Serum from preeclamptic patients increases rat aorta vascular reactivity independent of endothelial nitric oxide and prostaglandins

Cosmas J.M. Van De Ven, Susan A. Klarr, Robert H. Hayashi, R. Clinton Webb

Research output: Contribution to journalArticle

Abstract

Objective: To assess whether serum from preeclamptic patients increases vascular reactivity in an endothelium-dependent manner. Methods: Isolated rat thoracic aortae were incubated for 3 and 8 h in serum from preeclamptic patients, normotensive patients, or physiologic buffer. Vascular reactivity was assessed by phenylephrine-induced vasoconstriction in the presence and absence of N(ω)-nitro-L-arginine and indomethacin and by acetylcholine and S-nitroso-N-acetylpenicillamine-induced relaxation. Results: Aortae incubated in sera from preeclamptic patients showed a significant (P < 0.05) increase in sensitivity to phenylephrine (EC50 = 7.71 ± 0.09, -log M) when compared with aortae incubated in normotensive sera (EC50 7.49 ± 0.08, -log M) or buffer (EC50 = 7.41 + 0.08, -log M). After blocking nitric oxide production with N(ω)-nitro-L-arginine or after blocking prostaglandin production with indomethacin, vessels incubated in sera from preeclamptic patients remained more sensitive to phenylephrine than vessels incubated in sera from control patients. Acetylcholine-induced relaxation and S-nitroso-N-acetylpenicillamine concentration responses curves were not different. Conclusions: Serum from preeclamptic patients increases the sensitivity to phenylephrine. The increased sensitivity appears independent from endothelial nitric oxide or prostaglandin release. The serum-induced enhanced vascular smooth muscle reactivity therefore may be due to altered vascular smooth muscle function and not to altered endothelial function.

Original languageEnglish (US)
Pages (from-to)139-144
Number of pages6
JournalJournal of Maternal-Fetal Investigation
Volume7
Issue number3
StatePublished - Oct 2 1997

Fingerprint

Prostaglandins
Blood Vessels
Aorta
Nitric Oxide
Phenylephrine
Serum
S-Nitroso-N-Acetylpenicillamine
Vascular Smooth Muscle
Indomethacin
Acetylcholine
Arginine
Buffers
Vasoconstriction
Thoracic Aorta
Endothelium

Keywords

  • Nitric oxide
  • Preeclampsia
  • Prostaglandins
  • Rat aorta
  • Vascular reactivity

ASJC Scopus subject areas

  • Obstetrics and Gynecology

Cite this

Serum from preeclamptic patients increases rat aorta vascular reactivity independent of endothelial nitric oxide and prostaglandins. / Van De Ven, Cosmas J.M.; Klarr, Susan A.; Hayashi, Robert H.; Clinton Webb, R.

In: Journal of Maternal-Fetal Investigation, Vol. 7, No. 3, 02.10.1997, p. 139-144.

Research output: Contribution to journalArticle

@article{811785bc2abf480f8fb758318f08db10,
title = "Serum from preeclamptic patients increases rat aorta vascular reactivity independent of endothelial nitric oxide and prostaglandins",
abstract = "Objective: To assess whether serum from preeclamptic patients increases vascular reactivity in an endothelium-dependent manner. Methods: Isolated rat thoracic aortae were incubated for 3 and 8 h in serum from preeclamptic patients, normotensive patients, or physiologic buffer. Vascular reactivity was assessed by phenylephrine-induced vasoconstriction in the presence and absence of N(ω)-nitro-L-arginine and indomethacin and by acetylcholine and S-nitroso-N-acetylpenicillamine-induced relaxation. Results: Aortae incubated in sera from preeclamptic patients showed a significant (P < 0.05) increase in sensitivity to phenylephrine (EC50 = 7.71 ± 0.09, -log M) when compared with aortae incubated in normotensive sera (EC50 7.49 ± 0.08, -log M) or buffer (EC50 = 7.41 + 0.08, -log M). After blocking nitric oxide production with N(ω)-nitro-L-arginine or after blocking prostaglandin production with indomethacin, vessels incubated in sera from preeclamptic patients remained more sensitive to phenylephrine than vessels incubated in sera from control patients. Acetylcholine-induced relaxation and S-nitroso-N-acetylpenicillamine concentration responses curves were not different. Conclusions: Serum from preeclamptic patients increases the sensitivity to phenylephrine. The increased sensitivity appears independent from endothelial nitric oxide or prostaglandin release. The serum-induced enhanced vascular smooth muscle reactivity therefore may be due to altered vascular smooth muscle function and not to altered endothelial function.",
keywords = "Nitric oxide, Preeclampsia, Prostaglandins, Rat aorta, Vascular reactivity",
author = "{Van De Ven}, {Cosmas J.M.} and Klarr, {Susan A.} and Hayashi, {Robert H.} and {Clinton Webb}, R.",
year = "1997",
month = "10",
day = "2",
language = "English (US)",
volume = "7",
pages = "139--144",
journal = "Journal of Maternal-Fetal Investigation",
issn = "0939-6322",
publisher = "Springer Verlag",
number = "3",

