The role of endothelin A receptors in peripheral vascular control at rest and during exercise in patients with hypertension
Key points Exercise in patients with hypertension can be accompanied by an abnormal cardiovascular response that includes attenuated blood flow and an augmented pressor response. Endothelin‐1, a very potent vasoconstrictor, is a key modulator of blood flow and pressure during in health and has been...
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| Published in: | The Journal of physiology Vol. 598; no. 1; pp. 71 - 84 |
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01-01-2020
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| Abstract | Key points
Exercise in patients with hypertension can be accompanied by an abnormal cardiovascular response that includes attenuated blood flow and an augmented pressor response.
Endothelin‐1, a very potent vasoconstrictor, is a key modulator of blood flow and pressure during in health and has been implicated as a potential cause of the dysfunction in hypertension.
We assessed the role of endothelin‐1, acting through endothelin A (ETA) receptors, in modulating the central and peripheral cardiovascular responses to exercise in patients with hypertension via local antagonism of these receptors during exercise.
ETA receptor antagonism markedly increased leg blood flow, vascular conductance, oxygen delivery, and oxygen consumption during exercise; interestingly, these changes occurred in the presence of reduced leg perfusion pressure, indicating that these augmentations were driven by changes in vascular resistance.
These data indicate that ETA receptor antagonism could be a viable therapeutic approach to improve blood flow during exercise in hypertension.
Patients with hypertension can exhibit impaired muscle blood flow and exaggerated increases in blood pressure during exercise. While endothelin (ET)‐1 plays a role in regulating blood flow and pressure during exercise in health, little is known about the role of ET‐1 in the cardiovascular response to exercise in hypertension. Therefore, eight volunteers diagnosed with hypertension were studied during exercise with either saline or BQ‐123 (ETA receptor antagonist) infusion following a 2‐week withdrawal of anti‐hypertensive medications. The common femoral artery and vein were catheterized for drug infusion, blood collection and blood pressure measurements, and leg blood flow was measured by Doppler ultrasound. Patients exercised at both absolute (0, 5, 10, 15 W) and relative (40, 60, 80% peak power) intensities. BQ‐123 increased blood flow at rest (79 ± 87 ml/min; P = 0.03) and augmented the exercise‐induced hyperaemia at most intensities (80% saline: Δ3818±1222 vs. BQ‐123: Δ4812±1469 ml/min; P = 0.001). BQ‐123 reduced leg MAP at rest (−8 ± 4 mmHg; P < 0.001) and lower intensities (0–10 W; P < 0.05). Systemic diastolic blood pressure was reduced (0 W, 40%; P < 0.05), but systemic MAP was defended by an increased cardiac output. The exercise pressor response (ΔMAP) did not differ between conditions (80% saline: 25 ± 10, BQ‐123: 30 ± 7 mmHg; P = 0.17). Thus, ET‐1, acting through the ETA receptors, contributes to the control of blood pressure at rest and lower intensity exercise in these patients. Furthermore, the finding that ET‐1 constrains the blood flow response to exercise suggests that ETA receptor antagonism could be a therapeutic approach to improve blood flow during exercise in hypertension.
Key points
Exercise in patients with hypertension can be accompanied by an abnormal cardiovascular response that includes attenuated blood flow and an augmented pressor response.
Endothelin‐1, a very potent vasoconstrictor, is a key modulator of blood flow and pressure during in health and has been implicated as a potential cause of the dysfunction in hypertension.
We assessed the role of endothelin‐1, acting through endothelin A (ETA) receptors, in modulating the central and peripheral cardiovascular responses to exercise in patients with hypertension via local antagonism of these receptors during exercise.
ETA receptor antagonism markedly increased leg blood flow, vascular conductance, oxygen delivery, and oxygen consumption during exercise; interestingly, these changes occurred in the presence of reduced leg perfusion pressure, indicating that these augmentations were driven by changes in vascular resistance.
These data indicate that ETA receptor antagonism could be a viable therapeutic approach to improve blood flow during exercise in hypertension. |
|---|---|
| AbstractList | Key points
Exercise in patients with hypertension can be accompanied by an abnormal cardiovascular response that includes attenuated blood flow and an augmented pressor response.
Endothelin‐1, a very potent vasoconstrictor, is a key modulator of blood flow and pressure during in health and has been implicated as a potential cause of the dysfunction in hypertension.
We assessed the role of endothelin‐1, acting through endothelin A (ETA) receptors, in modulating the central and peripheral cardiovascular responses to exercise in patients with hypertension via local antagonism of these receptors during exercise.
