Nitric oxide inhibition as a mechanism for blood pressure increase during salt loading in normotensive postmenopausal women

Angelo Scuteri, Markus C. Stuehlinger, John P. Cooke, Jeanette G. Wright, Edward G. Lakatta, David E. Anderson, Jerome L. Fleg

Research output: Contribution to journalArticle

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Abstract

Objectives: Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide (NO), which plays an important role in natriuresis. We determined whether changes in endothelium-dependent vasodilation (EDD) and plasma ADMA predict changes in blood pressure (BP) after salt loading in normotensive postmenopausal women (PMW). Methods: In 15 normotensive PMW (age 50-60 years), not receiving estrogen, ambulatory 24-h BP, plasma lipids, and ADMA were measured after 4 days of a low-salt diet (70 mEq/day) and following 7 days of high-salt intake (260 mEq/day). Brachial artery diameter at rest, during reactive hyperemia, i.e. EDD, and after sublingual nitroglycerin, i.e. non-EDD, were measured by ultrasound. The 24-h urinary NO metabolite (NOx) was measured by Griess reaction. Plasma ADMA was measured by high-pressure liquid chromatography. Results: During low-salt, 24-h BP levels averaged 121 ± 11 and 69 ± 7 mmHg for systolic BP (SBP) and diastolic BP (DBP), respectively. After salt loading, average 24-h BP increases were: 7.6 mmHg for SBP, 2.2 mmHg for DBP, and 5.5 mmHg for pulse pressure (PP). Increases of 24-h SBP and 24-h PP after salt loading correlated directly with changes in ADMA (partial R2 = 0.16 for 24-h SBP and 0.17 for 24-h PP, P <0.05 for both) and inversely with changes in EDD (partial R2 = 0.13, P = 0.09 for 24 h SBP and partial R2 = 0.15, P = 0.07 for 24-h PP), after adjustment for age and cholesterol. Conclusions: Inhibition of NO bioavailability by ADMA and a subsequent reduction in EDD contribute to the increase in BP during high-salt intake in normotensive PMW not receiving estrogen.

Original languageEnglish
Pages (from-to)1339-1346
Number of pages8
JournalJournal of Hypertension
Volume21
Issue number7
DOIs
Publication statusPublished - Jul 1 2003

Fingerprint

Nitric Oxide
Salts
Blood Pressure
Vasodilation
Endothelium
Estrogens
Sodium-Restricted Diet
Natriuresis
Brachial Artery
Hyperemia
Nitroglycerin
Biological Availability
N,N-dimethylarginine
Cholesterol
High Pressure Liquid Chromatography
Hypertension
Lipids

Keywords

  • Arginine
  • Endothelium
  • Nitric oxide
  • Postmenopausal women
  • Salt sensitivity
  • Vasodilation

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology

Cite this

Scuteri, A., Stuehlinger, M. C., Cooke, J. P., Wright, J. G., Lakatta, E. G., Anderson, D. E., & Fleg, J. L. (2003). Nitric oxide inhibition as a mechanism for blood pressure increase during salt loading in normotensive postmenopausal women. Journal of Hypertension, 21(7), 1339-1346. https://doi.org/10.1097/00004872-200307000-00023

Nitric oxide inhibition as a mechanism for blood pressure increase during salt loading in normotensive postmenopausal women. / Scuteri, Angelo; Stuehlinger, Markus C.; Cooke, John P.; Wright, Jeanette G.; Lakatta, Edward G.; Anderson, David E.; Fleg, Jerome L.

In: Journal of Hypertension, Vol. 21, No. 7, 01.07.2003, p. 1339-1346.

Research output: Contribution to journalArticle

Scuteri, A, Stuehlinger, MC, Cooke, JP, Wright, JG, Lakatta, EG, Anderson, DE & Fleg, JL 2003, 'Nitric oxide inhibition as a mechanism for blood pressure increase during salt loading in normotensive postmenopausal women', Journal of Hypertension, vol. 21, no. 7, pp. 1339-1346. https://doi.org/10.1097/00004872-200307000-00023
Scuteri, Angelo ; Stuehlinger, Markus C. ; Cooke, John P. ; Wright, Jeanette G. ; Lakatta, Edward G. ; Anderson, David E. ; Fleg, Jerome L. / Nitric oxide inhibition as a mechanism for blood pressure increase during salt loading in normotensive postmenopausal women. In: Journal of Hypertension. 2003 ; Vol. 21, No. 7. pp. 1339-1346.
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abstract = "Objectives: Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide (NO), which plays an important role in natriuresis. We determined whether changes in endothelium-dependent vasodilation (EDD) and plasma ADMA predict changes in blood pressure (BP) after salt loading in normotensive postmenopausal women (PMW). Methods: In 15 normotensive PMW (age 50-60 years), not receiving estrogen, ambulatory 24-h BP, plasma lipids, and ADMA were measured after 4 days of a low-salt diet (70 mEq/day) and following 7 days of high-salt intake (260 mEq/day). Brachial artery diameter at rest, during reactive hyperemia, i.e. EDD, and after sublingual nitroglycerin, i.e. non-EDD, were measured by ultrasound. The 24-h urinary NO metabolite (NOx) was measured by Griess reaction. Plasma ADMA was measured by high-pressure liquid chromatography. Results: During low-salt, 24-h BP levels averaged 121 ± 11 and 69 ± 7 mmHg for systolic BP (SBP) and diastolic BP (DBP), respectively. After salt loading, average 24-h BP increases were: 7.6 mmHg for SBP, 2.2 mmHg for DBP, and 5.5 mmHg for pulse pressure (PP). Increases of 24-h SBP and 24-h PP after salt loading correlated directly with changes in ADMA (partial R2 = 0.16 for 24-h SBP and 0.17 for 24-h PP, P <0.05 for both) and inversely with changes in EDD (partial R2 = 0.13, P = 0.09 for 24 h SBP and partial R2 = 0.15, P = 0.07 for 24-h PP), after adjustment for age and cholesterol. Conclusions: Inhibition of NO bioavailability by ADMA and a subsequent reduction in EDD contribute to the increase in BP during high-salt intake in normotensive PMW not receiving estrogen.",
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AU - Scuteri, Angelo

