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Biomedical subjects

O Murakami

Publications and source records attributed to O Murakami.

At least 91 records · Page 5Linked to original sources
PubMed1990

[A case of glucocorticoid-responsive hyperaldosteronism: follow-up study for 21 years--comparison with cases of 17 alpha-hydroxylase deficiency in Japan].

A study of the pathophysiology in our previously reported case of glucocorticoid-responsive hyperaldosteronism (Case E.H., 17 yrs old, female; JCEM, 28: 1807, 1968), who had undergone a long-term successful treatment for 21 yrs of daily 0.5 mg dexamethasone (Dex), suggested again that the patient had 17 alpha-hydroxylase deficiency (17-OH-D) in the adrenal with minimum enzyme deficiency in the ovary. When Case E.H. was injected with zinc-ACTH for 3 days with daily 0.5 mg Dex administration, plasma levels of 17-deoxy-steroids were moderately or dramatically increased, but those of 17 alpha-hydroxy-steroids (17-OH-steroids) responded poorly or not at all. Plasma level of estradiol and urine estrogens were found to be normal in repeated measurements. Plasma basal levels of LH and FSH were normal, and their responses to LH-RH were high normal or slightly exaggerated. Her menstruation was almost regular, and the basal body temperature was at least biphasic with daily 0.5 mg Dex treatment. However, she did not become pregnant during the 17 yrs of her married life. Then, we surveyed 31 Japanese cases of 17-OH-D with suppressed plasma renin activity (PRA) to ascertain whether similar patients to our case, 17-OH-D with suppressed PRA and with hyperaldosteronism, has been reported or not. In this survey work, 9 such cases were found to have high plasma aldosterone (Ald) concentration (PAC) (group I). The other 21 cases had normal or low normal PAC, and the one remaining case had low urine Ald (group II). 17-Deoxy-steroids such as corticosterone, 11-deoxycorticosterone and progesterone, which were elevated in this disorder, were added to control plasma, and PAC was measured with Dainabot's "ALDOSTERONE.RIAKIT" used for the measurement of PAC in all group I patients. With the total of large amounts of 600 ng of these 17-deoxy-steroids (200 ng for each), however, the incremental PAC value was much less than the lowest PAC value in patients of group I. PAC of one group I patient was measured directly by "ALDOSTERONE.RIAKIT" and also by RIA after extraction and purification procedure using LH-20 column chromatography. The PAC values obtained by both methods were high and the same (285 pg/ml). In 5 out of 22 group II patients, PAC was also measured with the same RIA kit "ALDOSTERONE.RIAKIT" mentioned above, and yet it was low or low normal.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1990

Release of neuropeptide Y from pheochromocytomas.

To investigate the release of neuropeptide Y (NPY) from the pheochromocytomas, we studied the relationship between the plasma and tumor tissue immunoreactive (IR) NPY concentrations in 13 patients with pheochromocytoma and measured the IR-NPY concentration in plasma samples obtained by catheter from several veins (jugular veins, superior vena cava, renal veins, adrenal veins and inferior vena cava) in 2 patients with pheochromocytoma. The plasma IR-NPY concentration in 13 patients with pheochromocytoma ranged from 118 to 1460 pg/ml and the concentration in 10 of 13 patients with pheochromocytoma was above 290 pg/ml (the upper limit of normal range). The tumor tissue IR-NPY ranged from 0.025 to 95.3 micrograms/g wet tissue. Plasma IR-NPY was parallel with tumor tissue IR-NPY in 13 cases of pheochromocytoma (r = 0.76, P less than 0.01). The highest concentration of IR-NPY was found in plasma obtained from the drainage vein from a tumor among the plasma samples obtained from several veins in 2 cases of pheochromocytoma. These findings indicate that in patients with pheochromocytoma, NPY is in most cases excessively released from the tumors into the systemic circulation and plasma IR-NPY in the periphery is increased.

