Effects of combined inhibition of ATP-sensitive potassium channels, nitric oxide, and prostaglandins on hyperemia during moderate exercise
1 Department of Anesthesiology and 2 General Clinical Research Center, Mayo Clinic, Rochester, Minnesota Submitted 30 December 2005 ; accepted in final form 6 February 2006 ATP-sensitive potassium (K ATP ) channels have been suggested to contribute to coronary and skeletal muscle vasodilation during...
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| Published in | Journal of applied physiology (1985) Vol. 100; no. 5; pp. 1506 - 1512 |
|---|---|
| Main Authors | , , |
| Format | Journal Article |
| Language | English |
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Bethesda, MD
Am Physiological Soc
01.05.2006
American Physiological Society |
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| Online Access | Get full text |
| ISSN | 8750-7587 1522-1601 |
| DOI | 10.1152/japplphysiol.01639.2005 |
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| Abstract | 1 Department of Anesthesiology and 2 General Clinical Research Center, Mayo Clinic, Rochester, Minnesota
Submitted 30 December 2005
; accepted in final form 6 February 2006
ATP-sensitive potassium (K ATP ) channels have been suggested to contribute to coronary and skeletal muscle vasodilation during exercise, either alone or interacting in a parallel or redundant process with nitric oxide (NO), prostaglandins (PGs), and adenosine. We tested the hypothesis that K ATP channels, alone or in combination with NO and PGs, regulate exercise hyperemia in forearm muscle. Eighteen healthy young adults performed 20 min of moderate dynamic forearm exercise, with forearm blood flow (FBF) measured via Doppler ultrasound. After steady-state FBF was achieved for 5 min (saline control), the K ATP inhibitor glibenclamide (Glib) was infused into the brachial artery for 5 min (10 µg·dl 1 ·min 1 ), followed by saline infusion during the final 10 min of exercise ( n = 9). Exercise increased FBF from 71 ± 11 to 239 ± 24 ml/min, and FBF was not altered by 5 min of Glib. Systemic plasma Glib levels were above the therapeutic range, and Glib increased insulin levels by 50%, whereas blood glucose was unchanged (88 ± 2 vs. 90 ± 2 mg/dl). In nine additional subjects, Glib was followed by combined infusion of N G -nitro- L -arginine methyl ester ( L -NAME) plus ketorolac (to inhibit NO and PGs, respectively). As above, Glib had no effect on FBF but addition of L -NAME + ketorolac (i.e., triple blockade) reduced FBF by 15% below steady-state exercise levels in seven of nine subjects. Interestingly, triple blockade in two subjects caused FBF to transiently and dramatically decrease. This was followed by an acute recovery of flow above steady-state exercise values. We conclude 1 ) opening of K ATP channels is not obligatory for forearm exercise hyperemia, and 2 ) triple blockade of NO, PGs, and K ATP channels does not reduce hyperemia more than the inhibition of NO and PGs in most subjects. However, some subjects are sensitive to triple blockade, but they are able to restore FBF acutely during exercise. Future studies are required to determine the nature of these compensatory mechanisms in the affected individuals.