}

TY - JOUR

T1 - Serum from preeclamptic patients increases rat aorta vascular reactivity independent of endothelial nitric oxide and prostaglandins

AU - Van De Ven, Cosmas J.M.

AU - Klarr, Susan A.

AU - Hayashi, Robert H.

AU - Clinton Webb, R.

PY - 1997/10/2

Y1 - 1997/10/2

N2 - Objective: To assess whether serum from preeclamptic patients increases vascular reactivity in an endothelium-dependent manner. Methods: Isolated rat thoracic aortae were incubated for 3 and 8 h in serum from preeclamptic patients, normotensive patients, or physiologic buffer. Vascular reactivity was assessed by phenylephrine-induced vasoconstriction in the presence and absence of N(ω)-nitro-L-arginine and indomethacin and by acetylcholine and S-nitroso-N-acetylpenicillamine-induced relaxation. Results: Aortae incubated in sera from preeclamptic patients showed a significant (P < 0.05) increase in sensitivity to phenylephrine (EC50 = 7.71 ± 0.09, -log M) when compared with aortae incubated in normotensive sera (EC50 7.49 ± 0.08, -log M) or buffer (EC50 = 7.41 + 0.08, -log M). After blocking nitric oxide production with N(ω)-nitro-L-arginine or after blocking prostaglandin production with indomethacin, vessels incubated in sera from preeclamptic patients remained more sensitive to phenylephrine than vessels incubated in sera from control patients. Acetylcholine-induced relaxation and S-nitroso-N-acetylpenicillamine concentration responses curves were not different. Conclusions: Serum from preeclamptic patients increases the sensitivity to phenylephrine. The increased sensitivity appears independent from endothelial nitric oxide or prostaglandin release. The serum-induced enhanced vascular smooth muscle reactivity therefore may be due to altered vascular smooth muscle function and not to altered endothelial function.

AB - Objective: To assess whether serum from preeclamptic patients increases vascular reactivity in an endothelium-dependent manner. Methods: Isolated rat thoracic aortae were incubated for 3 and 8 h in serum from preeclamptic patients, normotensive patients, or physiologic buffer. Vascular reactivity was assessed by phenylephrine-induced vasoconstriction in the presence and absence of N(ω)-nitro-L-arginine and indomethacin and by acetylcholine and S-nitroso-N-acetylpenicillamine-induced relaxation. Results: Aortae incubated in sera from preeclamptic patients showed a significant (P < 0.05) increase in sensitivity to phenylephrine (EC50 = 7.71 ± 0.09, -log M) when compared with aortae incubated in normotensive sera (EC50 7.49 ± 0.08, -log M) or buffer (EC50 = 7.41 + 0.08, -log M). After blocking nitric oxide production with N(ω)-nitro-L-arginine or after blocking prostaglandin production with indomethacin, vessels incubated in sera from preeclamptic patients remained more sensitive to phenylephrine than vessels incubated in sera from control patients. Acetylcholine-induced relaxation and S-nitroso-N-acetylpenicillamine concentration responses curves were not different. Conclusions: Serum from preeclamptic patients increases the sensitivity to phenylephrine. The increased sensitivity appears independent from endothelial nitric oxide or prostaglandin release. The serum-induced enhanced vascular smooth muscle reactivity therefore may be due to altered vascular smooth muscle function and not to altered endothelial function.

KW - Nitric oxide

KW - Preeclampsia

KW - Prostaglandins

KW - Rat aorta

KW - Vascular reactivity

UR - http://www.scopus.com/inward/record.url?scp=0030828230&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030828230&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:0030828230

VL - 7

SP - 139

EP - 144

JO - Journal of Maternal-Fetal Investigation

JF - Journal of Maternal-Fetal Investigation

SN - 0939-6322

IS - 3

ER -