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Biomedical subjects

A G Robinson

Publications and source records attributed to A G Robinson.

At least 73 records · Page 4Linked to original sources
PubMed1982

Oxytocin, vasopressin, and estrogen-stimulated neurophysin: daily patterns of concentration in cerebrospinal fluid.

The concentrations of oxytocin, arginine vasopressin, and estrogen stimulated neurophysin in cerebrospinal fluid of monkeys showed a daily fluctuation with high concentrations occurring during the light period. The patterns of oxytocin and estrogen-stimulated neurophysin in the cerebrospinal fluid were not observed in the plasma nor were they altered after the administration of a dose of estradiol that increased concentrations of estrogen-stimulated neurophysin in plasma. The disassociation between these cerebrospinal fluid and plasma patterns and values suggests that the secretory activity of neurons that release estrogen-stimulated neurophysin and oxytocin into the cerebrospinal fluid is controlled by mechanisms different from those that control their release into the plasma.

Animals↗
PubMed1982

Identification of high molecular weight neurophysins in extracts of human neurohypophyseal tissue.

Acid extracts of human neurohypophyseal tissue were found to contain neurophysin-immunoreactive proteins in the 17,000-20,000 dalton molecular weight range by sodium dodecyl sulfate polyacrylamide gel electrophoresis. The 17,000-20,000 dalton neurophysins persisted under reducing conditions. Limited chymotrypsin proteolysis of the 17,000-20,000 dalton neurophysins generated both increased 10,000 dalton neurophysin and also 4000-8000 dalton vasopressin immunoreactivity. These 'big' neurophysins appear to represent precursor forms of the neurophysins and the neurohypophyseal hormones, which are present within the neurosecretory granules of the human posterior pituitary.

Electrophoresis, Polyacrylamide Gel↗
PubMed1982

Introduction to the general principles of hormone-receptor interactions.

This review presents a concise overview of the historical development of receptor theory and the molecular mechanisms of action of the three broad classes of hormones, steroids, tyrosine derivatives, and polypeptides. Key terms required for understanding the basic terminology and concepts currently utilized in membrane receptor research are defined. The basic information should enable the reader to critically assess and understand more detailed discussions of hormone-receptor interactions and their application to clinical medicine.

Animals↗
PubMed1982

Vasopressin-dependent and -independent control of the release of adrenocorticotropin.

We tested the possibility that vasopressin mediates the responses of adrenocorticotropin (ACTH) to electrical stimulation of various areas of the hypothalamus. Thirty-three cats were anesthetized with chloralose-urethane, immobilized with gallamine, and respired artificially. Plasma ACTH was measured by RIA. Intraventricular administration of antiserum to vasopressin blocked the release of ACTH induced by electrical stimulation of the paraventricular nucleus (PVN), suggesting a role for the vasopressinergic projection from PVN to the external zone of the median eminence. In contrast, the release of ACTH induced by stimulation of areas ventral to PVN was unaffected by the antiserum. Thus, there is at least one corticotropin releasing factor released from nuclei other than PVN that is distinct from vasopressin.

Adrenocorticotropic Hormone↗
PubMed1982

Reversible panhypopituitarism caused by a suprasellar aneurysm: the contribution of mass effect to pituitary dysfunction.

A case of panhypopituitarism and hyperprolactinemia caused by a giant intracranial aneurysm is presented. The case is unique because both the pattern of the pituitary dysfunction and the complete normalization of all pituitary function after decompression of the aneurysm demonstrate the importance of pure compressive effects of mass lesions on pituitary function. The literature regarding return of pituitary function after resection of sellar and suprasellar masses is reviewed, and a schema for classification of pituitary dysfunction caused by mass lesions is proposed.

Carotid Artery, Internal↗
PubMed1981

The role of calcitonin and parathyroid hormone in the pathogenesis of post-thyroidectomy hypocalcemia.

Permanent hypocalcemia complicating thyroidectomy is a rare complication, whereas transient post-thyroidectomy hypocalcemia occurs frequently. Ten patients were studied in an attempt to elucidate the underlying mechanisms. An early and transient postoperative rise in calcitonin (CT) corresponding to a decline in calcium levels was demonstrated. Though there was no significant depression of parathyroid hormone (PTH) levels, the failure of the parathyroids to respond to hypocalcemic stimuli suggests a degree of at least transient parathyroid insufficiency. Transiently elevated CT levels appear to play a significant role in the commonly observed early, transient post-thyroidectomy hypocalcemia following subtotal and total thyroidectomy.

Calcitonin↗
PubMed1981

Chlorpropamide effect: measurement of neurophysin and vasopressin in humans and rats.