Doppler ultrasound; N G -nitro- L -arginine methyl ester; blood flow; human; potassium; nitric oxide synthase; cyclooxygenase
Address for reprint requests and other correspondence: W. G. Schrage, Dept. of Anesthesiology, Joseph 4-184W, Mayo Clinic, Rochester, MN 55905 (e-mail: schrage.william{at}mayo.edu ) |
|---|---|
| AbstractList | ATP-sensitive potassium (KATP) channels have been suggested to contribute to coronary and skeletal muscle vasodilation during exercise, either alone or interacting in a parallel or redundant process with nitric oxide (NO), prostaglandins (PGs), and adenosine. We tested the hypothesis that KATP channels, alone or in combination with NO and PGs, regulate exercise hyperemia in forearm muscle. Eighteen healthy young adults performed 20 min of moderate dynamic forearm exercise, with forearm blood flow (FBF) measured via Doppler ultrasound. After steady-state FBF was achieved for 5 min (saline control), the KATP inhibitor glibenclamide (Glib) was infused into the brachial artery for 5 min (10 microg(symbol)dl-1(symbol)min-1), followed by saline infusion during the final 10 min of exercise (n = 9). Exercise increased FBF from 71 +/- 11 to 239 +/- 24 ml/min, and FBF was not altered by 5 min of Glib. Systemic plasma Glib levels were above the therapeutic range, and Glib increased insulin levels by approximately 50%, whereas blood glucose was unchanged (88 +/- 2 vs. 90 +/- 2 mg/dl). In nine additional subjects, Glib was followed by combined infusion of NG-nitro-L-arginine methyl ester (L-NAME) plus ketorolac (to inhibit NO and PGs, respectively). As above, Glib had no effect on FBF but addition of L-NAME + ketorolac (i.e., triple blockade) reduced FBF by approximately 15% below steady-state exercise levels in seven of nine subjects. Interestingly, triple blockade in two subjects caused FBF to transiently and dramatically decrease. This was followed by an acute recovery of flow above steady-state exercise values. We conclude 1) opening of KATP channels is not obligatory for forearm exercise hyperemia, and 2) triple blockade of NO, PGs, and KATP channels does not reduce hyperemia more than the inhibition of NO and PGs in most subjects. However, some subjects are sensitive to triple blockade, but they are able to restore FBF acutely during exercise. Future studies are required to determine the nature of these compensatory mechanisms in the affected individuals.[PUBLICATION ABSTRACT] ATP-sensitive potassium (K ATP ) channels have been suggested to contribute to coronary and skeletal muscle vasodilation during exercise, either alone or interacting in a parallel or redundant process with nitric oxide (NO), prostaglandins (PGs), and adenosine. We tested the hypothesis that K ATP channels, alone or in combination with NO and PGs, regulate exercise hyperemia in forearm muscle. Eighteen healthy young adults performed 20 min of moderate dynamic forearm exercise, with forearm blood flow (FBF) measured via Doppler ultrasound. After steady-state FBF was achieved for 5 min (saline control), the K ATP inhibitor glibenclamide (Glib) was infused into the brachial artery for 5 min (10 μg·dl −1 ·min −1 ), followed by saline infusion during the final 10 min of exercise ( n = 9). Exercise increased FBF from 71 ± 11 to 239 ± 24 ml/min, and FBF was not altered by 5 min of Glib. Systemic plasma Glib levels were above the therapeutic range, and Glib increased insulin levels by ∼50%, whereas blood glucose was unchanged (88 ± 2 vs. 90 ± 2 mg/dl). In nine additional subjects, Glib was followed by combined infusion of N G -nitro-l-arginine methyl ester (l-NAME) plus ketorolac (to inhibit NO and PGs, respectively). As above, Glib had no effect on FBF but addition of l-NAME + ketorolac (i.e., triple blockade) reduced FBF by ∼15% below steady-state exercise levels in seven of nine subjects. Interestingly, triple blockade in two subjects caused FBF to transiently and dramatically decrease. This was followed by an acute recovery of flow above steady-state exercise values. We conclude 1) opening of K ATP channels is not obligatory for forearm exercise hyperemia, and 2) triple blockade of NO, PGs, and K ATP channels does not reduce hyperemia more than the inhibition of NO and PGs in most subjects. However, some subjects are sensitive to triple blockade, but they are able to restore FBF acutely during exercise. Future studies are required to determine the nature of these compensatory mechanisms in the affected individuals. 