Biomedical subjects

K Shizume

Publications and source records attributed to K Shizume.

At least 235 records · Page 13Linked to original sources

PubMed1985

Synthetic rat atrial natriuretic factor inhibits in vitro and in vivo renin secretion in rats.

We investigated the action of a synthetic rat atrial natriuretic factor (ANF) with 28 amino acids on renin secretion in rats. Renin release by kidney cortex slices was determined after 90 min of incubation at 37C. ANF inhibited basal renin release in a dose-related fashion. ANF also decreased cAMP release and increased cGMP release in a dose-dependent manner. Renin release stimulated by 10(-7) M isoproterenol was inhibited by ANF with an ID50 of 5.8 x 10(-8) M. The renin-inhibitory effect was not calcium-dependent. In anesthetized rats, a bolus IV dose of ANF decreased plasma renin activity and cAMP concentration, but increased cGMP concentration. These data suggest that ANF inhibits renin secretion via the direct action on juxtaglomerular cells and that this effect may be partly mediated by the changes in cyclic nucleotide production.

Angiotensin I↗

PubMed1985

The effect of free fatty acids on growth hormone (GH)-releasing hormone-mediated GH secretion in man.

The effect of FFA on GH-releasing hormone (GHRH)-mediated secretion of GH was examined in six normal young men. Three of the men were infused with 250 ml of a lipid-heparin solution at 1.67 ml/min for 150 min, and the other three were given an equivalent volume of saline in the same manner. Thirty minutes after the start of infusion, 100 micrograms GHRH (the 44-amino acid form) were injected iv, and plasma GH and FFA were measured. One week later, the same men participated in an identical experiment, but the ones who had received lipid-heparin previously were given saline and vice versa. In both experiments, plasma FFA increased to 2.25 +/- 0.16 meq/liter (mean +/- SEM) 60 min after the start of lipid-heparin infusion, whereas FFA levels did not change significantly in the saline-treated group. Mean plasma GH levels reached peak concentrations in both groups 30 min after GHRH treatment. However, the peak GH response when lipid-heparin was given was significantly diminished (8.4 +/- 1.7 ng/ml), compared with the peak response when saline was given (28.9 +/- 7.1 ng/ml). These data suggest that plasma FFA elevations induced by lipid-heparin infusion inhibit GH secretion induced by GHRH.

Adult↗

PubMed1985

The effect of glucose on growth hormone (GH)-releasing hormone-mediated GH secretion in man.

The effect of glucose on GH-releasing hormone (GHRH)-mediated GH secretion was examined in six normal young men. In two paired experiments, the six men drank a 75-g glucose solution or an equal volume of water 30 min before receiving, iv, 100 micrograms of the 44-amino acid form of human pancreatic GHRH (hGHRH-44). One week later, the same men underwent an identical experimental protocol in a cross-over trial. Basal plasma GH concentrations before hGHRH-44 administration were not statistically different in the two experiments [glucose experiment, 2.1 +/- 0.1 (+/- SE) ng/ml; water experiment, 2.6 +/- 0.6 ng/ml]. The mean peak plasma GH level occurred 30 min after hGHRH-44 administration in both experiments. However, the mean GH response was significantly diminished when the men received glucose (8.12 +/- 1.12 ng/ml) compared to that when they received only water (23.70 +/- 8.46 ng/ml; P less than 0.01). Thus, hyperglycemia may exert an inhibitory effect on the plasma GH response to hGHRH-44.

Adult↗

PubMed1985

Plasma GH responses to GHRH and insulin-induced hypoglycemia in man.

Changes in plasma GH levels in response to an intravenous bolus injection of 200 micrograms GHRH-44 or 0.1 U/kg body weight regular insulin were examined in normal men who were pre-treated with 200 micrograms GHRH-44 or 0.1 U/kg body weight regular insulin 120 min in advance. The prior bolus injection of GHRH-44 inhibited the plasma GH response to the subsequent administration of GHRH-44 whereas the plasma GH response to the subsequent injection of insulin was not influenced by the prior administration of GHRH-44. The prior administration of insulin attenuated the plasma GH response to the subsequently given GHRH-44. These results suggest that desensitization of GHRH receptors in somatotrophs and/or somatostatin hypersecretion induced by increase in plasma GH levels following the prior GHRH-44 administration may be involved in the mechanism by which the prior GHRH-44 administration or insulin-induced hypoglycemia suppressed plasma GH responses to the following GHRH-44 administration. Sudden suppression of somatostatin secretion, which causes rebound of GH secretion, may occur in insulin-induced hypoglycemia.

