Release of prostaglandins by the mesenteric artery of the renovascular and spontaneously hypertensive rat

Abstract

The release of prostaglandin E2 (PGE2) and 6-ketoprostaglandin F1α (6-keto-PGF1α), the stable metabolite of prostacyclin (PGI2), by the perfused mesenteric arteries of renal and spontaneously hypertensive rats (SHR) have been measured. Unstimulated mesenteric arteries from two-kidney one-clip hypertensive rats (2K-1C) released 1.6 times as much PGE2 and 2.7 times as much 6-keto-PGF1α as those of control rats. The release of PGE2 by mesenteric arteries from one-kidney one-clip hypertensive rats (1K-1C) was not significantly different from that of uninephrectomized normotensive rats, but the release of 6-keto-PGF1α was 3.5 times higher in the former than in the latter. Norepinephrine (NE) induced a dose-related increase in perfusion pressure, in PGE2, and 6-keto-PGF1α release in all four groups. However, its effect on the release of PGE2 was more pronounced in 2K-1C than in sham-operated rats. There was no difference between 1K-1C and the uninephrectomized group. The effect of NE on the release of 6-keto-PGF1α was significantly higher for both renal hypertensive groups. These results indicate that the release of PGE2 is more dependent on the loss of renal mass than on hypertension, while the reverse applies to the release of 6-keto-PGF1α. Unstimulated mesenteric arteries from SHR released less PGE2 and less 6-keto-PGF1α than those of Wistar–Kyoto normotensive rats (WKY), but the release was not significantly different from Wistar rats. Under NE stimulation, WKY mesenteric arteries showed almost no increase in release of PGs. Compared with those of Wistar rats, SHR mesenteric arteries showed a greater pressor response to NE, a lower PGE2 release, and the same release of 6-keto-PGF1α. These findings reveal the difficulty of selecting an appropriate control group in studies involving SHR. We concluded that in renal hypertensive rats the specific increase of PGI2 release by arterial tissue may represent an important adaptive mechanism to the elevated blood pressure. However, this mechanism seems not to be involved in SHR.