A novel anti-lipolytic action of norepinephrine in uteri isolated from spayed rats appears subserved by the activation of alpha 1-adrenoreceptors diminishing the generation and release of lipolytic prostaglandins.

The effects of norepinephrine (NE: 3 x 10(-6) M) on the outputs of prostaglandins (PGs) E1, E2 and F2 alpha, from uterine horns isolated from ovariectomized rats and suspended in solutions with or without exogenous glucose, were explored. The releases of the different PGs into the external medium were determined after incubating for one hour uterine preparations, mounted within a tissue bath and receiving a constant preload tension. In glucose-containing solutions, NE enhanced the basal output of PGE2 and failed to alter the basal releases of PGE1 or of PGF2 alpha. In glucose-free media, the basal output of PGE2 was comparable to that detected in presence of exogenous glucose, and its augmentation following added NE was again evident. However, the basal outputs of PGE1 and of PGF2 alpha, greater in glucose-free solutions than in glucose-containing media, were significantly diminished by added NE. Uterine triglyceride (TG) levels were also explored, both immediately after sacrifice (0 min) or following suspending uterine segments during one hour (60 min) in solutions containing exogenous glucose or not. In glucose-containing media, tissue TGs did not differ at 0 min or at 60 min, neither in controls, nor in NE-challenged preparations, whereas in glucose-free solutions, TGs were significantly smaller at 60 min than at 0. interestingly, the addition of NE completely prevented the dimunition of uterine TGs, present at 60 min in glucose-free medium. Neither propranolol nor yohimbine (10(-6) M) altered this sparing action of added NE on tissue TGs, but phentolamine or prazocin (10(-6) M), effectively antagonized the preventive effect of the agonist.(ABSTRACT TRUNCATED AT 250 WORDS)