K<sup>+</sup> as a vasodilator in resting human muscle: implications for exercise hyperaemia

Juel, Carsten; Olsen, Steen; Rentsch, Rikke Louise; González‐Alonso, José; Rosenmeier, Jaya B.

doi:10.1111/j.1748-1716.2007.01678.x

Cited by 12 publications

(11 citation statements)

References 25 publications

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“…This result suggests that there are several other substances that may be contributing to this cardiovascular response, eg, potassium, oxygen, carbon dioxide and adenosine 39,40 . From the moment that C allele carriers have some vascular dysfunction, it is possible that other vasodilators are working to control responses to blood flow, thereby offsetting the reduced production of NO 17,40 .…”

Section: Figure 2 -Blood Flow (Panel a And B) And Vascular Resistancementioning

confidence: 89%

Efeito do exercício físico e do polimorfismo T-786C na pressão arterial e no fluxo sanguíneo de idosas

Zago¹,

Kokubun²,

Fenty-Stewart³

et al. 2010

Arq. Bras. Cardiol.

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Section: Figure 2 -Blood Flow (Panel a And B) And Vascular Resistancementioning

confidence: 89%

Efeito do exercício físico e do polimorfismo T-786C na pressão arterial e no fluxo sanguíneo de idosas

Zago¹,

Kokubun²,

Fenty-Stewart³

et al. 2010

Arq. Bras. Cardiol.

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“…Therefore, the observation that either infused ATP or K + stimulates vasodilatation in human skeletal muscle (K + response was Ba 2+ ‐sensitive) and their effects are additive (Juel et al . ) may put the current work in a more physiological context.…”

Section: Discussionmentioning

confidence: 99%

Conducted dilatation to ATP and K⁺in rat skeletal muscle arterioles

Dora

2016

Acta Physiol

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AimDuring exercise in humans, circulating levels of ATP and K+ increase at a time when blood flow increases to satisfy metabolic demand. Both molecules can activate arteriolar K+ channels to stimulate vasodilatation; here, it is established whether conducted dilatation is observed in a skeletal muscle bed.MethodsIsolated and cannulated rat cremaster arterioles were used to assess both local and conducted responses. Agents were either added to the bath, focally pulse‐ejected to the downstream end of arterioles, or in triple‐cannulated arterioles, luminally perfused into the downstream branches to assess both local and conducted responses.ResultsThe endothelium‐dependent agonist ACh and the KATP channel opener levcromakalim each stimulated both local and conducted vasodilatation. Focal, bolus delivery of ATP (10 μ m) or KCl (33 mm) to the outside of arterioles stimulated a biphasic vasomotor response: rapid vasoconstriction followed by dilatation as each washed away. At lower concentrations of KCl (19 mm), constriction was avoided, and instead, Ba2+‐sensitive local dilatation and conducted dilatation were both observed. Luminal perfusion of ATP avoided constriction and activated P2Y1 receptors stimulating vasodilatation secondary to opening of KC a channels. In triple‐cannulated arterioles, either ATP (10 μ m) or K+ (15 mm) luminally perfused into daughter branches of a bifurcation stimulated local dilatation which conducted into the parent arteriole.ConclusionThe recognized physiological autocrine and paracrine mediators ATP and K+ each act to evoke both local and conducted vasodilatation in rat cremaster arterioles. Therefore, in situations when circulating levels are raised, such as during exercise, these agents can act as important regulators of blood flow.

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“…In this context, prior studies in animal models established disruption of the endothelium attenuates the hyperemic response to muscle contraction (2, 44, 54) and subsequent studies have attempted to identify the endothelialderived substances that may regulate blood flow during exercise. Local metabolic substances independent of the endothelium, such as K ϩ , have also been suggested to be involved in exercise hyperemia (23,29,63), particularly at the onset of muscle contractions (1, 7, 40). However, to date, obligatory local vasodilators for the hyperemia at exercise onset and during steadystate conditions are still questioned in humans (28).…”

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confidence: 99%

K_IR channel activation contributes to onset and steady-state exercise hyperemia in humans

Crecelius

Luckasen

Larson

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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We tested the hypothesis that activation of inwardly rectifying potassium (KIR) channels and Na(+)-K(+)-ATPase, two pathways that lead to hyperpolarization of vascular cells, contributes to both the onset and steady-state hyperemic response to exercise. We also determined whether after inhibiting these pathways nitric oxide (NO) and prostaglandins (PGs) are involved in the hyperemic response. Forearm blood flow (FBF; Doppler ultrasound) was determined during rhythmic handgrip exercise at 10% maximal voluntary contraction for 5 min in the following conditions: control [saline; trial 1 (T1)]; with combined inhibition of KIR channels and Na(+)-K(+)-ATPase alone [via barium chloride (BaCl2) and ouabain, respectively; trial 2 (T2)]; and with additional combined nitric oxide synthase (N(G)-monomethyl-l-arginine) and cyclooxygenase inhibition [ketorolac; trial 3 (T3)]. In T2, the total hyperemic responses were attenuated ~50% from control (P < 0.05) at exercise onset, and there was minimal further effect in T3 (protocol 1; n = 11). In protocol 2 (n = 8), steady-state FBF was significantly reduced during T2 vs. T1 (133 ± 15 vs. 167 ± 17 ml/min; Δ from control: -20 ± 3%; P < 0.05) and further reduced during T3 (120 ± 15 ml/min; -29 ± 3%; P < 0.05 vs. T2). In protocol 3 (n = 8), BaCl2 alone reduced FBF during onset (~50%) and steady-state exercise (~30%) as observed in protocols 1 and 2, respectively, and addition of ouabain had no further impact. Our data implicate activation of KIR channels as a novel contributing pathway to exercise hyperemia in humans.

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K⁺ as a vasodilator in resting human muscle: implications for exercise hyperaemia

Cited by 12 publications

References 25 publications

Efeito do exercício físico e do polimorfismo T-786C na pressão arterial e no fluxo sanguíneo de idosas

Efeito do exercício físico e do polimorfismo T-786C na pressão arterial e no fluxo sanguíneo de idosas

Conducted dilatation to ATP and K⁺in rat skeletal muscle arterioles

K_IR channel activation contributes to onset and steady-state exercise hyperemia in humans

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K+ as a vasodilator in resting human muscle: implications for exercise hyperaemia

Cited by 12 publications

References 25 publications

Efeito do exercício físico e do polimorfismo T-786C na pressão arterial e no fluxo sanguíneo de idosas

Efeito do exercício físico e do polimorfismo T-786C na pressão arterial e no fluxo sanguíneo de idosas

Conducted dilatation to ATP and K+in rat skeletal muscle arterioles

KIR channel activation contributes to onset and steady-state exercise hyperemia in humans

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K⁺ as a vasodilator in resting human muscle: implications for exercise hyperaemia

Conducted dilatation to ATP and K⁺in rat skeletal muscle arterioles

K_IR channel activation contributes to onset and steady-state exercise hyperemia in humans