Role of nitric oxide, endothelin-1, and inflammatory cytokines in blood pressure regulation in hemodialysis patients

Elif Erkan, Prasad Devarajan, Frederick J. Kaskel

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

Background: Altered regulation of blood pressure (BP) in hemodialysis patients is associated with increased morbidity and mortality. Regulation of BP is dependent in part on such vasoactive agents as nitric oxide (NO) and endothelin-1 (ET-1). Cytokine-mediated NO synthase activation during dialysis previously has been reported. The purpose of this study is to investigate the relationship between cytokine-mediated activation of the NO and ET-1 systems and BP regulation in hemodialysis patients. Methods: Nine patients with chronic hypotension (predialysis systolic BP < 110 mm Hg, duration > 1 month), nine patients with hypertension (predialysis systolic BP ≥ 180 mm Hg), and nine age- and sex-matched normotensive controls were enrolled. Results: Predialysis NO end product levels in the hypotensive group were greater than in controls (17.63 ± 5.9 versus 11.06 ± 2.12 μm/mL; P = 0.01), whereas the hypertensive group showed lower levels (4.76 ± 2.33 μm/mL; P < 0.01). The hypotensive group had low postdialysis levels (3.45 ± 1.11 μm/mL; P = 0.01). Predialysis ET-1 levels in the hypotensive and hypertensive groups were greater in comparison to the normotensive group (7.54 ± 4.52 and 8.95 ± 3.52 versus 4.41 ± 0.6 pg/mL; P < 0.01). Postdialysis endothelin levels increased in both the control and hypertensive groups (P < 0.01). Interleukin-1 and tumor necrosis factor-α levels increased postdialysis in all groups, but not significantly. Conclusion: High levels of NO end products in hypotensive patients and low levels in hypertensive patients suggest a critical influence of NO in BP control. In addition, elevated ET-1 levels in hypertensive patients may contribute to systemic vasoconstriction and may suggest vascular dysfunction in this patient population.

Original languageEnglish (US)
Pages (from-to)76-81
Number of pages6
JournalAmerican Journal of Kidney Diseases
Volume40
Issue number1
DOIs
StatePublished - 2002

Fingerprint

Endothelin-1
Renal Dialysis
Nitric Oxide
Cytokines
Blood Pressure
Endothelins
Vasoconstriction
Interleukin-1
Nitric Oxide Synthase
Hypotension
Blood Vessels
Dialysis
Tumor Necrosis Factor-alpha
Hypertension
Morbidity
Control Groups
Mortality
Population

Keywords

  • Cytokines
  • Endothelin-1 (ET-1)
  • Hemodialysis (HD)
  • Nitric oxide (NO)

ASJC Scopus subject areas

  • Nephrology

Cite this

Role of nitric oxide, endothelin-1, and inflammatory cytokines in blood pressure regulation in hemodialysis patients. / Erkan, Elif; Devarajan, Prasad; Kaskel, Frederick J.

In: American Journal of Kidney Diseases, Vol. 40, No. 1, 2002, p. 76-81.

Research output: Contribution to journalArticle

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abstract = "Background: Altered regulation of blood pressure (BP) in hemodialysis patients is associated with increased morbidity and mortality. Regulation of BP is dependent in part on such vasoactive agents as nitric oxide (NO) and endothelin-1 (ET-1). Cytokine-mediated NO synthase activation during dialysis previously has been reported. The purpose of this study is to investigate the relationship between cytokine-mediated activation of the NO and ET-1 systems and BP regulation in hemodialysis patients. Methods: Nine patients with chronic hypotension (predialysis systolic BP < 110 mm Hg, duration > 1 month), nine patients with hypertension (predialysis systolic BP ≥ 180 mm Hg), and nine age- and sex-matched normotensive controls were enrolled. Results: Predialysis NO end product levels in the hypotensive group were greater than in controls (17.63 ± 5.9 versus 11.06 ± 2.12 μm/mL; P = 0.01), whereas the hypertensive group showed lower levels (4.76 ± 2.33 μm/mL; P < 0.01). The hypotensive group had low postdialysis levels (3.45 ± 1.11 μm/mL; P = 0.01). Predialysis ET-1 levels in the hypotensive and hypertensive groups were greater in comparison to the normotensive group (7.54 ± 4.52 and 8.95 ± 3.52 versus 4.41 ± 0.6 pg/mL; P < 0.01). Postdialysis endothelin levels increased in both the control and hypertensive groups (P < 0.01). Interleukin-1 and tumor necrosis factor-α levels increased postdialysis in all groups, but not significantly. Conclusion: High levels of NO end products in hypotensive patients and low levels in hypertensive patients suggest a critical influence of NO in BP control. In addition, elevated ET-1 levels in hypertensive patients may contribute to systemic vasoconstriction and may suggest vascular dysfunction in this patient population.",
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AU - Devarajan, Prasad