Adult↗

PubMed1985

Immunohistological evidence for renin in human endocrine tissues.

The peroxidase-labeled antibody method and the avidin-biotin-complex method with antiserum to purified human kidney renin were used to identify renin in human endocrine tissues. Renin immunoreactivity was found in some large cells of the anterior pituitary, the zona glomerulosa and the zona reticularis of the adrenal, the Leydig cells of the testis, and the follicular epithelial cells of the thyroid and prostate glands. The specificity of the immunohistochemical reaction was confirmed by immunoabsorption tests. The specific localization of immunoreactive renin in each tissue suggests a possible role of renin in the function of these tissues.

Adrenal Glands↗

PubMed1985

Characterization of insulin-like growth factor I receptor on human erythrocytes.

[125I]Insulin-like growth factor I (IGF-I) specifically bound to erythrocytes; the binding was saturable, and time and temperature dependent. Steady state binding was reached at 16 h at 4 C, and specific binding averaged 14.3 +/- 0.7% (+/- SEM) at a concentration of 3.6 X 10(9) cells/ml in seven normal subjects. [125I]IGF-I binding to the cells was displaced by unlabeled IGF-I in a dose-dependent manner. Scatchard analysis indicated a linear plot, and Ka and number of binding sites/cell were 1.43 +/- 0.07 X 10(9) M-1 and 20.7 +/- 2.2, respectively. Compared to IGF-I, the relative potencies of multiplication-stimulating activity and insulin for displacing [125I]IGF-I binding were 20% and 1%, respectively. [125I]IGF-I binding to erythrocytes from patients with acromegaly was lower than binding to cells from pituitary dwarfs. An inverse correlation between plasma IGF-I level and the number of IGF-I-binding sites per cell was found (r = -0.75; P less than 0.005). These results demonstrate that [125I]IGF-I binding to erythrocytes can be used for clinical measurement of the IGF-I receptor.

Acromegaly↗

PubMed1985

Thyroid-stimulating antibody bioassay using porcine thyroid cells cultured in follicles.

Isolated porcine thyroid cells were cultured in agarose-coated dishes and allowed to reform follicles with normal polarity. The thyroid cells reaggregated into follicles were compared with cells cultured in monolayer for cAMP responsiveness to TSH and thyroid-stimulating antibody (TSAb). The cells in follicles were sensitive to TSH stimulation and responded to the hormone at concentrations as low as 3.3-10 microU/ml with an increase in cAMP production. In contrast, 10-50 microU/ml TSH were required to elicit a cAMP response in cells cultured in monolayer using identical conditions. cAMP responsiveness to TSAb also was greater in the cells organized into follicles. TSAb was detected in serum from 89.4% of 66 untreated patients with hyperthyroid Graves' disease using thyroid follicles, but TSAb was detected in serum from only 60% of the patients when assayed using cells in monolayer. The assay using thyroid follicles was used to measure TSAb in 27 euthyroid patients who were euthyroid while receiving thionamide therapy and compared with 20-min thyroid 131I uptake after T3 suppression. TSAb was present in 11 of 12 nonsuppressible patients and in 5 of 15 suppressible patients. TSAb was positively correlated with 20-min 131I thyroid uptake. We conclude that thyroid cells cultured in follicles are suitable for measuring TSAb.

Adolescent↗

PubMed1985

The use of the corticotropin-releasing hormone test to monitor the recovery of patients with Cushing's disease or Cushing's syndrome due to an adrenal adenoma after adenomectomy.