ETA receptor antagonism markedly increased leg blood flow, vascular conductance, oxygen delivery, and oxygen consumption during exercise; interestingly, these changes occurred in the presence of reduced leg perfusion pressure, indicating that these augmentations were driven by changes in vascular resistance.
These data indicate that ETA receptor antagonism could be a viable therapeutic approach to improve blood flow during exercise in hypertension.
Patients with hypertension can exhibit impaired muscle blood flow and exaggerated increases in blood pressure during exercise. While endothelin (ET)‐1 plays a role in regulating blood flow and pressure during exercise in health, little is known about the role of ET‐1 in the cardiovascular response to exercise in hypertension. Therefore, eight volunteers diagnosed with hypertension were studied during exercise with either saline or BQ‐123 (ETA receptor antagonist) infusion following a 2‐week withdrawal of anti‐hypertensive medications. The common femoral artery and vein were catheterized for drug infusion, blood collection and blood pressure measurements, and leg blood flow was measured by Doppler ultrasound. Patients exercised at both absolute (0, 5, 10, 15 W) and relative (40, 60, 80% peak power) intensities. BQ‐123 increased blood flow at rest (79 ± 87 ml/min; P = 0.03) and augmented the exercise‐induced hyperaemia at most intensities (80% saline: Δ3818±1222 vs. BQ‐123: Δ4812±1469 ml/min; P = 0.001). BQ‐123 reduced leg MAP at rest (−8 ± 4 mmHg; P < 0.001) and lower intensities (0–10 W; P < 0.05). Systemic diastolic blood pressure was reduced (0 W, 40%; P < 0.05), but systemic MAP was defended by an increased cardiac output. The exercise pressor response (ΔMAP) did not differ between conditions (80% saline: 25 ± 10, BQ‐123: 30 ± 7 mmHg; P = 0.17). Thus, ET‐1, acting through the ETA receptors, contributes to the control of blood pressure at rest and lower intensity exercise in these patients. Furthermore, the finding that ET‐1 constrains the blood flow response to exercise suggests that ETA receptor antagonism could be a therapeutic approach to improve blood flow during exercise in hypertension.
Key points
Exercise in patients with hypertension can be accompanied by an abnormal cardiovascular response that includes attenuated blood flow and an augmented pressor response.
Endothelin‐1, a very potent vasoconstrictor, is a key modulator of blood flow and pressure during in health and has been implicated as a potential cause of the dysfunction in hypertension.
We assessed the role of endothelin‐1, acting through endothelin A (ETA) receptors, in modulating the central and peripheral cardiovascular responses to exercise in patients with hypertension via local antagonism of these receptors during exercise.
ETA receptor antagonism markedly increased leg blood flow, vascular conductance, oxygen delivery, and oxygen consumption during exercise; interestingly, these changes occurred in the presence of reduced leg perfusion pressure, indicating that these augmentations were driven by changes in vascular resistance.
These data indicate that ETA receptor antagonism could be a viable therapeutic approach to improve blood flow during exercise in hypertension. Patients with hypertension can exhibit impaired muscle blood flow and exaggerated increases in blood pressure during exercise. While endothelin (ET)‐1 plays a role in regulating blood flow and pressure during exercise in health, little is known about the role of ET‐1 in the cardiovascular response to exercise in hypertension. Therefore, eight volunteers diagnosed with hypertension were studied during exercise with either saline or BQ‐123 (ETA receptor antagonist) infusion following a 2‐week withdrawal of anti‐hypertensive medications. The common femoral artery and vein were catheterized for drug infusion, blood collection and blood pressure measurements, and leg blood flow was measured by Doppler ultrasound. Patients exercised at both absolute (0, 5, 10, 15 W) and relative (40, 60, 80% peak power) intensities. BQ‐123 increased blood flow at rest (79 ± 87 ml/min; P = 0.03) and augmented the exercise‐induced hyperaemia at most intensities (80% saline: Δ3818±1222 vs. BQ‐123: Δ4812±1469 ml/min; P = 0.001). BQ‐123 reduced leg MAP at rest (−8 ± 4 mmHg; P < 0.001) and lower