Concomitant inhibition of pulsatile luteinizing hormone (LH) and stimulation of prolactin release by prostacyclin (PGI2) in ovariectomized (OVX) conscious rats.
Prostacyclin (PGI2) or its stable metabolite, 6-keto-PGF1 alpha (1-5 micrograms) in 2.5 microliter 0.05 M phosphate buffer (pH 7.4), was injected into the third ventricle (3 V) of ovariectomized (OVX), freely moving rats. Control animals received 2.5 microliter of buffer. In the initial experiments a control blood sample was taken and then the PGI2 was injected and frequent samples taken thereafter. With this protocol injection of 2 micrograms of PGI2 produced a significant decrease in mean plasma LH only at 60 min after its injection (p less than .05), while the higher dose (5 micrograms) decreased plasma LH concentrations at 30 and 60 min (p less than .01 and p less than .001, respectively). In subsequent experiments, blood was removed from indwelling external jugular vein cannulae every 5-6 min during 2 hours and plasma LH and PRL levels were determined by radioimmunoassay. LH pulses were monitored and several parameters of LH pulsation were calculated during the hour before and after injection of phosphate buffer, PGI2 or 6-keto-PGF1 alpha. Intraventricular injection of phosphate buffer failed to modify the characteristic pulsatile release of LH and did not alter plasma PRL levels. The amplitude of LH pulses was significantly reduced by PGI2 and the inhibitory effect was dose-related. Even a dose of 1 microgram produced a significant reduction in pulse height and the response was graded with maximal reduction occurring with the 5 microgram dose which essentially abolished the LH pulses. Following the microinjection of 6-keto-PGF1 alpha, no significant changes were observed in plasma LH values and the pulses of the hormone. Five micrograms PGI2 considerably elevated plasma PRL values during the 20-25 min following its 3V injection, whereas the same dose of 6-keto-PGF1 alpha produced only a very slight stimulatory effect. Since PGI2 had no effect to alter LH release by cultured pituitary cells in vitro, it is concluded that PGI2 can act on structures near the 3V to inhibit pulsatile release of LHRH.
Ottlecz
A
A
University of Texas Health Science Center, Tyler, Texas 75701.
McCann
S M
SM
D015121:6-Ketoprostaglandin F1 alpha / Q000008:administration & dosage / Q000494:pharmacology; D000818:Animals; D002552:Cerebral Ventricles / Q000187:drug effects / Q000502:physiology*; D011464:Epoprostenol / Q000008:administration & dosage / Q000494:pharmacology*; D005260:Female; D007276:Injections, Intraventricular; D007700:Kinetics; D007986:Luteinizing Hormone / Q000097:blood / Q000378:metabolism*; D010052:Ovariectomy; D011388:Prolactin / Q000097:blood / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D015121:6-Ketoprostaglandin F1 alpha; D011388:Prolactin; D007986:Luteinizing Hormone; D011464:Epoprostenol