AU - Stuehlinger, Markus C.

AU - Cooke, John P.

AU - Wright, Jeanette G.

AU - Lakatta, Edward G.

AU - Anderson, David E.

AU - Fleg, Jerome L.

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N2 - Objectives: Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide (NO), which plays an important role in natriuresis. We determined whether changes in endothelium-dependent vasodilation (EDD) and plasma ADMA predict changes in blood pressure (BP) after salt loading in normotensive postmenopausal women (PMW). Methods: In 15 normotensive PMW (age 50-60 years), not receiving estrogen, ambulatory 24-h BP, plasma lipids, and ADMA were measured after 4 days of a low-salt diet (70 mEq/day) and following 7 days of high-salt intake (260 mEq/day). Brachial artery diameter at rest, during reactive hyperemia, i.e. EDD, and after sublingual nitroglycerin, i.e. non-EDD, were measured by ultrasound. The 24-h urinary NO metabolite (NOx) was measured by Griess reaction. Plasma ADMA was measured by high-pressure liquid chromatography. Results: During low-salt, 24-h BP levels averaged 121 ± 11 and 69 ± 7 mmHg for systolic BP (SBP) and diastolic BP (DBP), respectively. After salt loading, average 24-h BP increases were: 7.6 mmHg for SBP, 2.2 mmHg for DBP, and 5.5 mmHg for pulse pressure (PP). Increases of 24-h SBP and 24-h PP after salt loading correlated directly with changes in ADMA (partial R2 = 0.16 for 24-h SBP and 0.17 for 24-h PP, P <0.05 for both) and inversely with changes in EDD (partial R2 = 0.13, P = 0.09 for 24 h SBP and partial R2 = 0.15, P = 0.07 for 24-h PP), after adjustment for age and cholesterol. Conclusions: Inhibition of NO bioavailability by ADMA and a subsequent reduction in EDD contribute to the increase in BP during high-salt intake in normotensive PMW not receiving estrogen.

AB - Objectives: Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide (NO), which plays an important role in natriuresis. We determined whether changes in endothelium-dependent vasodilation (EDD) and plasma ADMA predict changes in blood pressure (BP) after salt loading in normotensive postmenopausal women (PMW). Methods: In 15 normotensive PMW (age 50-60 years), not receiving estrogen, ambulatory 24-h BP, plasma lipids, and ADMA were measured after 4 days of a low-salt diet (70 mEq/day) and following 7 days of high-salt intake (260 mEq/day). Brachial artery diameter at rest, during reactive hyperemia, i.e. EDD, and after sublingual nitroglycerin, i.e. non-EDD, were measured by ultrasound. The 24-h urinary NO metabolite (NOx) was measured by Griess reaction. Plasma ADMA was measured by high-pressure liquid chromatography. Results: During low-salt, 24-h BP levels averaged 121 ± 11 and 69 ± 7 mmHg for systolic BP (SBP) and diastolic BP (DBP), respectively. After salt loading, average 24-h BP increases were: 7.6 mmHg for SBP, 2.2 mmHg for DBP, and 5.5 mmHg for pulse pressure (PP). Increases of 24-h SBP and 24-h PP after salt loading correlated directly with changes in ADMA (partial R2 = 0.16 for 24-h SBP and 0.17 for 24-h PP, P <0.05 for both) and inversely with changes in EDD (partial R2 = 0.13, P = 0.09 for 24 h SBP and partial R2 = 0.15, P = 0.07 for 24-h PP), after adjustment for age and cholesterol. Conclusions: Inhibition of NO bioavailability by ADMA and a subsequent reduction in EDD contribute to the increase in BP during high-salt intake in normotensive PMW not receiving estrogen.

KW - Arginine

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KW - Nitric oxide

KW - Postmenopausal women

KW - Salt sensitivity

KW - Vasodilation

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