The role of nitric oxide in coronary vascular effects of estrogen in postmenopausal women

Victor Guetta, Arshed A. Quyyumi, Abhiram Prasad, Julio A. Panza, Myron Waclawiw, Richard O. Cannon

Research output: Contribution to journalArticle

215 Citations (Scopus)

Abstract

Background: At physiological concentrations, 17β-estradiol selectively enhances endothelium-dependent coronary vasodilation by an unknown mechanism in postmenopausal women. Methods and Results: To assess the contribution of nitric oxide (NO) to the vascular effects of estradiol, we measured coronary epicardial and microvascular responses to intracoronary acetylcholine (range, 3 to 300 μg/min for 2 minutes) before and after intracoronary estradiol 75 ng/min for 15 minutes in 20 estrogen-deficient women, 16 of whom had angiographic evidence of atherosclerosis or risk factors for atherosclerosis. This testing was repeated after inhibition of NO synthesis with intracoronary N(G)-monomethyl-L-arginine (L-NMMA) 64 μmol/min for 5 minutes. Estradiol increased acetylcholine-stimulated coronary flow from 54±48% (mean±SD) above baseline values before estradiol infusion to 100±63% above baseline values (P=.007) and decreased coronary resistance from 32±21% to 46±15% below baseline values (P=.007) at a coronary sinus estradiol concentration of 1725±705 pmol/L (470±192 pg/mL). Estradiol also tended to lessen the severity of acetylcholine-induced epicardial coronary artery vasoconstriction from 8±11% to 3±11% below baseline values (P=.123). However, during L-NMMA infusion, estradiol no longer potentiated the effects of acetylcholine on coronary flow dynamics; coronary flow increased 39±46% above baseline values and coronary resistance decreased 19±30% below baseline values (both P<.001 versus pre-L-NMMA responses). The epicardial diameter decreased 8±11% below baseline values (P=.06 versus pre-L-NMMA response). Conclusions: The effects of estradiol at physiological concentrations on endothelium-dependent coronary vasodilator responsiveness in postmenopausal women are mediated by enhanced bioavailability of NO, which may be responsible in part for the cardioprotective effects of estrogen.

Original languageEnglish (US)
Pages (from-to)2795-2801
Number of pages7
JournalCirculation
Volume96
Issue number9
StatePublished - Nov 4 1997
Externally publishedYes

Fingerprint

Blood Vessels
Estradiol
Nitric Oxide
Estrogens
omega-N-Methylarginine
Acetylcholine
Atherosclerosis
Endothelium-Dependent Relaxing Factors
Coronary Sinus
Vasoconstriction
Vasodilation
Biological Availability
Endothelium
Arginine
Coronary Vessels

Keywords

  • Atherosclerosis
  • Coronary disease
  • Endothelium
  • Hormones
  • Nitric oxide

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Guetta, V., Quyyumi, A. A., Prasad, A., Panza, J. A., Waclawiw, M., & Cannon, R. O. (1997). The role of nitric oxide in coronary vascular effects of estrogen in postmenopausal women. Circulation, 96(9), 2795-2801.

The role of nitric oxide in coronary vascular effects of estrogen in postmenopausal women. / Guetta, Victor; Quyyumi, Arshed A.; Prasad, Abhiram; Panza, Julio A.; Waclawiw, Myron; Cannon, Richard O.

In: Circulation, Vol. 96, No. 9, 04.11.1997, p. 2795-2801.

Research output: Contribution to journalArticle

Guetta, V, Quyyumi, AA, Prasad, A, Panza, JA, Waclawiw, M & Cannon, RO 1997, 'The role of nitric oxide in coronary vascular effects of estrogen in postmenopausal women', Circulation, vol. 96, no. 9, pp. 2795-2801.
Guetta V, Quyyumi AA, Prasad A, Panza JA, Waclawiw M, Cannon RO. The role of nitric oxide in coronary vascular effects of estrogen in postmenopausal women. Circulation. 1997 Nov 4;96(9):2795-2801.
Guetta, Victor ; Quyyumi, Arshed A. ; Prasad, Abhiram ; Panza, Julio A. ; Waclawiw, Myron ; Cannon, Richard O. / The role of nitric oxide in coronary vascular effects of estrogen in postmenopausal women. In: Circulation. 1997 ; Vol. 96, No. 9. pp. 2795-2801.
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abstract = "Background: At physiological concentrations, 17β-estradiol selectively enhances endothelium-dependent coronary vasodilation by an unknown mechanism in postmenopausal women. Methods and Results: To assess the contribution of nitric oxide (NO) to the vascular effects of estradiol, we measured coronary epicardial and microvascular responses to intracoronary acetylcholine (range, 3 to 300 μg/min for 2 minutes) before and after intracoronary estradiol 75 ng/min for 15 minutes in 20 estrogen-deficient women, 16 of whom had angiographic evidence of atherosclerosis or risk factors for atherosclerosis. This testing was repeated after inhibition of NO synthesis with intracoronary N(G)-monomethyl-L-arginine (L-NMMA) 64 μmol/min for 5 minutes. Estradiol increased acetylcholine-stimulated coronary flow from 54±48{\%} (mean±SD) above baseline values before estradiol infusion to 100±63{\%} above baseline values (P=.007) and decreased coronary resistance from 32±21{\%} to 46±15{\%} below baseline values (P=.007) at a coronary sinus estradiol concentration of 1725±705 pmol/L (470±192 pg/mL). Estradiol also tended to lessen the severity of acetylcholine-induced epicardial coronary artery vasoconstriction from 8±11{\%} to 3±11{\%} below baseline values (P=.123). However, during L-NMMA infusion, estradiol no longer potentiated the effects of acetylcholine on coronary flow dynamics; coronary flow increased 39±46{\%} above baseline values and coronary resistance decreased 19±30{\%} below baseline values (both P<.001 versus pre-L-NMMA responses). The epicardial diameter decreased 8±11{\%} below baseline values (P=.06 versus pre-L-NMMA response). Conclusions: The effects of estradiol at physiological concentrations on endothelium-dependent coronary vasodilator responsiveness in postmenopausal women are mediated by enhanced bioavailability of NO, which may be responsible in part for the cardioprotective effects of estrogen.",
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T1 - The role of nitric oxide in coronary vascular effects of estrogen in postmenopausal women