AU - Kaskel, Frederick J.

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N2 - Background: Altered regulation of blood pressure (BP) in hemodialysis patients is associated with increased morbidity and mortality. Regulation of BP is dependent in part on such vasoactive agents as nitric oxide (NO) and endothelin-1 (ET-1). Cytokine-mediated NO synthase activation during dialysis previously has been reported. The purpose of this study is to investigate the relationship between cytokine-mediated activation of the NO and ET-1 systems and BP regulation in hemodialysis patients. Methods: Nine patients with chronic hypotension (predialysis systolic BP < 110 mm Hg, duration > 1 month), nine patients with hypertension (predialysis systolic BP ≥ 180 mm Hg), and nine age- and sex-matched normotensive controls were enrolled. Results: Predialysis NO end product levels in the hypotensive group were greater than in controls (17.63 ± 5.9 versus 11.06 ± 2.12 μm/mL; P = 0.01), whereas the hypertensive group showed lower levels (4.76 ± 2.33 μm/mL; P < 0.01). The hypotensive group had low postdialysis levels (3.45 ± 1.11 μm/mL; P = 0.01). Predialysis ET-1 levels in the hypotensive and hypertensive groups were greater in comparison to the normotensive group (7.54 ± 4.52 and 8.95 ± 3.52 versus 4.41 ± 0.6 pg/mL; P < 0.01). Postdialysis endothelin levels increased in both the control and hypertensive groups (P < 0.01). Interleukin-1 and tumor necrosis factor-α levels increased postdialysis in all groups, but not significantly. Conclusion: High levels of NO end products in hypotensive patients and low levels in hypertensive patients suggest a critical influence of NO in BP control. In addition, elevated ET-1 levels in hypertensive patients may contribute to systemic vasoconstriction and may suggest vascular dysfunction in this patient population.

AB - Background: Altered regulation of blood pressure (BP) in hemodialysis patients is associated with increased morbidity and mortality. Regulation of BP is dependent in part on such vasoactive agents as nitric oxide (NO) and endothelin-1 (ET-1). Cytokine-mediated NO synthase activation during dialysis previously has been reported. The purpose of this study is to investigate the relationship between cytokine-mediated activation of the NO and ET-1 systems and BP regulation in hemodialysis patients. Methods: Nine patients with chronic hypotension (predialysis systolic BP < 110 mm Hg, duration > 1 month), nine patients with hypertension (predialysis systolic BP ≥ 180 mm Hg), and nine age- and sex-matched normotensive controls were enrolled. Results: Predialysis NO end product levels in the hypotensive group were greater than in controls (17.63 ± 5.9 versus 11.06 ± 2.12 μm/mL; P = 0.01), whereas the hypertensive group showed lower levels (4.76 ± 2.33 μm/mL; P < 0.01). The hypotensive group had low postdialysis levels (3.45 ± 1.11 μm/mL; P = 0.01). Predialysis ET-1 levels in the hypotensive and hypertensive groups were greater in comparison to the normotensive group (7.54 ± 4.52 and 8.95 ± 3.52 versus 4.41 ± 0.6 pg/mL; P < 0.01). Postdialysis endothelin levels increased in both the control and hypertensive groups (P < 0.01). Interleukin-1 and tumor necrosis factor-α levels increased postdialysis in all groups, but not significantly. Conclusion: High levels of NO end products in hypotensive patients and low levels in hypertensive patients suggest a critical influence of NO in BP control. In addition, elevated ET-1 levels in hypertensive patients may contribute to systemic vasoconstriction and may suggest vascular dysfunction in this patient population.

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