Six patients with Cushing's disease and three with Cushing's syndrome due to an adrenal adenoma were monitored after their adenomectomy with the corticotropin-releasing hormone test to evaluate the progress of recovery of their pituitary adrenal function. Before surgery the patients with Cushing's disease showed either high, normal or low responses of plasma ACTH and cortisol to 100 micrograms synthetic ovine corticotropin-releasing hormone (CRH) administered intravenously, whereas all three patients with Cushing's syndrome due to an adrenal adenoma showed no response of plasma ACTH or cortisol to CRH. One or two months after surgery, the patients who had Cushing's disease had low levels of basal plasma ACTH and cortisol and their responses to CRH were extremely low. However, the same patients were tested later, it was found that their responses to CRH gradually increased and reached normal ranges approximately within one year after tumor removal, which coincided with the overall improvement in their clinical signs and symptoms due to adrenal insufficiency. In contrast, the recovery of the pituitary adrenal function in patients who had Cushing's syndrome due to an adrenal adenoma was not complete even one year after surgery. Thus the corticotropin-releasing factor test is a useful criteria to evaluate the recovery of the pituitary adrenal function in these patients after surgery, since the responses of plasma ACTH and cortisol to the administered CRH are parallel with the improvements in clinical signs and symptoms due to adrenal insufficiency in patients with Cushing's disease.

Adenoma↗

PubMed1985

Plasma growth hormone and somatomedin-C responses to continuous growth hormone-releasing factor infusion in normal adult men.

The pituitary growth hormone (GH) responses during a 20-hour iv infusion of saline or human GH-releasing factor (hGRF-44) at 40 micrograms/h, followed by an iv bolus injection of hGRF at 2 micrograms/kg body weight, were studied in four normal adult men. During saline infusion only one or two pulses of plasma GH were observed. However, during hGRF infusion up to eight or ten pulses of GH were measured with an amplitude not different from that obtained during saline infusion. The mean +/- SEM integrated amount of GH secreted was 107 +/- 38.2 ng/ml.h in response to hGRF infusion, which was greater than the value of 25.4 +/- 3.5 ng/ml.h obtained during saline infusion. Plasma somatomedin-C also increased after hGRF infusion, but not after saline. After saline or hGRF infusion most of the subjects still responded to an iv bolus injection of the peptide (2 micrograms/kg). These results indicate that hGRF infusion augments GH secretion by increasing the number, but not the amplitude of GH pulses and that the infusion does not cause the pituitary somatotrophs to lose their capacity and ability to respond to hGRF subsequently.

Adult↗

PubMed1985

Effects of hGRF treatment of a patient with hGRF deficiency.

A 12-year old girl was admitted to our hospital for evaluation of her short stature. Her height was below -3.5 SD of the mean height for her age. She was diagnosed as having craniopharyngioma and treated surgically. Thereafter she was treated with thyroxine and hydrocortisone. One and a half years later, she revisited our hospital for treatment of short stature. Her plasma GH did not respond to insulin-induced hypoglycemia but increased after hGRF-44 administration, indicating hGRF deficiency. hGRF was therefore administered at a dosage of 100 micrograms twice a day subcutaneously for three months. Her height increased 1.6 cm during treatment, which corresponded to a height increase of 6.4 cm/year. These findings indicate that hGRF treatment stimulates height increase in patients with GRF deficiency. For complete evaluation of hGRF therapy, further studies will be required.

Child↗

PubMed1985

The inter- and intra-subject variabilities of plasma GH response to human growth hormone-releasing hormone (1-44) NH2 in men.

The effects of intravenously given human growth hormone-releasing hormone (1-44) NH2 (hGRH-44) on growth hormone (GH) secretion were studied in normal men. A wide variability of intersubject GH response to hGRH-44 was observed. The peak plasma GH levels in response to 50, 100 and 200 micrograms hGRH-44 in 7 normal men were 9.1 +/- 3.2 ng/ml (Mean + SEM), 19.3 +/- 3.3 ng/ml and 22.4 +/- 4.0 ng/ml, respectively. Both the mean peak values for plasma GH response to 100 and 200 micrograms were significantly greater than that for 50 micrograms hGRH-44 injection (p less than 0.01), although there was no significant difference of the mean peak plasma GH values and mean concentrations at each time point, except for those at 120 min, when 100 or 200 micrograms hGRH-44 was administered. A significant difference in the mean amount of plasma GH secreted in response to hGRH-44 was observed only between 50 and 200 micrograms hGRH-44 injection (p less than 0.01). Furthermore, a dose-related plasma GH increase in response to hGRH-44 was not always observed in each subject. In contrast to the wide intersubject variability, the difference among responses of plasma GH to 100 micrograms or 200 micrograms of hGRH-44 given at multiple times separated by intervals of at least 1 week in each individual was relatively small.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed1985

Plasma GH and somatomedin C responses to single and repeated administrations of human growth hormone releasing factor (hGRF).

