Synthetic TRF (pyroglutamylhistidyl-proline amide) was infused (1 ng/min) for 20 min (1) into the anterior pituitary of 10 rats by way of a cannulated hypophysial stalk portal vessel or (2) into a femoral vein of 10 rats. At the end of the 20-min infusion period, the plasma concentration of TSH in 8 of 10 rats given TRF via a cannulated portal vessel was significantly greater than the pre-infusion level. In contrast, in only 3 of 10 rats given TRF via a femoral vein was the plasma concentration of TSH significantly greater than the pre-infusion level of TSH (Endocrinology89: 1054, 1971)
Corticosterone-4-14C, Na131I, ovine LH-KI1I, rat prolactin-131I, or bovine hemoglobin- 131I was injected into the third ventricle of rats. In 30 min, significant quantities of corticosterone- 4-14C, Na131I, and LH-131I were recovered in the pituitary stalk blood of the recipient animals. At the same time, little radioactivity was present in arterial blood. The radioactivity recovered in stalk blood after ovine LH-131I was injected into the third ventricle was associated with a substance which reacted with an antiserum to ovine LH, indicating that LH per se passed from CSF to stalk blood. These data show that certain compounds in the CSF of the third ventricle can pass through the median eminence and enter hypophysial blood. (Endocrinology91: 1239, 1972)
The capacity of the median eminence to transport LRF from CSF to hypophysial portal blood and the efficacy of intraventricularly and intravenously administered LRF in releasing LH were studied. Ten to 15 min after 125 ng LRF was injected intraventricularly, LRF was detected in portal blood. The maximal rate of transport ranged from 35 to more than 200 pg'min. The rates of transport were much less following the administration of 25 or 5 ng LRF. When these same quantities of LRF were injected intraventricularly into rats with intact pituitary glands, plasma LH levels increased in proportion to the dose of LRF. The releasing action of LRF was long, and 120 min after the administration of 125 ng LRF, the concentration of plasma LH was 40- to 50-fold greater than the control level. Intravenous injection of 5, 25, or 125 ng LRF caused corresponding increases in LH release. Intravenously administered LRF stimulated LH release slightly faster than did LRF given intraventricularly, but the effect of intraventricular LRF injections lasted much longer. The disappearance curve of LRF from systemic plasma after an intravenous injection consisted of a fast and a slow component with estimated half-times of 7 and 48 min, respectively. The half-time for the disappearance curve of LRF from plasma after intraventricular injection was 107 min, indicating slow, prolonged entry of LRF into the systemic vasculature from CSF. It is concluded that LRF can be transported from CSF to hypophysial portal blood in significant quantity. In addition, LRF given intraventricularly is more effective on a prolonged basis in stimulating LH release than when given intravenously. (Endocrinology95: 18, 1974)
Pituitary halves incubated in pituitary stalk plasma release more luteinizing hormone than their opposite halves incubated in plasma from peripheral blood. Glands incubated in stalk plasma from dopamine-treated rats release more luteinizing hormone than glands incubated in stalk plasma from untreated controls. Luteinizing hormone-releasing activity in stalk plasma may be due to the luteinizing hormone-releasing factor, and the secretion of luteinizing hormone-releasing factor may be controlled by a dopaminergic mechanism.
