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

Abstract

The release of prostaglandin E2 (PGE2) and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha), 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-PGF1 alpha 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-PGF1 alpha 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-PGF1 alpha 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-PGF1 alpha 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-PGF1 alpha. Unstimulated mesenteric arteries from SHR released less PGE2 and less 6-keto-PGF1 alpha 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-PGF1 alpha. These findings reveal the difficulty of selecting an appropriate control group in studies involving SHR.(ABSTRACT TRUNCATED AT 250 WORDS)

Altered Aortic Production of 6-Keto-Prostaglandin F_1αfrom Aldosterone-Salt Hypertensive Rats

“…we cannot at the present time be certain whether it is one or a combination of altera tions in our hypertensive model. The combination of altered mechanisms in the arachidonic acid cascade may in fact vary among hypertensive models [29],…”

Release of fatty acids by perfused vascular tissue in normotensive and hypertensive rats.

“…The procedure has been described in detail previously. 33 Sensitivities.of the assays, determined by the amount of standard per assay tube required to inhibit binding of the label to the antibody by 10%, were 8 pg for 6-keto-PGF lo and 5 pg for thromboxane B 2 . Cross-reactivity of the 6-keto-PGF, o antiserum was less than 1% for thromboxane and for E and F prostaglandins.…”