Increased renal vasoconstriction and gene expression of cyclooxygenase-1 in renovascular hypertension

Beatriz Vazquez-Cruz, Pedro Lopez, Patricia Talamas-Rohana, Bruno Escalante

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Vascular responses to arachidonic acid (AA) in the renal circulation are increased in hypertensive rats. We have suggested that these differences are related to changes in AA metabolism. In this study we investigated the mechanism involved in the increased AA-induced renal vasoconstriction. We evaluated vascular renal reactivity in the isolated perfused kidney, cyclooxygenase activity, protein content, and mRNA expression of kidneys from sham operated and aortic coarctation rats. Bolus injection of AA (1, 2, 4, and 8 μg) increased perfusion pressure in a dose-dependent manner by 20 ± 4, 28 ± 5, 38 ± 6, and 44 ± 7 mm Hg in sham-operated rats and 30 ± 3, 55 ± 5, 78 ± 5, and 113 ± 8 mm Hg in rats with aortic coarctation. Indomethacin (1 μg/ml) or the endoperoxide/thromboxane blocker SQ29548 (1 μM) prevented AA renal vasoconstriction. Cyclooxygenase activity, cyclooxygenase-1 protein content, and mRNA expression were also increased in the renal tissue from the aortic coarctation rats compared with sham-operated rats. In conclusion, we suggest that during development of hypertension, the cyclooxygenase-1 mRNA is induced, and consequently cyclooxygenase-1 activity and AA metabolism are increased, resulting in augmented production of vasoconstrictor prostaglandins that mediate the potentiated responsiveness to AA or other vascular agonists that release AA, thus increasing peripheral vascular resistance.
Original languageAmerican English
Pages (from-to)577-583
Number of pages518
JournalJournal of Cardiovascular Pharmacology
DOIs
StatePublished - 1 Jan 2000
Externally publishedYes

Fingerprint

vasoconstriction
hypertension
Cyclooxygenase 1
Renovascular Hypertension
gene expression
Vasoconstriction
Arachidonic Acid
Gene expression
rats
Kidney
Gene Expression
Rats
acids
Acids
Aortic Coarctation
Blood Vessels
kidneys
metabolism
Prostaglandin-Endoperoxide Synthases
Metabolism

Cite this

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abstract = "Vascular responses to arachidonic acid (AA) in the renal circulation are increased in hypertensive rats. We have suggested that these differences are related to changes in AA metabolism. In this study we investigated the mechanism involved in the increased AA-induced renal vasoconstriction. We evaluated vascular renal reactivity in the isolated perfused kidney, cyclooxygenase activity, protein content, and mRNA expression of kidneys from sham operated and aortic coarctation rats. Bolus injection of AA (1, 2, 4, and 8 μg) increased perfusion pressure in a dose-dependent manner by 20 ± 4, 28 ± 5, 38 ± 6, and 44 ± 7 mm Hg in sham-operated rats and 30 ± 3, 55 ± 5, 78 ± 5, and 113 ± 8 mm Hg in rats with aortic coarctation. Indomethacin (1 μg/ml) or the endoperoxide/thromboxane blocker SQ29548 (1 μM) prevented AA renal vasoconstriction. Cyclooxygenase activity, cyclooxygenase-1 protein content, and mRNA expression were also increased in the renal tissue from the aortic coarctation rats compared with sham-operated rats. In conclusion, we suggest that during development of hypertension, the cyclooxygenase-1 mRNA is induced, and consequently cyclooxygenase-1 activity and AA metabolism are increased, resulting in augmented production of vasoconstrictor prostaglandins that mediate the potentiated responsiveness to AA or other vascular agonists that release AA, thus increasing peripheral vascular resistance.",
author = "Beatriz Vazquez-Cruz and Pedro Lopez and Patricia Talamas-Rohana and Bruno Escalante",
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Increased renal vasoconstriction and gene expression of cyclooxygenase-1 in renovascular hypertension. / Vazquez-Cruz, Beatriz; Lopez, Pedro; Talamas-Rohana, Patricia; Escalante, Bruno.

In: Journal of Cardiovascular Pharmacology, 01.01.2000, p. 577-583.

Research output: Contribution to journalArticle

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