The concentration of luteinizing hormone releasing hormone (LHRH) in hypophysial portal plasma was determined in pentobarbitalanesthetized, intact and castrated rats of both sexes, including proestrous rats following electrochemical stimulation of the medial preoptic area (MPOA). Mean LHRH levels in portal plasma obtained between 1400–1700 h from estrous and diestrous rats and from rats ovariectomized for 8 weeks were similar and ranged from 50–55 pg/ml, but the LHRH levels in proestrous rats were less than 12 pg/ml. In addition, hypophysial portal plasma collected during lldO to 1400 h from animals orchidectomized for 8 weeks and from intact male rats contained mean LHRH concentrations that ranged from 50–65 pg/ml and 30–35 pg/ml, respectively. Electrochemical stimulation of the MPOA in the female rat on the afternoon of proestrus resulted in a marked increase in the concentration of LHRH in portal plasma. LHRH levels in portal plasma during the 0 to 30, 30 to 60, 60 to 90, 90 to 120, and 120 to 150-min periods after electrochemical stimulation of the MPOA were 105 ± 24.2, 61 ± 10.8, 51 ± 8.2, 36 ± 5.3, and 32 ±4.1 pg/ml, respectively. LHRH levels in portal plasma from the unstimulated lats were not detectable (<12 pg/ml) in most of the animals. In another group of proestrous rats, the effect of rabbit anti- LHRH serum or normal rabbit serum (NRS) on the release of LH after electrochemical stimulation of the MPOA was examined. Pretreatment of proestrous rats with anti-LHRH serum blocked the release of LH due to MPOA stimulation, whereas pretreatment with NRS did not inhibit LH release. On the basis of these findings, it is concluded that electrochemical stimulation of the MPOA in proestrous rats increases LHRH levels in portal blood and that the enhanced secretion of LHRH stimulates the release of LH from the pituitary gland. (Endocrinology 100: 263, 1977)
Melatonin as well as serotonin, when injected into the third ventricle of the brain of male rats, appeared to stimulate the release of prolactin and inhibit the release of FSH as judged by the changes in the concentrations of these hormones in the plasma of the recipient animals. (FSH and prolactin were determined by radioimmunoassay.) For example, 30 min after the injection into the third ventricle of doses of 1, 5 and 50 μg melatonin, the plasma prolactin concentrations were 199 ± 11.3 % (mean and SE), 235±16.1% and 304±12.7%, respectively, of the pre-injection levels. The corresponding FSH values were 88±3.7%, 85±3.7% and 74±2.6%. After 2 hr, the plasma prolactin concentration had returned to the pre-injection level; however, the plasma FSH concentration after 2 hr was only 50% of the pre-injection level. The effects of intraventricularly administered serotonin were similar to those seen with melatonin. Isotonic saline solution (2.5 μl) had no effect on the release of prolactin and FSH. When melatonin or serotonin was infused directly into the anterior pituitary by way of a cannulated portal vessel, no significant alterations in the plasma concentrations of prolactin and FSH were observed. These results suggest that melatonin or serotonin may have suppressed the discharge of PIF and FRF and thereby indirectly affected the release of prolactin and FSH. (Endocrinology88:1288,1971)
The acute effect of selective surgical interruption of the anterior pituitary’s blood supply on the release of ACTH has been investigated in surgically stressed rats. The corticosterone secretory rate was used to evaluate the release of ACTH. In intact, sham-operated animals, corticosterone secretion was near maximal throughout a 50-min observation period. Removal of the pituitary greatly suppressed the secretion of corticosterone. Posterior lobectomy or transection of the portal vessels in the upper stalk had no apparent effect on ACTH release. This finding was interpreted to mean that the posterior pituitary and post-chiasmatic eminence are not obligatory sources of CRF. Transection of the pituitary stalk greatly suppressed ACTH release. This finding supports the view that the caudal hypophysial arteries do not provide the anterior pituitary with a significant amount of blood via the short portal vessels. Transection of the peduncular arteries or the stalk portal vessels in the lower stalk suppressed ACTH release. This finding is consistent with the notion that CRF enters portal blood via the post-peduncular and/or pituitary stalk capillaries. These findings indicate that CRF comes from the stalk, postpedunuclar eminence and/or the cerebrospinal fluid. (Endocrinology86: 590, 1970)
Extracts of hypothalamic tissue (HE) or of cerebrocortical tissue were infused into stalk portal vessels of anesthetized male rats. The extract of cerebrocortical tissue, equal in weight to ½ of a hypothalamic fragment, had no effect on the release of LH, FSH, or prolactin. HE caused an increase in the levels of LH and FSH in arterial plasma and simultaneously a decrease in the level of prolactin. The responses to HE were related to the concentration of the extract. For example, in rats given HE equivalent to ½1 ⅙, or ½ of a hypothalamic fragment per 30 min, the concentrations of LH in plasma at the end of the infusion period were 2.5, 4.5 and 6.9 times the control values, respectively. The corresponding levels of FSH were 1.6, 2.2 and 2.9, and of prolactin 0.73, 0.55 and 0.37. After the infusion of HE was terminated, the concentrations of LH and FSH in plasma fell and that of prolactin rose. The half-times of the disappearance functions of prolactin, LH and FSH in plasma of rats after hypophysectomy were 14.4, 28.9 and 123 min, respectively. The disappearance rates of prolactin during the infusion of HE and of FSH after the infusion (equivalent to ⅙ or ½ of a hypothalamic fragment) appeared to be slower than those seen in hypophysectomized animals. The disappearance rate of LH after the infusion of HE was the same as that seen in hypophysectomized rats. (Endocrinology88: 1294, 1971)
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