AU - Guetta, Victor

AU - Quyyumi, Arshed A.

AU - Prasad, Abhiram

AU - Panza, Julio A.

AU - Waclawiw, Myron

AU - Cannon, Richard O.

PY - 1997/11/4

Y1 - 1997/11/4

N2 - Background: At physiological concentrations, 17β-estradiol selectively enhances endothelium-dependent coronary vasodilation by an unknown mechanism in postmenopausal women. Methods and Results: To assess the contribution of nitric oxide (NO) to the vascular effects of estradiol, we measured coronary epicardial and microvascular responses to intracoronary acetylcholine (range, 3 to 300 μg/min for 2 minutes) before and after intracoronary estradiol 75 ng/min for 15 minutes in 20 estrogen-deficient women, 16 of whom had angiographic evidence of atherosclerosis or risk factors for atherosclerosis. This testing was repeated after inhibition of NO synthesis with intracoronary N(G)-monomethyl-L-arginine (L-NMMA) 64 μmol/min for 5 minutes. Estradiol increased acetylcholine-stimulated coronary flow from 54±48% (mean±SD) above baseline values before estradiol infusion to 100±63% above baseline values (P=.007) and decreased coronary resistance from 32±21% to 46±15% below baseline values (P=.007) at a coronary sinus estradiol concentration of 1725±705 pmol/L (470±192 pg/mL). Estradiol also tended to lessen the severity of acetylcholine-induced epicardial coronary artery vasoconstriction from 8±11% to 3±11% below baseline values (P=.123). However, during L-NMMA infusion, estradiol no longer potentiated the effects of acetylcholine on coronary flow dynamics; coronary flow increased 39±46% above baseline values and coronary resistance decreased 19±30% below baseline values (both P<.001 versus pre-L-NMMA responses). The epicardial diameter decreased 8±11% below baseline values (P=.06 versus pre-L-NMMA response). Conclusions: The effects of estradiol at physiological concentrations on endothelium-dependent coronary vasodilator responsiveness in postmenopausal women are mediated by enhanced bioavailability of NO, which may be responsible in part for the cardioprotective effects of estrogen.

AB - Background: At physiological concentrations, 17β-estradiol selectively enhances endothelium-dependent coronary vasodilation by an unknown mechanism in postmenopausal women. Methods and Results: To assess the contribution of nitric oxide (NO) to the vascular effects of estradiol, we measured coronary epicardial and microvascular responses to intracoronary acetylcholine (range, 3 to 300 μg/min for 2 minutes) before and after intracoronary estradiol 75 ng/min for 15 minutes in 20 estrogen-deficient women, 16 of whom had angiographic evidence of atherosclerosis or risk factors for atherosclerosis. This testing was repeated after inhibition of NO synthesis with intracoronary N(G)-monomethyl-L-arginine (L-NMMA) 64 μmol/min for 5 minutes. Estradiol increased acetylcholine-stimulated coronary flow from 54±48% (mean±SD) above baseline values before estradiol infusion to 100±63% above baseline values (P=.007) and decreased coronary resistance from 32±21% to 46±15% below baseline values (P=.007) at a coronary sinus estradiol concentration of 1725±705 pmol/L (470±192 pg/mL). Estradiol also tended to lessen the severity of acetylcholine-induced epicardial coronary artery vasoconstriction from 8±11% to 3±11% below baseline values (P=.123). However, during L-NMMA infusion, estradiol no longer potentiated the effects of acetylcholine on coronary flow dynamics; coronary flow increased 39±46% above baseline values and coronary resistance decreased 19±30% below baseline values (both P<.001 versus pre-L-NMMA responses). The epicardial diameter decreased 8±11% below baseline values (P=.06 versus pre-L-NMMA response). Conclusions: The effects of estradiol at physiological concentrations on endothelium-dependent coronary vasodilator responsiveness in postmenopausal women are mediated by enhanced bioavailability of NO, which may be responsible in part for the cardioprotective effects of estrogen.

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