Effect of converting enzyme inhibitors on prostaglandin synthesis by isolated glomeruli and aortic strips from rats

M. Galler, R. Backenroth, Vaughn Wesley Folkert, D. Schlondorff

Research output: Contribution to journalArticle

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Abstract

In addition to their effect on angiotensin and bradykinin metabolism, converting enzyme inhibitors (CEI) may also alter prostaglandin (PG) synthesis. We therefore examined two CEI, SQ 14,225 (captopril) and SQ 20,881, for their in vitro effect on PG synthesis by glomeruli and aortic strips from rats. Glomeruli incubated in test tubes produced predominantly PGE2 and PGF(2α). Both CEI selectively stimulated PGE2 synthesis with maximal effects at 25 μM. During superfusion of glomeruli with captopril (25 μM) synthesis of PGE2 increased 5- to 10-fold and that of 6-keto-PGF(1α) doubled. No significant change in PGF(2α) or thromboxane B2 occurred. This effect of CEI was independent of angiotensin or bradykinin. In contrast captopril had no effect on PG synthesis by aortic strips, which produced predominantly prostacyclin assayed as 6-keto-PGF(1α) and little PGE2 and PGF(2α). These results demonstrate that CEI can directly stimulate PG synthesis in glomeruli. This additional mechanism of action of CEI may require reinterpretation of the role of angiotensin based on results obtained with CEI.

Original languageEnglish (US)
Pages (from-to)23-28
Number of pages6
JournalJournal of Pharmacology and Experimental Therapeutics
Volume220
Issue number1
StatePublished - 1982

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Enzyme Inhibitors
Prostaglandins
Prostaglandins F
Captopril
Angiotensins
Dinoprostone
Bradykinin
Thromboxane B2
Epoprostenol

ASJC Scopus subject areas

  • Pharmacology

Cite this

Effect of converting enzyme inhibitors on prostaglandin synthesis by isolated glomeruli and aortic strips from rats. / Galler, M.; Backenroth, R.; Folkert, Vaughn Wesley; Schlondorff, D.

In: Journal of Pharmacology and Experimental Therapeutics, Vol. 220, No. 1, 1982, p. 23-28.

Research output: Contribution to journalArticle

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abstract = "In addition to their effect on angiotensin and bradykinin metabolism, converting enzyme inhibitors (CEI) may also alter prostaglandin (PG) synthesis. We therefore examined two CEI, SQ 14,225 (captopril) and SQ 20,881, for their in vitro effect on PG synthesis by glomeruli and aortic strips from rats. Glomeruli incubated in test tubes produced predominantly PGE2 and PGF(2α). Both CEI selectively stimulated PGE2 synthesis with maximal effects at 25 μM. During superfusion of glomeruli with captopril (25 μM) synthesis of PGE2 increased 5- to 10-fold and that of 6-keto-PGF(1α) doubled. No significant change in PGF(2α) or thromboxane B2 occurred. This effect of CEI was independent of angiotensin or bradykinin. In contrast captopril had no effect on PG synthesis by aortic strips, which produced predominantly prostacyclin assayed as 6-keto-PGF(1α) and little PGE2 and PGF(2α). These results demonstrate that CEI can directly stimulate PG synthesis in glomeruli. This additional mechanism of action of CEI may require reinterpretation of the role of angiotensin based on results obtained with CEI.",
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AB - In addition to their effect on angiotensin and bradykinin metabolism, converting enzyme inhibitors (CEI) may also alter prostaglandin (PG) synthesis. We therefore examined two CEI, SQ 14,225 (captopril) and SQ 20,881, for their in vitro effect on PG synthesis by glomeruli and aortic strips from rats. Glomeruli incubated in test tubes produced predominantly PGE2 and PGF(2α). Both CEI selectively stimulated PGE2 synthesis with maximal effects at 25 μM. During superfusion of glomeruli with captopril (25 μM) synthesis of PGE2 increased 5- to 10-fold and that of 6-keto-PGF(1α) doubled. No significant change in PGF(2α) or thromboxane B2 occurred. This effect of CEI was independent of angiotensin or bradykinin. In contrast captopril had no effect on PG synthesis by aortic strips, which produced predominantly prostacyclin assayed as 6-keto-PGF(1α) and little PGE2 and PGF(2α). These results demonstrate that CEI can directly stimulate PG synthesis in glomeruli. This additional mechanism of action of CEI may require reinterpretation of the role of angiotensin based on results obtained with CEI.

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