Intravenous T26A dose-dependently potentiates the hypotensive effect of intravenous PGE₂ in anesthetized normotensive rats, and lowers BP in hypertensive > normotensive rats.

<p>Anesthetized rats were injected intravenously via the femoral vein and arterial BP was monitored continuously via the carotid artery. <b>A,</b> BP of a Sprague-Dawley rat after two intravenous PGE_<b>2</b> injections at the same dose (250 ng). The reduction in BP is highly reproducible and non-additive, indicating that the first dose of PGE_<b>2</b> has been rapidly metabolized. <b>B,</b> BP of a Sprague-Dawley rat measured after each of a series of stepwise intravenous PGE_<b>2</b> injections (25–500 ng) before and after T26A injection. T26A potentiates the hypotensive effect of each does of PGE_<b>2</b>. <b>C,</b> Summary of a series of studies performed as in panel B, after injecting 0 nmoles, 200 nmoles, or 300 nmoles of T26A in the second phase. Percent reduction of BP was calculated as per Methods. T26A shifted the dose-response curve of PGE_<b>2</b> on BP to the left in a dose-dependent fashion. Values are mean ± SEM, n = 5 rats for each point. # p < 0.05 for 200 nmoles versus 0 nmoles T26A. * p < 0.05 and * p < 0.01 for 300 nmoles versus 0 nmoles T26A. <b>D,</b> Effect of intravenous T26A alone on BP of normotensive Wistar-Kyoto rats (blue) and SHR rats (red). Percent reduction of BP was calculated as per Methods. T26A produced a greater fractional reduction in BP in SHR versus Wistar-Kyoto rats. Mean ± SEM, n = 5 rats each. * p < 0.05.