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Biomedical subjects

O M Cramer

Publications and source records attributed to O M Cramer.

12 recordsLinked to original sources
PubMed1979

Estrogen inhibition of dopamine release into hypophysial portal blood.

The hypothesis that 17 beta-estradiol suppresses dopamine secretion into hypophysial portal blood was tested. Portal plasma concentrations of dopamine were significantly lower in proestrous rats (1.0 +/- 0.1 ng/ml; mean +/- SE) than in estrous rats (1.9 +/- 0.38 ng/ml). To deplete the animal of endogenous steroid hormones, proestrous rats were adrenalectomized (Adx) and ovariectomized (Ovx). Twenty-four hours later, hypophysial portal blood was collected for 60 min, and the plasma from this blood was analyzed for dopamine. Arterial plasma from these rats was assayed for 17 beta-estradiol and progesterone. The concentrations of dopamine in the portal plasma of sham-operated rats and bilaterally Adx-Ovx rats were similar to those in estrous animals. The concentration of dopamine in portal plasma of Adx-Ovs rats injected 24 h earlier with 50 micrograms 17 beta-estradiol was 1.0 +/- 0.31 ng/ml, which was comparable to that in proestrous animals but less than that in the estrous rats. The concentrations of 17 beta-estradiol in arterial plasma were as follows: 24 +/- 8.3 pg/ml in proestrous rats, 40 +/- 2.9 pg/ml in estrous rats, 10 +/- 1.3 pg/ml in Adx-ovx rats, and 96 +/- 17.3 pg/ml in Adx-Ovx rats injected with 50 micrograms 17 beta-estradiol. Twenty-four hours after injection of 25 micrograms 17beta-extradiol into Adx-Ovx rats, the plasma 17beta-estradiol levels were 51 +/- 7.4 pg/ml, and the dopamine concentrations in portal plasma were 1.9 +/- 0.57 ng/ml. It is concluded that an acute effect of 17 beta-estradiol is suppression of hypothalamic secretion of dopamine into hypophysial portal blood.

Adrenalectomy↗
PubMed1979

Stimulation of dopamine release into hypophysial portal blood by administration of progesterone.

To test the hypothesis that progesterone is involved in the regulation of dopamine release into hypophysial portal blood, female rats were adrenalectomized and ovariectomized at 1200 h on the day of proestrus and, immediately after the operation, injected sc with sesame oil or progesterone. Approximately 24 h later, hypophysial portal blood was collected and the plasma from this blood was analyzed for dopamine. The concentration of dopamine in portal plasma from rats given sesame oil or progesterone (50 mg) was 1.8 +/- 0.24 or 6.0 +/- 1.2 ng/ml (mean +/- SE), respectively. At the time of collection of portal blood, the progesterone concentration in arterial plasma was less than 0.8 ng/ml in rats given sesame oil and was 93 +/- 11 ng/ml in animals given progesterone. Conversely, the circulating concentrations of PRL was less (25 +/- 3 ng/ml) in animals given progesterone and higher (42 +/- 5 ng/ml) in animals given sesame oil. Twenty-four hours after the injection of progesterone (50 mg) into intact proestrous rats, the dopamine concentration in portal plasma was 5.8 +4- 1.29 ng/ml, a concentration which was significantly (P less thann 0.01) higher than that in untreated proestrous rats (1.1 +/- 0.24 ng/ml) but only slightly higher than that in untreated estrous rats (3.7 +/- 1.0 ng/ml). It is proposed 1) that progesterone administered sc can lead to an increased secretion of dopamine into hypophysial portal blood and 2) that the increased concentration of dopamine in portal plasma of intact pregnant rats relative to that of proestrous rats is, in part, a consequence of augmented progesterone secretion.

Adrenalectomy↗
PubMed1978

The actions of serotonin, norepinephrine, and epinephrine on hypothalamic processes leading to adenohypophyseal luteinizing hormone release.

The effects of third ventricle (3V) infusion of exogenous monoamines on the secretion of LH were investigated in Nembutal-blocked proestrous rats after electrochemical stimulation (ECS) of the medial preoptic area (MPOA). Two microcannulae were anatomically oriented through the ventral surface of the brain to establish a push-pull flow system in the 3V at the rate of 3.9 microliter/min for 160 min. Serotonin perfusions (2.6 x 10(-3) M for 160 min at 3.9 microgram/min) significantly depressed the MPOA-ECS-induced rise in plasma LH at 160 and 200 min, but did not diminish the secretion of LH after an intraatrial injection of 250 ng LRH. Seemingly, the reduced plasma LH which follows MPOA-ECS in serotonin-treated rats is the consequence of decreased hypothalamic LRH secretion. Desipramine (3.6 x 10(-4) M), a norepinephrine (NE) uptake inhibitor, did not prevent serotonin inhibition. In contrast, the specific serotonin uptake inhibitor. Lilly 110140 (3.2 X 10(-4) M), and cyproheptadine (2.9 x 10(-4) M) blocked the inhibitory effects of serotonin. Serotonin was also tested in proestrous rats anesthetized with Nembutal within 1 h after the beginning of the light cycle (morning rats) and in proestrous rats at least 15 min after the start of the dark cycle (night rats). Serotonin (2.6 x 10(-3) M) failed to diminish the rise in plasma LH after ECS in morning rats, but depressed the ECS-induced increase of LH in night rats. Perfusions of 3 X 10(-8) M NE at 3.9 microliter/min for 160 min augmented the plasma LH increase after MPOA-ECS but only at 160 and 200 min, while its response to LRH was not tested. At higher concentrations, 3 x 10(-6) M NE markedly suppressed the rise in plasma LH after ECS and also depressed the secretion of LH after an intraatrial injection of LRH. In contrast, 3 x 10(-6) M epinephrine which inhibited the response to LRH, potentiated the MPOA-ECS-induced rise in plasma LH. Higher concentrations of epinephrine (3 x 10(-4) M), however, inhibited both the ECS and LRH-induced secretion of LH.

Animals↗
PubMed1975

Failure to detect luteinizing hormone-releasing hormone in third ventricle cerebral spinal fluid under a variety of experimental conditions.

Cerebral spinal fluid (CSF) was examined for the presence of luteinizing hormone-releasing hormone (LH-RH) at times when copious amounts of LH were being secreted by the adenohypophysis. A "push-pull" apparatus was designed which permitted the perfusion of artificial CSF through the 3rd ventricle from the region of the medial preoptic area (MPOA) to the site of recollection adjacent to the median eminence (ME). It was observed on radioimmunoassay that LH-RH concentrations were low in CSF and peripheral plasma of Nembutal-blocked proestrous rats. Intraarterial injections of LH-RH did not increase CSF concentrations of this decapeptide, although a significant release of pituitary LH occurred. Further, electrochemical stimulation of the MPOA also elevated plasma LH without altering CSF-LH-RH levels. When synthetic LH-RH, dissolved in artificial CSF, was perfused through the 3rd ventricle, plasma LH levels rose dramatically, and a significant decrease in the concentration of LH-RH in the CSF efflux was observed on collection and assay. CSF collected from MPOA-stimulated rats also was tested for biologically active LH-RH by its reinjection into Nembutal-blocked proestrous recipients. While such injections failed to induce pituitary LH release, it was observed that LH-RH, when mixed with artificial CSF, and allowed to stand at room temperature (24 C), also lost all biological potency even though immunoreactivity was retained. The results suggest that CSF does not serve as a vehicle for transport of LH-RH to the median eminence under physiological conditions.

Animals↗