1 Department of Anesthesiology and 2 General Clinical Research Center, Mayo Clinic, Rochester, Minnesota Submitted 30 December 2005 ; accepted in final form 6 February 2006 ATP-sensitive potassium (K ATP ) channels have been suggested to contribute to coronary and skeletal muscle vasodilation during exercise, either alone or interacting in a parallel or redundant process with nitric oxide (NO), prostaglandins (PGs), and adenosine. We tested the hypothesis that K ATP channels, alone or in combination with NO and PGs, regulate exercise hyperemia in forearm muscle. Eighteen healthy young adults performed 20 min of moderate dynamic forearm exercise, with forearm blood flow (FBF) measured via Doppler ultrasound. After steady-state FBF was achieved for 5 min (saline control), the K ATP inhibitor glibenclamide (Glib) was infused into the brachial artery for 5 min (10 µg·dl 1 ·min 1 ), followed by saline infusion during the final 10 min of exercise ( n = 9). Exercise increased FBF from 71 ± 11 to 239 ± 24 ml/min, and FBF was not altered by 5 min of Glib. Systemic plasma Glib levels were above the therapeutic range, and Glib increased insulin levels by 50%, whereas blood glucose was unchanged (88 ± 2 vs. 90 ± 2 mg/dl). In nine additional subjects, Glib was followed by combined infusion of N G -nitro- L -arginine methyl ester ( L -NAME) plus ketorolac (to inhibit NO and PGs, respectively). As above, Glib had no effect on FBF but addition of L -NAME + ketorolac (i.e., triple blockade) reduced FBF by 15% below steady-state exercise levels in seven of nine subjects. Interestingly, triple blockade in two subjects caused FBF to transiently and dramatically decrease. This was followed by an acute recovery of flow above steady-state exercise values. We conclude 1 ) opening of K ATP channels is not obligatory for forearm exercise hyperemia, and 2 ) triple blockade of NO, PGs, and K ATP channels does not reduce hyperemia more than the inhibition of NO and PGs in most subjects. However, some subjects are sensitive to triple blockade, but they are able to restore FBF acutely during exercise. Future studies are required to determine the nature of these compensatory mechanisms in the affected individuals. Doppler ultrasound; N G -nitro- L -arginine methyl ester; blood flow; human; potassium; nitric oxide synthase; cyclooxygenase Address for reprint requests and other correspondence: W. G. Schrage, Dept. of Anesthesiology, Joseph 4-184W, Mayo Clinic, Rochester, MN 55905 (e-mail: schrage.william{at}mayo.edu ) ATP-sensitive potassium (KATP) channels have been suggested to contribute to coronary and skeletal muscle vasodilation during exercise, either alone or interacting in a parallel or redundant process with nitric oxide (NO), prostaglandins (PGs), and adenosine. We tested the hypothesis that KATP channels, alone or in combination with NO and PGs, regulate exercise hyperemia in forearm muscle. Eighteen healthy young adults performed 20 min of moderate dynamic forearm exercise, with forearm blood flow (FBF) measured via Doppler ultrasound. After steady-state FBF was achieved for 5 min (saline control), the KATP inhibitor glibenclamide (Glib) was infused into the brachial artery for 5 min (10 microg.dl(-1).min(-1)), followed by saline infusion during the final 10 min of exercise (n = 9). Exercise increased FBF from 71 +/- 11 to 239 +/- 24 ml/min, and FBF was not altered by 5 min of Glib. Systemic plasma Glib levels were above the therapeutic range, and Glib increased insulin levels by approximately 50%, whereas blood glucose was unchanged (88 +/- 2 vs. 90 +/- 2 mg/dl). In nine additional subjects, Glib was followed by combined infusion of NG-nitro-L-arginine methyl ester (L-NAME) plus ketorolac (to inhibit NO and PGs, respectively). As above, Glib had no effect on FBF but addition of L-NAME + ketorolac (i.e., triple blockade) reduced FBF by approximately 15% below steady-state exercise levels in seven of nine subjects. Interestingly, triple blockade in two subjects caused FBF to transiently and dramatically decrease. This was followed by an acute recovery of flow above steady-state exercise values. We conclude 1) opening of KATP channels is not obligatory for forearm exercise hyperemia, and 2) triple blockade of NO, PGs, and KATP channels does not reduce hyperemia more than the inhibition of NO and PGs in most