The effect of chlorpropamide on neurohypophyseal function was studied by measurement of neurophysin and vasopressin in humans and in rats. Administration of chlorpropamide was shown to inhibit the ability of the human subjects and of the rats to maximally dilute their urine after administration of water. Comparison of the levels of vasopressin and neurophysin before and after the administration of chlorpropamide in the basal state and after water loading in both the human subjects and in rats showed no lack of suppression due to the chlorpropamide. The levels of both peptides were measured at the limits of detection. In other studies where neurophysin and vasopressin were readily detected, administration of chlorpropamide did not result in any augmented release of neurophysin or vasopressin in response to stimulation of the neurohypophysis in humans nor in rats. Levels of neurophysin in the pituitaries of rats showed no change in rats given chlorpropamide, while the content of vasopressin was increased, possibly indicating a chronic decreased secretion of vasopressin in rats given chlorpropamide.

Adult↗
PubMed1981

Control of release of adrenocorticotropin and vasopressin by the supraoptic and paraventricular nuclei.

To determine the relative roles of the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei in the control of the release of vasopressin and of ACTH, we have examined the hormonal responses to electrical stimulation (200 microA, 0.2 msec, 100 Hz, 20 sec) of these regions. Cats were anesthetized with chloralose-urethane. Blood samples were taken 30 sec before stimulation and 1.5 min poststimulation. ACTH and vasopressin were measured by RIA. Electrical stimulation of the caudal pole of the SON increased vasopressin in plasma (1.82 +/- 0.41 microU/ml, n = 17, P less than 0.01) and decreased ACTH (-26 +/- 4 pg/ml, n = 13, P less than 0.01). In contrast, stimulation of the PVN increased vasopressin (2.01 +/- 0.60 microU/ml, n = 7, P less than 0.001) and increased ACTH (107 +/- 20 pg/ml, n = 32, P less than 0.01). Previous work has shown that vasopressinergic neurons of PVN, but not of SON, project to the zona externa of the median eminence. Other have suggested that the retrograde flow of blood from the neural lobe to the median eminence and thence to the anterior lobe would allow vasopressin to influence the release of ACTH. The present results indicate that both SON and PVN facilitate the release of vasopressin. However, PVN facilitates, but SON inhibits the release of ACTH. These findings suggest that the projection from PVN to the zona externa of the median eminence mediates the release of ACTH and that retrograde flow from the neural lobe is not important in the control of ACTH release during modest and transient increases in the release of vasopressin.

Adrenocorticotropic Hormone↗
PubMed1981

Oxytocin in human plasma: correlation with neurophysin and stimulation with estrogen.

RIA for the measurement of oxytocin in human plasma is described. Extraction of oxytocin from larger peptides in plasma used acetone precipitation with a 75% +/- 2 SEM recovery of oxytocin. Nonspecific binding of the assay was less than 4%, and the minimum level of detection was 0.2 microunits/tube. No cross-reactivity was noted with neurophysins, arginine, or lysine vasopressin. The mean basal level (+/- SEM) of oxytocin in men was 1.80 +/- 0.07 microunits/ml and was not different in normal women (1.71 +/- 0.07 microunits/ml). Changes in posture had no effect on the levels of oxytocin. Samples obtained every 15 min over 4 h showed no pulsatile secretion of oxytocin. In women chronically receiving estrogen as an oral contraceptive, oxytocin was greater than normal, (4.59 +/- 0.51 microunits/ml; P less than 0.01). Estrogen-stimulated neurophysin was also elevated (8.45 +/- 1.99 ng/ml; P less than 0.005). Acute ingestion of estrogen caused an increase in the level of oxytocin in plasma by 12 h and a concomitant elevation of estrogen-stimulated neurophysin. When the neurophysin was isolated from plasma obtained from a subject after ingestion of estrogen, the neurophysin from plasma comigrated on a polyacrylamide gel with a human pituitary standard of estrogen-stimulated neurophysin. In the studies in which neurophysin was elevated, the correlation between the level of oxytocin and the level of estrogen-stimulated neurophysin in plasma was significant (P less than 0.01). The observation that estrogen administration stimulates the release of oxytocin and estrogen-stimulated neurophysin provides additional evidence that this neurophysin is the oxytocin-neurophysin of man.

Animals↗
PubMed1981

Elevation of oxytocin and the oxytocin-associated neurophysin in the plasma of normal women during midcycle.

A positive correlation was observed between the midcycle elevation of estrogen (E) and the level of oxytocin- and estrogen-stimulated neurophysin (ESN), the protein carrier of oxytocin, in the plasma of five of six women. The time of the maximal level of E was associated with a level of oxytocin significantly greater than that in either the early follicular or late luteal phase (P less than 0.025). Likewise, the level of ESN at midcycle was greater than the level of ESN in the early follicular or late luteal phase (P less than 0.01). Other than states of lactation or pregnancy, this is the only described cyclic secretion of oxytocin in humans. Since oxytocin chronologically correlates with a rise in the level of E at midcycle, a role for oxytocin in ovulation may be considered.