intensities (0–10 W; P < 0.05). Systemic diastolic blood pressure was reduced (0 W, 40%; P < 0.05), but systemic MAP was defended by an increased cardiac output. The exercise pressor response (ΔMAP) did not differ between conditions (80% saline: 25 ± 10, BQ‐123: 30 ± 7 mmHg; P = 0.17). Thus, ET‐1, acting through the ETA receptors, contributes to the control of blood pressure at rest and lower intensity exercise in these patients. Furthermore, the finding that ET‐1 constrains the blood flow response to exercise suggests that ETA receptor antagonism could be a therapeutic approach to improve blood flow during exercise in hypertension. Patients with hypertension can exhibit impaired muscle blood flow and exaggerated increases in blood pressure during exercise. While endothelin (ET)-1 plays a role in regulating blood flow and pressure during exercise in health, little is known about the role of ET-1 in the cardiovascular response to exercise in hypertension. Therefore, eight volunteers diagnosed with hypertension were studied during exercise with either saline or BQ-123 (ET A receptor antagonist) infusion following a 2-week withdrawal of anti-hypertensive medications. The common femoral artery and vein were catheterized for drug infusion, blood collection, and blood pressure measurements and leg blood flow was measured by Doppler ultrasound. Patients exercised at both absolute (0, 5, 10, 15 W) and relative (40, 60, 80 % peak power) intensities. BQ-123 increased blood flow at rest (79±87 ml/min; p=0.03) and augmented the exercise-induced hyperemia at most intensities (80% Saline: Δ3818±1222 vs BQ-123: Δ4812±1469 ml/min; p=0.001). BQ-123 reduced leg MAP at rest (−8±4 mmHg; p<0.001) and lower intensities (0-10 W; p<0.05). Systemic diastolic blood pressure was reduced (0 W-40 %; p<0.05), but systemic MAP was defended by an increased cardiac output. The exercise pressor response (ΔMAP) did not differ between conditions (80% saline: 25±10, BQ-123: 30±7 mmHg; p=0.17). Thus, ET-1, acting through the ET A receptors, contributes to the control of blood pressure at rest and lower intensity exercise in these patients. Furthermore, the finding that ET-1 constrains the blood flow response to exercise suggests that ET A receptor antagonism could be a therapeutic approach to improve blood flow during exercise in hypertension. KEY POINTSExercise in patients with hypertension can be accompanied by an abnormal cardiovascular response that includes attenuated blood flow and an augmented pressor response. Endothelin-1, a very potent vasoconstrictor, is a key modulator of blood flow and pressure during in health and has been implicated as a potential cause of the dysfunction in hypertension. We assessed the role of endothelin-1, acting through endothelin A (ETA ) receptors, in modulating the central and peripheral cardiovascular responses to exercise in patients with hypertension via local antagonism of these receptors during exercise. ETA receptor antagonism markedly increased leg blood flow, vascular conductance, oxygen delivery, and oxygen consumption during exercise; interestingly, these changes occurred in the presence of reduced leg perfusion pressure, indicating that these augmentations were driven by changes in vascular resistance. These data indicate that ETA receptor antagonism could be a viable therapeutic approach to improve blood flow during exercise in hypertension. ABSTRACTPatients with hypertension can exhibit impaired muscle blood flow and exaggerated increases in blood pressure during exercise. While endothelin (ET)-1 plays a role in regulating blood flow and pressure during exercise in health, little is known about the role of ET-1 in the cardiovascular response to exercise in hypertension. Therefore, eight volunteers diagnosed with hypertension were studied during exercise with either saline or BQ-123 (ETA receptor antagonist) infusion following a 2-week withdrawal of anti-hypertensive medications. The common femoral artery and vein were catheterized for drug infusion, blood collection and blood pressure measurements, and leg blood flow was measured by Doppler ultrasound. Patients exercised at both absolute (0, 5, 10, 15 W) and relative (40, 60, 80% peak power) intensities. BQ-123 increased blood flow at rest (79 ± 87 ml/min; P = 0.03) and augmented the