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Ovarian tissue from immature rats treated with pregnant mare serum gonadotrophin (PMSG) or PMSG and human chorionic gonadotrophin was incubated in Medium 199. Stimulation of the formation of cyclic AMP in follicular and luteal tissue by terbutaline (10(-5) mol/l), a selective beta 2-agonist, was blocked by butoxamine (10(-5) mol/l), a selective beta 2-antagonist, whereas practolol (10(-5) mol/l), a selective beta 1-antagonist, was ineffective. Propranolol (10(-5) mol/l) a non-selective beta-antagonist, butoxamine nor practolol affected the increase in cyclic AMP promoted by the addition of 1 microgram LH. Stimulation of the production of progesterone in both follicular and luteal tissue by terbutaline was blocked by butoxamine, but not by practolol. These findings indicated that beta-adrenergic stimulation of ovarian cyclic AMP and progesterone is mediated by beta 2-adrenergic receptors.

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We randomly assigned 42 subjects for treatment with transcutaneous electrical nerve stimulation (TENS) to one of three groups: conventional TENS--80 Hz; low frequency TENS--2 Hz; and a control group--TENS without batteries. Pain threshold measurements and blood beta-endorphin levels were obtained at regular intervals before, during, and for 17 hours after TENS application. We found no significant difference in blood beta-endorphin levels between the groups before, during, or immediately after TENS application. The differences in pain threshold and beta-endorphin levels appeared to be a function of the patient-selection process and not the application of TENS. The results indicated that TENS, with the stimulation characteristics used in this study, did not significantly change the measured plasma levels of beta-endorphin. The blind administration of naloxone hydrochloride, an opiate antagonist, did not significantly alter the perceived experimental pain of these subjects. We could find no evidence that TENS altered experimental pain threshold or plasma beta-endorphin levels.

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