Plasma growth hormone (GH) and somatomedin C responses to single and repeated administrations of synthetic human growth hormone releasing factor (hGRF-44) were studied in 29 patients with GH deficiency. hGRF-44 administered by single iv bolus (10 micrograms/kg), repeated iv boluses (50 or 100 micrograms, once a day), repeated iv infusions (2.5 micrograms/min for 90 min, once a day), and/or repeated im injections (100 micrograms, twice a day) for three to six consecutive days. Ten of 16 patients had plasma GH responses to a single iv bolus injection, i.e., their plasma GH increased above 5 ng/ml or twice the basal level. However none of them showed a plasma somatomedin C increase. To repeated iv bolus injections and repeated iv infusions of hGRF-44, 7 of 17 patients showed plasma GH responses, however in none of 7 patients did somatomedin C increase. Plasma somatomedin C did not increase after repeated im administrations of hGRF-44 for 5 days. Plasma somatomedin C increase was observed in two patients, from 0.32 to 0.54 U/ml and from 0.16 to 0.46 U/ml, in response to repeated iv boluses and repeated iv infusions, respectively. These results suggest that hGRF-44 stimulates plasma GH secretion in some patients with GH deficiency, however the increases are not enough to stimulate somatomedin generation.

Adolescent↗

PubMed1985

Oro-maxillofacial development in patients with Turner's syndrome.

Detailed oro-maxillofacial studies using dental casts, pantomograms and cephalograms were performed in 28 patients with Turner's syndrome and compared statistically to the results from 23 normal short children. Small tooth crown size, short tooth roots and advanced dental age were characteristic of patients with Turner's syndrome. However, the incidence of peg shaped teeth, malocclusion, high arched palate and congenital anodontia were not characteristic of patients with Turner's syndrome. The coronal arch width (C.A.W.) and basal arch width (B.A.W.) were greater and the coronal arch length (C.A.L.) and basal arch length (B.A.L.) were less in patient's with Turner's syndrome. These data indicate underdevelopment of the maxilla in the forward direction forming the wide-, flat-shaped facial characteristic of patients with Turner's syndrome.

Adolescent↗

PubMed1985

Plasma growth hormone (GH) responses to single and repetitive subcutaneous administration of GH releasing factor (hpGRF-44) in normal and GH deficient children.

Synthetic human pancreatic GRF (hpGRF-44) was administered sc to 8 normal children with short stature and 11 patients with GH deficiency. After a dose of 100-200 micrograms hpGRF-44, mean plasma GH levels reached a peak at 15 min of 27.2 +/- 6.4 (+/- SE) ng/ml in normal children. However the responses were variable and peak plasma GH varied from 10.1 to 56.5 ng/ml. Eight of 11 patients with idiopathic GH deficiency did not respond to sc administration of 100-300 micrograms hpGRF-44. However, a plasma GH increase of more than 5 ng/ml occurred in 2 patients and to twice the basal level in 1 patient. Their GH values were 14.3, 5.2 and 3.4 ng/ml, respectively. After repetitive administration of hpGRF-44 (200 micrograms, twice a day) sc for 5 consecutive days, 2 of 8 patients restored their responsiveness, but the remaining patients did not show GH rise in response to both sc and iv bolus administration of hpGRF-44. Repetitive hpGRF-44 administrations for 5 days had no effect on somatomedin-C production.

Adolescent↗

PubMed1985

Triiodothyronine binding immunoglobulin in a euthyroid man without apparent thyroid disease; its properties and effects on triiodothyronine metabolism.

