Low-dose aspirin. I. Effect on angiotensin II pressor responses and blood prostaglandin concentrations in pregnant women sensitive to angiotensin II

Bernard Spitz, Ronald R. Magness, Susan M. Cox, Charles E L Brown, Charles R. Rosenfeld, Norman F. Gant

Research output: Contribution to journalArticle

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Abstract

Decreased incidence of proteinuric hypertension after low-dose aspirin therapy is hypothesized to be a consequence of selective thromboxane A2 inhibition and sparing of prostacyclin. This study was designed to ascertain if low-dose aspirin therapy (81 mg/day for 1 week) alters vascular refractoriness to angiotensin II and the prostacyclin/thromboxane A2 ratio in pregnant women sensitive to angiotensin II (n = 17). Low-dose aspirin increased the effective pressor dose of angiotensin II from 5.9 ± 2.4 to 10.2 ± 5.5 ng/kg/min (p < 0.01, mean ± SD). Platelet-derived serum thromboxane B2 (a metabolite of thromboxane A2), a measure of therapy compliance, decreased from 1804 ± 1771 to 132 ± 206 pg/ml (p < 0.01). Plasma thromboxane B2 decreased from 130 ± 107 to 19 ± 12 pg/ml (p < 0.01). Inhibition was not selective because 6-keto-prostaglandin F (a metabolite of prostacyclin) also decreased from 243 ± 90 to 163 ± 90 pg/ml (p = 0.039) and prostaglandin E2 was reduced from 155 ± 67 to 95 ± 40 pg/ml (p = 0.014). Decreases in thromboxane B2, however, were significantly greater (75% ± 19%) than decreases in 6-keto-prostaglandin F (21% ± 33%) or prostaglandin E2 (29% ± 36%); thus the 6-keto-prostaglandin F/thromboxane B2 ratio increased from 3.1 ± 2.0 to 12.4 ± 9.9 (p < 0.01). Although low-dose aspirin increases the effective pressor dose of angiotensin II, it does not return to normal pregnancy values. This observation is consistent with the hypothesis that this represents only a partial selective prostaglandin inhibition.

Original languageEnglish (US)
Pages (from-to)1035-1043
Number of pages9
JournalAmerican Journal of Obstetrics and Gynecology
Volume159
Issue number5
DOIs
StatePublished - 1988

Fingerprint

Thromboxane B2
Angiotensin II
Thromboxane A2
Aspirin
Prostaglandins
Pregnant Women
Epoprostenol
Dinoprostone
Blood Vessels
Reference Values
Therapeutics
Blood Platelets
Hypertension
Pregnancy
Incidence
Serum
prostaglandin F1

Keywords

  • angiotensin II
  • baroreceptor
  • blood pressure control
  • Low-dose aspirin
  • preeclampsia
  • pressor responses
  • prostaglandins

ASJC Scopus subject areas

  • Medicine(all)
  • Obstetrics and Gynecology

Cite this

Low-dose aspirin. I. Effect on angiotensin II pressor responses and blood prostaglandin concentrations in pregnant women sensitive to angiotensin II. / Spitz, Bernard; Magness, Ronald R.; Cox, Susan M.; Brown, Charles E L; Rosenfeld, Charles R.; Gant, Norman F.

In: American Journal of Obstetrics and Gynecology, Vol. 159, No. 5, 1988, p. 1035-1043.

Research output: Contribution to journalArticle

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abstract = "Decreased incidence of proteinuric hypertension after low-dose aspirin therapy is hypothesized to be a consequence of selective thromboxane A2 inhibition and sparing of prostacyclin. This study was designed to ascertain if low-dose aspirin therapy (81 mg/day for 1 week) alters vascular refractoriness to angiotensin II and the prostacyclin/thromboxane A2 ratio in pregnant women sensitive to angiotensin II (n = 17). Low-dose aspirin increased the effective pressor dose of angiotensin II from 5.9 ± 2.4 to 10.2 ± 5.5 ng/kg/min (p < 0.01, mean ± SD). Platelet-derived serum thromboxane B2 (a metabolite of thromboxane A2), a measure of therapy compliance, decreased from 1804 ± 1771 to 132 ± 206 pg/ml (p < 0.01). Plasma thromboxane B2 decreased from 130 ± 107 to 19 ± 12 pg/ml (p < 0.01). Inhibition was not selective because 6-keto-prostaglandin F1α (a metabolite of prostacyclin) also decreased from 243 ± 90 to 163 ± 90 pg/ml (p = 0.039) and prostaglandin E2 was reduced from 155 ± 67 to 95 ± 40 pg/ml (p = 0.014). Decreases in thromboxane B2, however, were significantly greater (75{\%} ± 19{\%}) than decreases in 6-keto-prostaglandin F1α (21{\%} ± 33{\%}) or prostaglandin E2 (29{\%} ± 36{\%}); thus the 6-keto-prostaglandin F1α/thromboxane B2 ratio increased from 3.1 ± 2.0 to 12.4 ± 9.9 (p < 0.01). Although low-dose aspirin increases the effective pressor dose of angiotensin II, it does not return to normal pregnancy values. This observation is consistent with the hypothesis that this represents only a partial selective prostaglandin inhibition.",
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