ml papain (10 -15 min) and 3 mg/ml collagenase (10 -15 min).…”

Section: Preparation Of Dfas and Isometric Tension Measurementmentioning

confidence: 99%

“…We previously characterized the deep femoral artery (DFA; diameter: 150 -200 m) of rats as a model of small feeding artery having prominent myogenic tone at physiological luminal pressure (40 -100 mmHg; Refs. 2,15). In a pilot study using DFA, we found that hypoxia (PO 2 , 3-6%) consistently induces strong vasoconstriction when pretreated with phenylephrine (PhE), an ␣-adrenergic agonist.…”

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confidence: 99%

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Hypoxia-augmented constriction of deep femoral artery mediated by inhibition of eNOS in smooth muscle

Han

Seo

Kim

et al. 2013

American Journal of Physiology-Cell Physiology

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In contrast to the conventional belief that systemic arteries dilate under hypoxia, we found that α-adrenergic contraction of rat deep femoral artery (DFA) is largely augmented by hypoxia (HVC(DFA)) while hypoxia (3% Po(2)) alone had no effect. HVC(DFA) was consistently observed in both endothelium-intact and -denuded vessels with partial pretone by phenylephrine (PhE) or by other conditions (e.g., K(+) channel blocker). Patch-clamp study showed no change in the membrane conductance of DFA myocytes by hypoxia. The RhoA-kinase inhibitor Y27632 attenuated HVC(DFA). The nitric oxide synthase inhibitor [nitro-L-arginine methyl ester (L-NAME)] and soluble guanylate cyclase inhibitor [oxadiazole quinoxalin (ODQ)] strongly augmented the PhE-pretone, while neither of the agents had effect without pretone. NADPH oxidase type 4 (NOX4) inhibitors (diphenylene iodonium and plumbagin) also potentiated PhE-pretone, which was reversed by NO donor. No additive HVC(DFA) was observed under the pretreatment with L-NAME, ODQ, or plumbagin. Western blot and immunohistochemistry analysis showed that both NOX4 and endothelial nitric oxide synthase (eNOS) are expressed in smooth muscle layer of DFA. Various mitochondria inhibitors (rotenone, myxothiazol, and cyanide) prevented HVC(DFA). From the pharmacological data, as a mechanism for HVC(DFA), we suggest hypoxic inhibition of eNOS in myocytes. The putative role of NOX4 and mitochondria requires further investigation. The HVC(DFA) may prevent imbalance between cardiac output and skeletal blood flow under emergent hypoxia combined with increased sympathetic tone.

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Exercise training increases inwardly rectifying K+ current and augments K+-mediated vasodilatation in deep femoral artery of rats

Cited by 14 publications

References 35 publications

Regulation of Increased Blood Flow (Hyperemia) to Muscles During Exercise: A Hierarchy of Competing Physiological Needs

Regulation of Increased Blood Flow (Hyperemia) to Muscles During Exercise: A Hierarchy of Competing Physiological Needs

Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles

Hypoxia-augmented constriction of deep femoral artery mediated by inhibition of eNOS in smooth muscle

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