subjects. However, some subjects are sensitive to triple blockade, but they are able to restore FBF acutely during exercise. Future studies are required to determine the nature of these compensatory mechanisms in the affected individuals. ATP-sensitive potassium (KATP) channels have been suggested to contribute to coronary and skeletal muscle vasodilation during exercise, either alone or interacting in a parallel or redundant process with nitric oxide (NO), prostaglandins (PGs), and adenosine. We tested the hypothesis that KATP channels, alone or in combination with NO and PGs, regulate exercise hyperemia in forearm muscle. Eighteen healthy young adults performed 20 min of moderate dynamic forearm exercise, with forearm blood flow (FBF) measured via Doppler ultrasound. After steady-state FBF was achieved for 5 min (saline control), the KATP inhibitor glibenclamide (Glib) was infused into the brachial artery for 5 min (10 microg.dl(-1).min(-1)), followed by saline infusion during the final 10 min of exercise (n = 9). Exercise increased FBF from 71 +/- 11 to 239 +/- 24 ml/min, and FBF was not altered by 5 min of Glib. Systemic plasma Glib levels were above the therapeutic range, and Glib increased insulin levels by approximately 50%, whereas blood glucose was unchanged (88 +/- 2 vs. 90 +/- 2 mg/dl). In nine additional subjects, Glib was followed by combined infusion of NG-nitro-L-arginine methyl ester (L-NAME) plus ketorolac (to inhibit NO and PGs, respectively). As above, Glib had no effect on FBF but addition of L-NAME + ketorolac (i.e., triple blockade) reduced FBF by approximately 15% below steady-state exercise levels in seven of nine subjects. Interestingly, triple blockade in two subjects caused FBF to transiently and dramatically decrease. This was followed by an acute recovery of flow above steady-state exercise values. We conclude 1) opening of KATP channels is not obligatory for forearm exercise hyperemia, and 2) triple blockade of NO, PGs, and KATP channels does not reduce hyperemia more than the inhibition of NO and PGs in most subjects. However, some subjects are sensitive to triple blockade, but they are able to restore FBF acutely during exercise. Future studies are required to determine the nature of these compensatory mechanisms in the affected individuals.ATP-sensitive potassium (KATP) channels have been suggested to contribute to coronary and skeletal muscle vasodilation during exercise, either alone or interacting in a parallel or redundant process with nitric oxide (NO), prostaglandins (PGs), and adenosine. We tested the hypothesis that KATP channels, alone or in combination with NO and PGs, regulate exercise hyperemia in forearm muscle. Eighteen healthy young adults performed 20 min of moderate dynamic forearm exercise, with forearm blood flow (FBF) measured via Doppler ultrasound. After steady-state FBF was achieved for 5 min (saline control), the KATP inhibitor glibenclamide (Glib) was infused into the brachial artery for 5 min (10 microg.dl(-1).min(-1)), followed by saline infusion during the final 10 min of exercise (n = 9). Exercise increased FBF from 71 +/- 11 to 239 +/- 24 ml/min, and FBF was not altered by 5 min of Glib. Systemic plasma Glib levels were above the therapeutic range, and Glib increased insulin levels by approximately 50%, whereas blood glucose was unchanged (88 +/- 2 vs. 90 +/- 2 mg/dl). In nine additional subjects, Glib was followed by combined infusion of NG-nitro-L-arginine methyl ester (L-NAME) plus ketorolac (to inhibit NO and PGs, respectively). As above, Glib had no effect on FBF but addition of L-NAME + ketorolac (i.e., triple blockade) reduced FBF by approximately 15% below steady-state exercise levels in seven of nine subjects. Interestingly, triple blockade in two subjects caused FBF to transiently and dramatically decrease. This was followed by an acute recovery of flow above steady-state exercise values. We conclude 1) opening of KATP channels is not obligatory for forearm exercise hyperemia, and 2) triple blockade of NO, PGs, and KATP channels does not reduce hyperemia more than the inhibition of NO and PGs in most subjects. However, some subjects are sensitive to triple blockade, but they are able to restore FBF acutely during exercise. Future studies are required to determine the nature of these compensatory mechanisms in the affected individuals. ATP-sensitive potassium (K sub(ATP)) channels have been