Estrogens↗
PubMed1981

The effect of maternal smoking on carboxyhemoglobin levels and acid-base balance of the fetus.

Results are presented showing a dose-related effect of maternal smoking during pregnancy on cord blood carboxyhemoglobin levels. These elevated cord blood carboxyhemoglobin levels are associated with decreased pH and pO2 levels and raised pCO2 levels. This evidence of chronic intrauterine hypoxia in the infants of mothers who smoke during pregnancy provides a potential mechanism for the reduced birthweight found in these infants.

Acid-Base Equilibrium↗
PubMed1981

Hyponatremia in intracranial disease: perhaps not the syndrome of inappropriate secretion of antidiuretic hormone (SIADH).

Patients with intracranial disorders are prone to develop hyponatremia with inability to prevent the loss of sodium in their urine. This was originally referred to as "cerebral salt wasting," but more recently is thought to be secondary to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Blood volume determinations were made in 12 unselected neurosurgical patients with intracranial disease who fulfilled the laboratory criteria for SIADH. Ten of the 12 patients had significant decreases in their red blood cell mass, plasma volume, and total blood volume. The finding of a decreased blood volume in patients who fulfill the laboratory criteria for SIADH is better explained by the original concepts of cerebral salt wasting than by SIADH. The primary defect may be the inability of the kidney to conserve sodium.

Blood Volume↗
PubMed1980

Neurohypophyseal peptides in the developing rat fetus.

The quantitative changes in the content of the neurohypophyseal peptides, neurophysins, oxytocin, and vasopressin, were determined in the developing rat fetus. No neurohypophyseal peptides were found in 12-day fetuses. Neurophysins were first detected at day 13 and increased dramatically on day 14. The hormones vasopressin and oxytocin were not detected at day 13 and were measured at low levels at day 14. A 350-fold molar excess of neurophysin to hormones existed at day 14. From day 14 to day 19 the total content of neurophysin decreased while the content of vasopressin and oxytocin slowly increased. At day 19 there was a near molar equivalency between the content of neurophysin and that of the neurohypophyseal hormones. From day 18 to day 22 there was a sharp increase in the content of vasopressin while the content of neurophysin and oxytocin increased less dramatically. At term there was a molar excess of vasopressin, and the molar ratio of neurophysin to hormone at the time of delivery was 0.12. Measurement of vasopressin by different radioimmunoassays and by bioassay indicated no contribution of arginine-vasotocin to the measured vasopressin.

Age Factors↗
PubMed1980

Levels of neurohypophyseal peptides in the rat during the first month of life. I. Basal levels in plasma, pituitary, and hypothalamus.

Vasopressin, oxytocin, and neurophysin were measured by RIA in the pituitary, hypothalamus, and plasma (except oxytocin) of the rat during the first month of life. In plasma, vasopressin was less than 1.7 microU/ml in most animals. Neurophysin was elevated above adult levles on day 2 and decreased with age. The three peptides were present in the pituitary at birth, but in amounts less than 1% of the adult level. The vasopressin content of the pituitary increased rapidly in the first days after birth, while the levels of oxytocin and neurophysin remained low until 8 days and then increased between 8-21 days. The ratio of vasopressin to oxytocin in the pituitary was 4.4 at birth and reached unity (the ratio in the adult) at 30 days. At birth, the moles of neurophysin in the pituitary relative to the moles of hormone (oxytocin plus vasopressin) was low (0.15), largely due to a molar excess of vasopressin. The ratio of neurophysin to hormone reached unity at 21-30 days. Assays to detect vasotocin gave negative results. It is postulated that a precursor neurophysin which was related to vasopressin was present in the fetal rat but was not measured in our study.

Aging↗
PubMed1980

Levels of neurohypophyseal peptides in the rat during the first month of life. II. Response to physiological stimuli.

Levels of vasopressin, oxytocin, and neurophysin were measured by RIA in the hypothalamus, pituitary, and plasma of infant rats (2-30 days old). At all ages, ip injection of a hypertonic solution of 5 g/100 ml NaCl produced a marked increase in levels of vasopressin and neurophpysin in plasma, up to 21 microU/ml and 51 ng/ml, respectively. After dehydration, there was a decrease of 26-38% in the levels of neurohypophyseal peptides in the pituitary. Depletion of neurohypophyseal peptides from the pituitary was greater after 24 h of dehydration in younger rats (26%) than in older rats (7%). Levels of vasopressin in plasma were less than 1.7 microU/ml after dehydration in younger rats but were greater in older rats. Immaturity of the neurohypophysis may contribute to the inability of newborn rats to withstand prolonged dehydration.

Animals↗