exercise-induced hyperaemia at most intensities (80% saline: Δ3818±1222 vs. BQ-123: Δ4812±1469 ml/min; P = 0.001). BQ-123 reduced leg MAP at rest (-8 ± 4 mmHg; P < 0.001) and lower intensities (0-10 W; P < 0.05). Systemic diastolic blood pressure was reduced (0 W, 40%; P < 0.05), but systemic MAP was defended by an increased cardiac output. The exercise pressor response (ΔMAP) did not differ between conditions (80% saline: 25 ± 10, BQ-123: 30 ± 7 mmHg; P = 0.17). Thus, ET-1, acting through the ETA receptors, contributes to the control of blood pressure at rest and lower intensity exercise in these patients. Furthermore, the finding that ET-1 constrains the blood flow response to exercise suggests that ETA receptor antagonism could be a therapeutic approach to improve blood flow during exercise in hypertension. Exercise in patients with hypertension can be accompanied by an abnormal cardiovascular response that includes attenuated blood flow and an augmented pressor response. Endothelin-1, a very potent vasoconstrictor, is a key modulator of blood flow and pressure during in health and has been implicated as a potential cause of the dysfunction in hypertension. We assessed the role of endothelin-1, acting through endothelin A (ET ) receptors, in modulating the central and peripheral cardiovascular responses to exercise in patients with hypertension via local antagonism of these receptors during exercise. ET receptor antagonism markedly increased leg blood flow, vascular conductance, oxygen delivery, and oxygen consumption during exercise; interestingly, these changes occurred in the presence of reduced leg perfusion pressure, indicating that these augmentations were driven by changes in vascular resistance. These data indicate that ET receptor antagonism could be a viable therapeutic approach to improve blood flow during exercise in hypertension. Patients with hypertension can exhibit impaired muscle blood flow and exaggerated increases in blood pressure during exercise. While endothelin (ET)-1 plays a role in regulating blood flow and pressure during exercise in health, little is known about the role of ET-1 in the cardiovascular response to exercise in hypertension. Therefore, eight volunteers diagnosed with hypertension were studied during exercise with either saline or BQ-123 (ET receptor antagonist) infusion following a 2-week withdrawal of anti-hypertensive medications. The common femoral artery and vein were catheterized for drug infusion, blood collection and blood pressure measurements, and leg blood flow was measured by Doppler ultrasound. Patients exercised at both absolute (0, 5, 10, 15 W) and relative (40, 60, 80% peak power) intensities. BQ-123 increased blood flow at rest (79 ± 87 ml/min; P = 0.03) and augmented the exercise-induced hyperaemia at most intensities (80% saline: Δ3818±1222 vs. BQ-123: Δ4812±1469 ml/min; P = 0.001). BQ-123 reduced leg MAP at rest (-8 ± 4 mmHg; P < 0.001) and lower intensities (0-10 W; P < 0.05). Systemic diastolic blood pressure was reduced (0 W, 40%; P < 0.05), but systemic MAP was defended by an increased cardiac output. The exercise pressor response (ΔMAP) did not differ between conditions (80% saline: 25 ± 10, BQ-123: 30 ± 7 mmHg; P = 0.17). Thus, ET-1, acting through the ET receptors, contributes to the control of blood pressure at rest and lower intensity exercise in these patients. Furthermore, the finding that ET-1 constrains the blood flow response to exercise suggests that ET receptor antagonism could be a therapeutic approach to improve blood flow during exercise in hypertension. Exercise in patients with hypertension can be accompanied by an abnormal cardiovascular response that includes attenuated blood flow and an augmented pressor response. Endothelin‐1, a very potent vasoconstrictor, is a key modulator of blood flow and pressure during in health and has been implicated as a potential cause of the dysfunction in hypertension. We assessed the role of endothelin‐1, acting through endothelin A (ET A ) receptors, in modulating the central and peripheral cardiovascular responses to exercise in patients with hypertension via local antagonism of these receptors during exercise. ET A receptor antagonism markedly increased leg blood flow, vascular conductance, oxygen delivery, and oxygen consumption during exercise; interestingly, these changes occurred in the presence of reduced leg perfusion pressure, indicating that these augmentations were driven by changes in vascular resistance. These data indicate that ET A receptor antagonism could be a viable therapeutic approach to improve blood flow during exercise in hypertension. |