suggested to contribute to coronary and skeletal muscle vasodilation during exercise, either alone or interacting in a parallel or redundant process with nitric oxide (NO), prostaglandins (PGs), and adenosine. We tested the hypothesis that K sub(ATP) channels, alone or in combination with NO and PGs, regulate exercise hyperemia in forearm muscle. Eighteen healthy young adults performed 20 min of moderate dynamic forearm exercise, with forearm blood flow (FBF) measured via Doppler ultrasound. After steady-state FBF was achieved for 5 min (saline control), the K sub(ATP) inhibitor glibenclamide (Glib) was infused into the brachial artery for 5 min (10 mu g.dl super(-1).min super(-1)), followed by saline infusion during the final 10 min of exercise (n = 9). Exercise increased FBF from 71 plus or minus 11 to 239 plus or minus 24 ml/min, and FBF was not altered by 5 min of Glib. Systemic plasma Glib levels were above the therapeutic range, and Glib increased insulin levels by similar to 50%, whereas blood glucose was unchanged (88 plus or minus 2 vs. 90 plus or minus 2 mg/dl). In nine additional subjects, Glib was followed by combined infusion of N super(G)-nitro-L-arginine methyl ester (L-NAME) plus ketorolac (to inhibit NO and PGs, respectively). As above, Glib had no effect on FBF but addition of L-NAME + ketorolac (i.e., triple blockade) reduced FBF by similar to 15% below steady-state exercise levels in seven of nine subjects. Interestingly, triple blockade in two subjects caused FBF to transiently and dramatically decrease. This was followed by an acute recovery of flow above steady-state exercise values. We conclude 1) opening of K sub(ATP) channels is not obligatory for forearm exercise hyperemia, and 2) triple blockade of NO, PGs, and K sub(ATP) channels does not reduce hyperemia more than the inhibition of NO and PGs in most subjects. However, some subjects are sensitive to triple blockade, but they are able to restore FBF acutely during exercise. Future studies are required to determine the nature of these compensatory mechanisms in the affected individuals. |
| Author | Dietz, Niki M Schrage, William G Joyner, Michael J |
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| Keywords | Physical exercise Prostaglandin-endoperoxide synthase NG-nitro-L-arginine methyl ester Ionic channel Inorganic element Doppler ultrasound Arginine Eicosanoid Inhibition nitric oxide synthase Ultrasound Human Prostaglandin Enzyme Arachidonic acid derivatives cyclooxygenase Nitric-oxide synthase Blood flow Vertebrata Mammalia Aminoacid Nitric oxide Hemodynamics Oxidoreductases ATP Potassium |
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| Snippet | 1 Department of Anesthesiology and 2 General Clinical Research Center, Mayo Clinic, Rochester, Minnesota
Submitted 30 December 2005
; accepted in final form 6... ATP-sensitive potassium (K ATP ) channels have been suggested to contribute to coronary and skeletal muscle vasodilation during exercise, either alone or... ATP-sensitive potassium (KATP) channels have been suggested to contribute to coronary and skeletal muscle vasodilation during exercise, either alone or... ATP-sensitive potassium (K sub(ATP)) channels have been suggested to contribute to coronary and skeletal muscle vasodilation during exercise, either alone or... |
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| SubjectTerms | Adenosine Adenosine Triphosphate - physiology Adult ATP Biological and medical sciences Enzyme Inhibitors - pharmacology Exercise Exercise - physiology Female Forearm - blood supply Forearm - physiology Fundamental and applied biological sciences. Psychology Glyburide - pharmacology Human subjects Humans Hyperemia - physiopathology Inhibitor drugs Ketorolac - pharmacology Male Muscle, Skeletal - blood supply Muscle, Skeletal - physiopathology NG-Nitroarginine Methyl Ester - pharmacology Nitric oxide Nitric Oxide - antagonists & inhibitors Nitric Oxide - physiology Potassium Potassium Channels - drug effects Potassium Channels - physiology Prostaglandins - physiology Regional Blood Flow - drug effects Regional Blood Flow - physiology Ultrasonic imaging Vasodilation - drug effects Vasodilation - physiology Young adults |
| Title | Effects of combined inhibition of ATP-sensitive potassium channels, nitric oxide, and prostaglandins on hyperemia during moderate exercise |
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