Action of oxygen and potassium on vascular resistance of dog skeletal muscle

Ns, Skinner; Wj, Powell

doi:10.1152/ajplegacy.1967.212.3.533

Cited by 69 publications

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“…Oxygen has been reported to alter the response of the peripheral vasculature to potassium (19,20,26). Since the solution Po 2 was rather arbitrarily set at low levels, the effect of potassium at higher solution Po 2 levels was also investigated.…”

Section: 8 Dulingmentioning

confidence: 99%

“…Many investigators have shown that potassium at the increased concentrations observed in venous blood during exercise and hypoxia can relax smooth muscle both in vivo (5)(6)(7)(8)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20) and in vitro (21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31). Therefore, this ion.…”

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confidence: 99%

“…However, interstitial fluid potassium concentration can be estimated if one knows arterial and venous potassium concentrations, flow, and the permeability-surface area product of the tissue; fortunately, such measurements are available during rest and exercise for the dog gracilis muscle (7,20,38). These data have been used to estimate interstitial potassium levels, and the calculated values are shown in Table 5.…”

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confidence: 99%

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Effects of potassium ion on the microcirculation of the hamster.

Duling¹

1975

Circulation Research

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The vasoactive properties of potassium were assessed in the microcirculation of the hamster cremaster muscle and the muscular and epithelial portions of the hamster cheek pouch. Tissues were transilluminated and suffused with a physiological salt solution whose potassium concentration varied from 0 to 20 mM. Vessel diameters were measured and normalized as a percent of the control diameter (± SE) observed during exposure to 4.7 mM K + . Altering the potassium concentration in the suffusion solution caused a transient vascular response. The peak changes in the vascular diameter of the arterioles supplying striated muscle varied directly with the suffusion solution potassium concentration from a minimum of 78 ± 3% in 0 mM K + to 155 ± 15% in 15 mM K". Vascular diameter increases were sustained for the full 5-minute test period only in 15 mM K+. In the epithelial portions of the cheek pouch, only the constrictor component of the potassium response was observed. The data indicate that potassium is sufficiently potent to participate in initiating functional hyperemia in striated muscle and might cause as much as a 6.3-fold increase in flow. Functional hyperemias exceeding approximately 3 minutes cannot be due to potassium ion, since the dilation induced by this agent is transient.• Cells contain a large store of labile potassium that can be released by various stimuli such as muscle contraction and hypoxia (1-9). Many investigators have shown that potassium at the increased concentrations observed in venous blood during exercise and hypoxia can relax smooth muscle both in vivo (5)(6)(7)(8)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20) and in vitro (21-31). Therefore, this ion. may be important in the local control of blood flow. However, further quantification of the reactivity of resistance vessels to the ion must be carried out before accurate estimates of the importance of potassium in blood flow regulation can be made. These data can be obtained by studying microvessel responses to alterations in suffusion solution potassium concentrations, but such experiments have only been performed on pial vessels (11,16,17). Furthermore, no data are currently available showing the temporal response pattern of microvessels during variations in potassium concentration. These data are of particular interest in view of the transient potassium ion release during functional hyperemia in striated muscle (7,8) and the transient vascular smooth muscle response to potassium both in vitro (26-32) and in vivo (10). A preliminary report of this work was presented at the Fall Meeting of the American Physiological Society, August, 1974. This work was done during Dr. Duling's tenure as an Established Investigator of the American Heart Association.Received September 20, 1974. Accepted for publication June 4, 1975. I have therefore studied the responses of the arterioles of the hamster cremaster muscle and cheek pouch to changes in the potassium concentration of a superfusion solution. The aims of the experiment were to: (1) estab...

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Section: 8 Dulingmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Effects of potassium ion on the microcirculation of the hamster.