A 54 year old man with markedly elevated serum T3, but without an apparent thyroid disease, was found to have a specific antibody to T3. His serum thyroxine, TBG and TSH were in normal range, but T3-RSU was markedly low. Antibodies to thyroglobulin and microsome were negative. He was judged euthyroid because of a normal basal metabolic rate and a normal thyroidal 123I uptake which was suppressed by T3 administration. When serum was extracted with ethanol prior to assay, serum T3 was found to be in the upper border of normal range. Several experiments revealed the presence of an antibody to T3 in his serum with an affinity constant of 3.3 X 10(9) M-1. The binding capacity of the antibody was 7.6 ng/mg of IgG. The binding of [125I]T3 was almost specific to T3, and potencies of T4 and fT3 in displacing [125I]T3 binding were only 1.0 and 0.3%, respectively, of that of T3. The antibody contained both kappa and lambda chains and was therefore polyclonal. The T3 metabolic clearance rate, which was determined by disappearance of injected [125I]T3 from serum, was lower in this patient (7.44 1/day) than in normal. The T3-production rate was decreased to 14.9 micrograms/day, and serum free T3 concentration as well as urinary T3 excretion rate were also reduced. Since both serum total and free T4 concentrations were normal, the supply of T4 to peripheral tissues would be sufficient to keep this patient in a euthyroid state in spite of the anti-T3 antibody.

Chemical Precipitation↗

PubMed1985

Renin and angiotensins in cultured mouse adrenocortical tumour cells.

Mouse adrenal tissue has been reported to contain high renin activity. However, it is not clear whether the renin is produced inside the tissue or is derived from a blood-borne component. We have investigated a cloned cell line of mouse adrenocortical tumour (Y-1) which has a steroidogenic activity. Sizable quantities of renin were demonstrated, predominantly in the cell lysate. This renin activity was distinguished from cathepsin D in view of its specific affinity to anti-renin antibody, optimal pH was determined, and the substrate specificity was checked with haemoglobin. Immunoreactive angiotensins were also detectable, but were demonstrated both in the cell and in the culture medium. This study provides further evidence for the existence of renin intrinsic to the adrenal gland. This study also suggests an intracellular role for renin and possible secretion of generated angiotensins.

Adrenal Cortex Neoplasms↗

PubMed1985

Plasma growth hormone (GH) and somatomedin C response to continuous growth hormone-releasing factor (GRF) infusion in patients with GH deficiency.

Pituitary growth hormone (GH) responses during a 10-h iv infusion of saline or human GH-releasing factor (hGRF-44) at 500 ng/kg/h, followed by an iv bolus injection of hGRF-44 at 2 micrograms/kg body weight, were studied in 10 patients with GH deficiency. During saline infusion in 4 patients, small plasma GH increase were observed in 2 patients. However, during hGRF infusion in 6 patients, up to 4 or 13 pulses of GH secretion were observed. The mean integrated GH pulse area during hGRF infusion was 22.5 +/- 5.2 (SE) ng/ml X h, which was greater than that obtained during saline infusion. Plasma somatomedin C levels did not increase after hGRF infusion. After saline or hGRF infusion all patients responded to an iv bolus injection of the peptide. These results indicate that hGRF infusion augments GH secretion by increasing the number and amplitude of GH pulses and that the infusion does not cause pituitary somatotrophs to lose their capacity to respond to hGRF subsequently.

Adolescent↗

PubMed1985

Changes in computed tomographic findings in microprolactinomas before and after bromocriptine.

Computed tomography (CT) of the pituitary before and after bromocriptine treatment were performed in 10 patients with microprolactinoma. Intrapituitary low densities were demonstrated in 7 out of the 10 patients before bromocriptine. Low densities shrank in size and increased in density after normalization of the plasma prolactin (Prl) level following bromocriptine. At the same time, various degrees of empty sella were demonstrated in these patients and in 2 out of the 3 without noticeable changes before treatment. It was concluded that enhanced CT scans, especially sagittal reconstruction images, were very informative for the diagnosis of microprolactinoma and that bromocriptine reduced the size of the microprolactinoma and often led to empty sella.

Adult↗