Key result
Hypertensive rat arteries shift arachidonic acid metabolism away from PGI2 toward proportionally more PGE2.
Why the study?
Does arachidonic acid alter the release of prostaglandins E2 and I2 in aortic strips from hypertensive versus normotensive rats?
Does arachidonic acid alter the release of prostaglandins E2 and I2 in aortic strips from hypertensive versus normotensive rats?
Answers are grounded in this paper and cite their sources.
Arteries from spontaneously hypertensive rats exhibit altered arachidonic acid metabolism, preferentially synthesizing PGE2 over PGI2 compared to normotensive rats.
The ability of aortic strips from 5, 10 and 20 week old spontaneously hypertensive (SH) and normotensive Wistar-Kyoto (WKY) and Wistar (W) rats to release prostaglandin (PG) E2 and I2 was examined both in the presence and absence of arachidonic acid (AA). Strips from SH rats older than 5 weeks generally synthesized more PGE2 than those from age-matched control rats. Strips from age-matched SH and W rats synthesized the same amounts of PGI2 and both released more than those from age-matched WKY rats. Although the actual quantities of PGE2 or PGI2 released varied between strips from W and WKY rats, the PGI2/PGE2 ratio was always the same and doubled with the addition of AA. In contrast, the PGI2/PGE2 ratio for SH rats did not increase with the addition of AA and was only one-half that of W or WKY rats. These data demonstrate that arteries from normotensive rats preferentially synthesize PGI2 whereas those from SH rats metabolize AA to proportionally more PGE2.
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Peter Lukacsko (1983) studied Hypertension. Arachidonic acid vs. Absence of arachidonic acid was evaluated on Release of prostaglandin (PG) E2 and I2. Arteries from normotensive rats preferentially synthesize PGI2, whereas those from spontaneously hypertensive rats metabolize arachidonic acid to proportionally more PGE2.
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