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Biomedical subjects

J C Porter

Publications and source records attributed to J C Porter.

At least 199 records · Page 11Linked to original sources
PubMed1975

Differential sub-cellular compartmentalization of thyrotropin releasing hormone (TRH) and gonadotropin releasing hormone (LRH) in hypothalamic tissue.

Homogenates of male rat hypothalami were fractionated by differential centrifugation. Of the total quantity of TRH and LRH in the homogenate, about 50% was in particles sedimenting at 11,500 X g. and 15-20% was in particles sedimenting between 20,000 and 105,000 X g. No LRH or TRH was recovered in the 105,000 X g supernatant fluid. When the 900 X g supernatant fluid was subjected to continuous sucrose density gradient centrifugation, TRH-containing particles distributed as two peaks located at 0.9 and 1.1 M sucrose. On the other hand, LRH-containing particles distributed as only one peak located at 1.2 M sucrose. The 11,500 X g pellet contained those particles comprising the 1.2 M peak of LRH and the 1.1 M peak of TRH. Acid phosphatase activity was found in the gradient fractions containing TRH and LRH, whereas NADPH-cytochrome c reductase and cytochrome c oxidase activities were separated from the peaks of TRH and LRH. Norepinephrine, dopamine, and TRH distributed identically on the gradient. Hypo-osmotic treatment changed the gradient profile of TRH but not that of LRH. Most of the TRH was found near the top of the gradient, but a small amount of TRH was associated with particles which were lighter than those previously noted. The peak of LRH was reduced but its location on the gradient was unchanged. It is concluded that in hypothalamic homogenates TRH and LRH are localized in synaptosome-like particles which have different physical properties.

Animals↗
PubMed1975

Transformation of 3H-dopamine during transport from CSF to hypophysial portal blood.

The capacity of the hypothalamus to transport dopamine from brain tissue into hypophysial portal blood was investigated. One hour after injection 10 muCi of 3H-dopamine into a lateral ventricle of male rats, radioactivity was present in the brain, in the anterior pituitary gland, and in systemic plasma. The highest concentration of radioactivity was found in the hypothalamus, whereas the lowest was found in systemic plasma. The cerebrum and systemic plasma contained over 50% of the dose injected, whereas the anterior pituitary gland contained no more than 0.2%. Three doses of 3H-dopamine (0.1, 1, 1nd 10 muCi) were injected into a lateral ventricle, and hypophysial portal and arterial blood were collected at 7 mu1/min for two hours. Ten min after injection, radioactivity was detected in hypophysial portal blood, reached a peak within 15-20 min, and then declined gradually to attain a concentration similar to that in arterial blood. Portal and arterial plasma and tissue extracts from rats injected intraventricularly with 3H-dopamine were subjected to gel filtration on a Sephadex G-10 comumn and to paper electrophoresis. The hypothalamus as well as the cerebrum contained several radiolabeled substances one of which appeared to behave like 3H-dopamine. However, no free 3H-dopamine was evident at this time either in blood or in the anterior pituitary gland. The results of chromatography and electrophoresis of dialyzed portal plasma indicate that much of the radioactivity was bound to macromolecules (probably plasma proteins) larger than 10,000-12,000 molecular weight. When the radioactive compound was dissociated from the macromolecule with perchloric acid, the dissociated compound did not behave as free 3H-dopamine as judged by gel filtration and electrophoresis. It is concluded that a transformation of 3H-dopamine occurred during passage from the CSF to blood and that no 3H-dopamine was present in portal blood. A large portion of the radioactivity was bound to plasma macromolecules.

Animals↗
PubMed1975

Prostaglandin E2-induced release of LHRH into hypophysial portal blood(1).

Prostaglandin E2 (PGE2) was infused into a lateral ventricle of adult male rats or infused into a hypophysial portal vessel. Intraventricularly administered PGE2 stimulated the release of LH, FSH, and prolactin but not TSH. Intraventricular infusion of the control solution did not alter the basal release of any of these hormones. PGE2 was found to be a potent stimulator of LH release, but larger quantities were needed to stimulate the release of FSH or prolactin. In addition, lateral ventricle infusion of 5 mug or 20 mug of PGE2 stimulated a 2- to 3-fold increase in the concentration of LHRH in hypophysial portal plasma but did not affect LHRH levels in arterial plasma. PGE2 infused into a hypophysial portal vessel at a rate of 0.167 mug/min for 30 min, or infusion of the control solution, resulted in similar changes in the concentration of FSH, LH, and prolactin in arterial plasma. The results of this investigation suggest that PGE2 stimulates the release of gonadotropins in vivo by enhancing the release of LHRH. The portal vessel infusion studies do not support a direct stimulatory effect of PGE2 on the pituitary gonadotrophs.

Animals↗
PubMed1975

Transport of thyrotropin-releasing hormone from cerebrospinal fluid to hypophysial portal blood and the release of thyrotropin.

The capacity of the medium eminence to transport thyrotropin-releasing hormone (TRH) from cerebrospinal fluid (CSF) to hypophysial portal blood, and the ability of TRH when introduced into a lateral ventricle to stimulate TSH release from the pituitary gland were investigated. Male rats were injected either intraventricularly or intravenously with 0, 1, 10, or 100 ng of TRH, and plasma TSH concentrations were determined at various times thereafter. TRH administration via both routes resulted in substantial release of TSH. Following intraventricular injection of TRH, there was a delay in reached maximal TSH concentration when compared with the faster elevation and faster decline in TSH concentrations which followed intravenous injection of the same dose of TRH. In a second experiment, 7 muCi of [3H]TRH were introduced intraventricularly or intravenously, and hypophysial portal and arterial blood were simultaneously collected and examined for the presence of radioactivity. The intraventricular injection of [3H]TRH resulted in a peak of radioactivity in portal blood within minutes, which was maintained for 20--30 min and then declined. The concentration of radioactivity in arterial blood from the same animals was considerably lower than that in portal blood. The intravenous administration of [3H]TRH resulted in radioactive peaks in both portal and arterial blood with a higher concentration of radioactive substances in arterial blood. However, the level of radioactivity in portal blood following intravenous injection of [3H]TRH comprised no more than 5--10% of that found following intraventricular administration of the saem dose. The data support the view that TRH is able to cross the medium eminence from CSF into hypophysial portal blood and that it is capable of stimulating the pituitary gland to release TSH.

Animals↗
PubMed1975

Fetal plasma prolactin levels.

Prolactin levels were measured by radioimmunoassay in umbilical cord plasma from fetuses, in capillary plasma from neonates, and in venous plasma from adults. The concentrations of prolactin in cord plasma from fetuses having gestational ages of 16 to 19 weeks, 20 to 34 weeks, and 35 to 42 weeks were 53 +/- 16 (mean and SE), 233 +/- 30 and 371 +/- 7 ng/ml, respectively. The prolactin levels decreased to 218 +/- 35 ng/ml during the first neonatal week. The similarity of the patterns of prolactin levels, reported gestational estrogen levels and adrenal weights, as well as the known biological properties of prolactin, estrogen, and ACTH is consistent with the view that these three factors may be involved in the growth of the fetal adrenal cortex and its involution in the newborn.

Adrenal Glands↗