| Author | Bunsawat, Kanokwan Richardson, Russell S. Cerbie, James Nelson, Ashley D. Gifford, Jayson R. Morgan, David E. Broxterman, Ryan M. Trinity, Joel D. Craig, Jesse C. Ratchford, Stephen M. Wray, D. Walter La Salle, D. Taylor Bledsoe, Amber D. |
| AuthorAffiliation | 3 Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, Utah 4 Department of Anesthesiology, University of Utah, Salt Lake City, Utah 1 Department of Internal Medicine, University of Utah, Salt Lake City, Utah 2 Geriatric Research, Education, and Clinical Center, Veterans Affairs Medical Center, Salt Lake City, Utah |
| AuthorAffiliation_xml | – name: 3 Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, Utah – name: 2 Geriatric Research, Education, and Clinical Center, Veterans Affairs Medical Center, Salt Lake City, Utah – name: 1 Department of Internal Medicine, University of Utah, Salt Lake City, Utah – name: 4 Department of Anesthesiology, University of Utah, Salt Lake City, Utah |
| Author_xml | – sequence: 1 givenname: Jesse C. orcidid: 0000-0001-5959-4139 surname: Craig fullname: Craig, Jesse C. email: jesse.craig@utah.edu organization: University of Utah – sequence: 2 givenname: Ryan M. orcidid: 0000-0002-7388-2214 surname: Broxterman fullname: Broxterman, Ryan M. organization: Veterans Affairs Medical Center – sequence: 3 givenname: D. Taylor orcidid: 0000-0001-7956-8704 surname: La Salle fullname: La Salle, D. Taylor organization: University of Utah – sequence: 4 givenname: James surname: Cerbie fullname: Cerbie, James organization: University of Utah – sequence: 5 givenname: Stephen M. orcidid: 0000-0002-6300-7600 surname: Ratchford fullname: Ratchford, Stephen M. organization: Veterans Affairs Medical Center – sequence: 6 givenname: Jayson R. orcidid: 0000-0002-6034-306X surname: Gifford fullname: Gifford, Jayson R. organization: Veterans Affairs Medical Center – sequence: 7 givenname: Kanokwan surname: Bunsawat fullname: Bunsawat, Kanokwan organization: University of Utah – sequence: 8 givenname: Ashley D. surname: Nelson fullname: Nelson, Ashley D. organization: University of Utah – sequence: 9 givenname: Amber D. surname: Bledsoe fullname: Bledsoe, Amber D. organization: University of Utah – sequence: 10 givenname: David E. surname: Morgan fullname: Morgan, David E. organization: University of Utah – sequence: 11 givenname: D. Walter surname: Wray fullname: Wray, D. Walter organization: University of Utah – sequence: 12 givenname: Russell S. surname: Richardson fullname: Richardson, Russell S. organization: University of Utah – sequence: 13 givenname: Joel D. orcidid: 0000-0001-8271-6536 surname: Trinity fullname: Trinity, Joel D. organization: University of Utah |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31705661$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1113_JP279344 crossref_primary_10_1152_japplphysiol_00218_2022 crossref_primary_10_3389_fimmu_2022_835953 |
| Cites_doi | 10.1249/01.mss.0000230342.86870.94 10.1161/HYPERTENSIONAHA.107.088294 10.1152/japplphysiol.00219.2004 10.1152/japplphysiol.00357.2007 10.1161/01.CIR.97.8.752 10.1097/HJH.0000000000000777 10.1113/jphysiol.2010.203026 10.1161/01.CIR.100.12.1305 10.1038/sj.bjp.0704304 10.1152/ajpheart.00575.2013 10.1161/01.HYP.31.1.68 10.1016/j.amjhyper.2006.02.001 10.1152/ajpheart.00689.2008 10.1042/CS20030302 10.1113/jphysiol.2011.209353 10.1113/jphysiol.2006.121558 10.1056/NEJM199007053230105 10.1016/j.autneu.2014.10.010 10.1253/jcj.47.802 10.1097/00004872-198706000-00007 10.1152/ajpheart.00603.2012 10.1152/ajpheart.00556.2010 10.1152/japplphysiol.01281.2006 10.1161/01.CIR.100.16.1680 10.1152/jappl.1993.75.4.1911 10.1113/jphysiol.2003.059717 10.1136/gut.52.3.410 10.1139/apnm-2018-0101 10.1093/gerona/glu065 10.1152/jappl.1998.84.1.277 10.1152/jappl.1997.83.4.1383 10.1111/j.1469-7793.1999.00621.x 10.1161/HYPERTENSIONAHA.107.094649 10.1152/ajpheart.00867.2007 10.1152/ajpheart.00206.2011 10.1161/HYPERTENSIONAHA.118.11076 10.1152/physrev.00035.2013 10.7326/0003-4819-124-1_Part_1-199601010-00008 10.1113/jphysiol.2011.225136 10.1152/ajpheart.1991.260.2.H632 10.1113/jphysiol.2007.150060 10.1161/HYP.0000000000000066 10.1113/jphysiol.1985.sp015794 10.1161/01.HYP.33.2.753 10.1113/JP271335 10.1161/01.CIR.91.6.1732 10.1161/01.HYP.0000024218.04872.F3 10.1161/01.HYP.29.3.736 |
