Angiotensin II and Catecholamines Increase Plasma Levels of 8-Epi-Prostaglandin F 2α With Different Pressor Dependencies in Rats

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Abstract
We investigated the extent of oxidative stress evoked in the hypertensive rat by measuring plasma levels of 8-epi-prostaglandin F 2α (8-epi-PGF 2α ), a marker of in vivo oxidative stress. Administration of angiotensin (Ang) II and norepinephrine at doses of 0.7 and 2.8 mg · kg −1 · d −1 , respectively, resulted in similar significant elevations in plasma levels of 8-epi-PGF 2α . A 7-day infusion of Ang II at a nonpressor dose, but not norepinephrine at a nonpressor dose, also increased plasma levels of 8-epi-PGF 2α . The norepinephrine-induced increase in 8-epi-PGF 2α levels could be completely normalized by 3 different classes of antihypertensive drugs: prazosin, an α-adrenergic receptor blocker; hydralazine, a nonspecific vasodilator; and losartan, a specific angiotensin type 1 (AT 1 ) receptor antagonist. This finding suggests that the norepinephrine-induced increase is a pressor-dependent event. In contrast, among these antihypertensive drugs, only losartan was effective in inhibiting the Ang II–induced increase in plasma 8-epi-PGF 2α , suggesting that Ang II increases plasma levels of 8-epi-PGF 2α in both a pressor-independent and an AT 1 receptor–dependent manner. In summary, continuous infusion of both Ang II and norepinephrine potently increases plasma levels of 8-epi-PGF 2α and thus in vivo oxidative stress. Ang II and norepinephrine seem to induce this increase in 8-epi-PGF 2α via mechanisms with different pressor dependencies.

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