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
Externally publishedYes

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.; Webb, R Clinton.

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

Research output: Contribution to journalArticle

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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.",
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AU - Klarr, Susan A.

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AU - Webb, R Clinton

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