Duling¹

1975

Circulation Research

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“…A number of investigations have strongly suggested that K + manifests as an important regulatory factor, which enhances blood flow and meets the metabolic needs of active tissues. For instance, the exercise-induced increase in blood flow to skeletal muscle is associated with an increase in the K + of the venous outflow [19][20][21][22] . Many studies have been carried out to elucidate the mechanisms underlying the vasorelaxing effect of K + .…”

Section: Discussionmentioning

confidence: 99%

Potentiation of EDHF-mediated relaxation by chloride channel blockers

et al. 2010

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Aim: To investigate the involvement of Cl -channels in endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation in rat mesenteric arteries. Methods: Cl -channel and K ir channel activities were studied using whole-cell patch clamping in rat mesenteric arterial smooth muscle cells. Isometric tension of arterial rings was measured in organ chambers. Results: The volume-activated Cl -current in rat mesenteric arterial smooth muscle cells was abolished by Cl -channel blockers NPPB or DIDS. The EDHF-mediated vasorelaxation was potentiated by NPPB and DIDS. The EDHF response was diminished by a combination of apamin and charybdotoxin, which agreed with the hypothesis that EDHF response involves the release of K + via the Ca 2+ -activated K + channels in endothelial cells. The elevation of K + concentration in bathing solution from 1.2 mmol/L to 11.2 mmol/L induced an arterial relaxation, which was abolished by the combination of BaCl 2 and ouabain. It is consistent to the hypothesis that K + activates K + /Na + -ATPase and inward rectifier K + (K ir ) channels, leading to the hyperpolarization and relaxation of vascular smooth muscle. The K + -induced relaxation was augmented by NPPB, DIDS, or withdrawal of Cl -from the bathing solution, which could be reversed by BaCl 2 , but not ouabain. The potentiating effect of Cl -channel blockers on K + -induced relaxation was probably due to the interaction between Cl -channels and K ir channels. Moreover, the K + -induced relaxation was potentiated when the arteries were incubated in hyperosmotic solution, which is known to inhibit volume-activated Cl -channels. Conclusion: The inhibition of Cl -channels, particularly the volume-activated Cl -channels, may potentiate the EDHF-induced vasorelaxation through the K ir channels.

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“…There is strong evidence supporting a role for at least three factors in the production of metabolic vasodilation. These factors are the potassium ion (27), osmolarity (28), and a substance related to oxidative metabolism (29,30). The concept that two or more factors are involved in the control of vascular resistance during active hyperemia has received considerable experimental support.…”

Section: Mohrman Cant Sparksmentioning

confidence: 99%

Time Course of Vascular Resistance and Venous Oxygen Changes following Brief Tetanus of Dog Skeletal Muscle

Mohrman

Cant

Sparks

1973

Circulation Research

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The time courses of vascular resistance and venous blood oxygen (O 2 ) saturation following a brief tetanus of isolated dog calf muscle were studied during free-flow (constant-pressure), high constant-flow (>30 ml/100 g min-1 ), and low constant-flow (<24 ml/100 g mirr 1 ) perfusion. A monophasic decrease in resistance followed a 1-second tetanus during either free-flow or high constant-flow perfusion. The transient decrease in vascular resistance during high constant-flow perfusion returned to control before the return of the decrease in end-capillary oxygen tension. Thus, it seems unlikely that the vascular response to a brief tetanus during free-flow or high constant-flow perfusion was controlled by a factor related to oxidative metabolism. A biphasic resistance response followed a brief tetanus during low constant-flow perfusion. This vascular response had a longer duration than the response during free-flow or high constant-flow perfusion. It returned to control with approximately the same time course as that for tissue O 2 consumption and could therefore be controlled by factors related to oxidative metabolism. These findings support the hypothesis that exercise hyperemia is due to multiple factors. Moreover, they indicate that, under the conditions of free-flow perfusion or high constant-flow perfusion, the vascular response to a brief tetanus is not solely controlled by factors directly associated with tissue oxidative metabolism. KEY WORDS flow washoutexercise hyperemia constant-flow perfusion metabolic vasodilator blood flow constant-pressure perfusion• Several factors contributing to exercise hyperemia have been identified (1-3), and most of these factors have been implicated as metabolic vasodilators on the basis of two criteria: (1) steady-state exercise produces changes in the venous level of the substance which correlate with changes in the vascular resistance and (2) the substance produces vasodilation when it is infused into the arterial supply of resting skeletal muscle. However, such experiments are difficult to interpret, because steady-state exercise produces many alterations in the chemical composition of the venous effluent of

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Action of oxygen and potassium on vascular resistance of dog skeletal muscle

Cited by 69 publications

References 0 publications

Effects of potassium ion on the microcirculation of the hamster.

Effects of potassium ion on the microcirculation of the hamster.

Potentiation of EDHF-mediated relaxation by chloride channel blockers

Time Course of Vascular Resistance and Venous Oxygen Changes following Brief Tetanus of Dog Skeletal Muscle

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