Activation of ATP-sensitive potassium channels contributes to reactive hyperemia in humans

Banitt, Peter F.; Smits, Paul; Williams, Stephen B.; Ganz, Patricia A.; Creager, Mark A.

doi:10.1152/ajpheart.1996.271.4.h1594

Cited by 48 publications

(51 citation statements)

References 6 publications

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“…A study in the forearm circulation found that adenosine-induced vasodilation was not attenuated by the K ATP channel inhibitor, tolbutamide. 18 In our study, coronary K ATP channel inhibition resulted in a diminution of the peak vasodilator response to adenosine. However, the observation that CFR did not change significantly with glibenclamide infusion suggests that K ATP channels are not critical to the vasodilator response to adenosine and that other mechanisms are involved.…”

Section: Circulation Research February 8 2002supporting

confidence: 48%

Effect of ATP-Sensitive Potassium Channel Inhibition on Resting Coronary Vascular Responses in Humans

Farouque

Worthley

Meredith

et al. 2002

Circulation Research

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Abstract-Experimental data suggest that vascular ATP-sensitive potassium (K ATP ) channels regulate coronary blood flow (CBF), but their role in regulating human CBF is unclear. We sought to determine the contribution of K ATP channels to resting conduit vessel and microvascular function in the human coronary circulation. Twenty-five patients (19 male/6 female, aged 56Ϯ12 years) were recruited. Systemic and coronary hemodynamics were assessed in 20 patients before and after K ATP channel inhibition with graded intracoronary glibenclamide infusions (4, 16, and 40 g/min), in an angiographically smooth or mildly stenosed coronary artery following successful elective percutaneous coronary intervention to another vessel.

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Section: Circulation Research February 8 2002supporting

confidence: 48%

Effect of ATP-Sensitive Potassium Channel Inhibition on Resting Coronary Vascular Responses in Humans

Farouque

Worthley

Meredith

et al. 2002

Circulation Research

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“…Glibenclamide has been reported to have no effect on resting vascular resistance in several vascular beds. [40][41][42][43] The reason for these differences is not obvious and has not been experimentally explored. The differences may indicate species or regional differences in the activity and regulation of these channels or methodological differences among the studies described above.…”

Section: Regulation Of Vascular Tone By K + Channels and Voltage-gatementioning

confidence: 99%

Ion Channels and Vascular Tone

2000

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Ion channels in the plasma membrane of vascular muscle cells that form the walls of resistance arteries and arterioles play a central role in the regulation of vascular tone. Current evidence indicates that vascular smooth muscle cells express at least 4 different types of K + channels, 1 to 2 types of voltage-gated Ca 2+ channels, ≥2 types of Cl − channels, store-operated Ca + (SOC) channels, and stretch-activated cation (SAC) channels in their plasma membranes, all of which may be involved in the regulation of vascular tone. Calcium influx through voltage-gated Ca 2+, SOC, and SAC channels provides a major source of activator Ca 2+ used by resistance arteries and arterioles. In addition, K + and Cl − channels and the Ca 2+ channels mentioned previously all are involved in the determination of the membrane potential of these cells. Membrane potential is a key variable that not only regulates Ca +2 influx through voltage-gated Ca 2+ channels, but also influences release of Ca 2+ from internal stores and Ca 2+ -sensitivity of the contractile apparatus. By controlling Ca 2+ delivery and membrane potential, ion channels are involved in all aspects of the generation and regulation of vascular tone. Keywords muscle; smooth; vascular; arterioles; potassium channels; calcium channels; vascular resistance; vasoconstriction Vascular tone, the contractile activity of vascular smooth muscle cells in the walls of small arteries and arterioles, is the major determinant of the resistance to blood flow through the circulation. Thus, vascular tone plays an important role in the regulation of blood pressure and the distribution of blood flow between and within the tissues and organs of the body. Regulation of the contractile activity of vascular smooth muscle cells in the systemic circulation is dependent on a complex interplay of vasodilator and vasoconstrictor stimuli from circulating hormones, neurotransmitters, endothelium-derived factors, and blood pressure. All of these signals are integrated by vascular muscle cells to determine the activity of the contractile apparatus of the muscle cells and hence the diameter and hydraulic resistance of a blood vessel. Ion channels play a central role in this process. Like all muscle cells, vascular smooth muscle uses Ca 2+ as the trigger for contraction. Calcium influx through channels in the plasma membrane and Ca 2+ release from intracellular stores are the major source of activator Ca 2+ . In addition, the movement of ions through ion channels determines, to a large extent, membrane potential. Membrane potential, along with cytosolic Ca 2+ concentration, regulates and modulates the influx 1,2 and release 3-5 of Ca 2+ through ion channels and the sensitivity of the contractile machinery to Ca 2+.6 Vascular smooth muscle cells express ≥4 different types of K + channels, 7,8 1 to 2 types of voltage-gated Ca 2+ channels, 1,2 ≥2 types of Cl − channels, 9-11 store-operated Ca + channels, 12,13 and stretch-activated cation channels 14-16 in their plasma membranes, all of which may...

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“…PORH has been studied extensively in the past, and it is thought that the hyperaemic response involves endothelial, myogenic, metabolic, and physical mechanisms (Banitt et al, 1996;Beinder and Schlembach, 2001;Lombard and Duling, 1981) PORH can be used as an instrument to investigate microvascular function in a variety of vascular diseases. The method has been used to study the effect of diabetes (Yamamoto-Suganuma and Aso, 2009), heart failure (van Langen et al, 2001), peripheral vascular disease (Cheng et al, 2004), preeclampsia, (Beinder and Schlembach, 2001) and cigarette smoking (Hashimoto, 1994).…”

Section: Introductionmentioning

confidence: 99%

Hyperaemic changes in forearm skin perfusion and RBC concentration after increasing occlusion times

Farnebo

Thorfinn

Henricson

et al. 2010

Microvascular Research

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Activation of ATP-sensitive potassium channels contributes to reactive hyperemia in humans

Abstract: , channels contribute to reactive hyperemia in the forePeter Ganz, and Mark A. Creager. Activation of ATP-arm of healthy humans.

Cited by 48 publications

References 6 publications

Effect of ATP-Sensitive Potassium Channel Inhibition on Resting Coronary Vascular Responses in Humans

Effect of ATP-Sensitive Potassium Channel Inhibition on Resting Coronary Vascular Responses in Humans

Ion Channels and Vascular Tone

Hyperaemic changes in forearm skin perfusion and RBC concentration after increasing occlusion times

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