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| Copyright | 2019 The Authors. The Journal of Physiology © 2019 The Physiological Society 2019 The Authors. The Journal of Physiology © 2019 The Physiological Society. Journal compilation © 2020 The Physiological Society |
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| Keywords | ETA receptor exercise pressor response exercise hyperaemia |
| Language | English |
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| Notes | Edited by: Harold Schultz & Caroline Rickards ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Author contributions. JCC, RMB, DWW, RSR, and JDT conceived and designed the study. JCC, RMB, DTL, JC, SMR, JRG, KB, AND, ADB, DEM, DWW, RSR, and JDT acquired, analyzed and interpreted the data. JCC prepared the first draft of the manuscript. All authors critically reviewed and approved the final version of the manuscript and agree to be accountable for all aspects of the work. The experiments were performed in the Utah Vascular Research Laboratory. All persons designated as authors qualify for authorship, and all those who qualify for authorship are listed. |
| ORCID | 0000-0002-6300-7600 0000-0001-5959-4139 0000-0002-6034-306X 0000-0001-8271-6536 0000-0001-7956-8704 0000-0002-7388-2214 |
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| References | 2007; 103 1997; 83 1995; 91 1990; 323 2015; 70 2015; 95 2015; 188 2006; 38 1987; 5 2013; 304 2009; 297 1985; 366 1997; 29 2006; 19 1999; 520 2007; 50 1999; 100 2008; 586 1998; 84 2006; 577 1996; 124 2003; 52 2004; 106 2016; 34 2011; 589 2012; 590 2014; 306 2011; 301 2001; 134 2004; 556 2007; 293 2019; 44 2002; 40 1991; 260 2010; 299 1993; 75 1999; 33 2016; 594 2005; 98 2018; 72 2018; 71 1998; 31 1998; 97 1983; 47 31856308 - J Physiol. 2020 Feb;598(3):441-442 e_1_2_5_27_1 e_1_2_5_28_1 e_1_2_5_49_1 e_1_2_5_25_1 e_1_2_5_48_1 e_1_2_5_26_1 e_1_2_5_47_1 e_1_2_5_23_1 e_1_2_5_46_1 e_1_2_5_24_1 e_1_2_5_45_1 e_1_2_5_21_1 e_1_2_5_44_1 e_1_2_5_22_1 e_1_2_5_43_1 e_1_2_5_29_1 e_1_2_5_42_1 e_1_2_5_20_1 e_1_2_5_41_1 e_1_2_5_40_1 e_1_2_5_15_1 e_1_2_5_38_1 e_1_2_5_14_1 e_1_2_5_39_1 e_1_2_5_17_1 e_1_2_5_36_1 e_1_2_5_9_1 e_1_2_5_16_1 e_1_2_5_37_1 e_1_2_5_8_1 e_1_2_5_11_1 e_1_2_5_34_1 e_1_2_5_7_1 e_1_2_5_10_1 e_1_2_5_35_1 e_1_2_5_6_1 e_1_2_5_13_1 e_1_2_5_32_1 e_1_2_5_5_1 e_1_2_5_12_1 e_1_2_5_33_1 e_1_2_5_4_1 e_1_2_5_3_1 e_1_2_5_2_1 e_1_2_5_19_1 e_1_2_5_18_1 e_1_2_5_30_1 e_1_2_5_31_1 |
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Exercise in patients with hypertension can be accompanied by an abnormal cardiovascular response that includes attenuated blood flow and an... Exercise in patients with hypertension can be accompanied by an abnormal cardiovascular response that includes attenuated blood flow and an augmented pressor... Patients with hypertension can exhibit impaired muscle blood flow and exaggerated increases in blood pressure during exercise. While endothelin (ET)‐1 plays a... KEY POINTSExercise in patients with hypertension can be accompanied by an abnormal cardiovascular response that includes attenuated blood flow and an augmented... Patients with hypertension can exhibit impaired muscle blood flow and exaggerated increases in blood pressure during exercise. While endothelin (ET)-1 plays a... |
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| SubjectTerms | Antihypertensives Blood flow Blood Pressure Doppler effect Endothelin ETA receptors Endothelin Receptor Antagonists - pharmacology Endothelin-1 - physiology ETA receptor Exercise exercise hyperaemia exercise pressor response Femoral artery Humans Hyperemia Hypertension Hypertension - physiopathology Leg Muscle, Skeletal - blood supply Peptides, Cyclic - pharmacology Receptor, Endothelin A - physiology Regional Blood Flow Ultrasound |
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| Title | The role of endothelin A receptors in peripheral vascular control at rest and during exercise in patients with hypertension |
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