Adrenal Gland Neoplasms↗
PubMed1990

Failure to visualize bilateral adrenal glands in a patient with primary aldosteronism.

Failure to visualize either adrenal gland by adrenal imaging was experienced in a patient with biochemical evidence of primary aldosteronism. Visualization of the adrenal glands was not possible after the administration of ACTH-Z (1 mg/day) for 3 days. The administration of ACTH and dexamethasone elicited an increase in blood pressure. Although the reason for this failure to visualize the adrenal glands by scanning and for the rise in blood pressure brought on by ACTH and dexamethasone remain unclear, we think that the case herein reported is a rare type of primary aldosteronism.

Adosterol↗
PubMed1989

Plasma aldosterone level in a female case of pseudohyperaldosteronism (Liddle's syndrome).

A 22-yr-old female suffering from hypertension, hypokalemic alkalosis and suppressed plasma renin activity was studied. The plasma aldosterone concentration (PAC) ranged between subnormal and normal levels while the other adrenal mineralocorticoids were normal. Examinations through computed tomography and ultrasonography showed no abnormal findings. For differential diagnosis, dexamethasone, spironolactone and triamterene were administered. Triamterene alone corrected the abnormalities in this case, and the therapeutic effect was further enhanced by sodium restriction. Therefore, the present case is strongly suggested to be one of Liddle's syndrome, which is characterized by a primary defect in renal tubular sodium handling and can be corrected with triamterene. However, the patient in our study is different from the first reported case in which aldosterone secretion was estimated to be low. Analysis of the changes in PAC has shown that PAC is parallel with the level of plasma progesterone in accordance with the rhythm of the menstrual cycle and, in the follicular phase, PAC is rather low. It is concluded that the patient was suffering from Liddle's syndrome, and it is assumed that PAC is not always subnormal and, as same as in normal females, PAC may change in accordance with the rhythm of the menstrual cycle in a female case of Liddle's syndrome.

Adult↗
PubMed1989

Corticotropin-releasing hormone in the human hypothalamus. Free-floating immunostaining method.

We have clearly demonstrated corticotropin-releasing hormone (CRH) immunoreactive cell bodies and nerve fibers in the human hypothalamus by immunocytochemistry using free-floating sections instead of paraffin-embedded sections. Human hypothalami were obtained at autopsy, fixed and cryostat-sectioned at 40 microns. Free-floating sections were immunostained with antibody to CRH using the Vector ABC system. Most of CRH immunoreactive nerve fibers from the paraventricular nucleus pass under the fornix, while some CRH immunoreactive nerve fibers pass beyond the fornix and some through the fornix. Then the CRH immunoreactive nerve fibers run downward, medially to the supraoptic nucleus and toward the pituitary stalk. This method of immunocytochemistry is a very sensitive and suitable means for immunocytochemical studies of neuropeptides in the human brain.

Aged↗
PubMed1989

Calcitonin gene-related peptide in the human hypothalamus.

Calcitonin gene-related peptide (CGRP)-like immunoreactivity (LI) in the human hypothalamus was investigated by radioimmunoassay and by immunocytochemistry. CGRP-LI was detected from two hypothalami obtained at autopsy (2.1 and 7.0 ng/g wet tissue) by radioimmunoassay. Reverse phase high performance liquid chromatography revealed that most of the CGRP-LI in the human hypothalamus was eluted in an identical position with synthetic human CGRP. For immunocytochemistry, human hypothalami obtained at autopsy were fixed and cryostat-sectioned at 40 microns. Free floating sections were immunostained with antibody to CGRP. CGRP-immunoreactive cell bodies were found in the supraoptic nucleus, paraventricular nucleus and infundibular nucleus. These findings indicate that CGRP exists in the cell bodies of the supraoptic nucleus, paraventricular nucleus and infundibular nucleus in the human hypothalamus and CGRP may play some roles in the endocrine and other functions of the human hypothalamus.

Aged↗
PubMed1989

Neuropeptide Y and blood pressure in haemodialysis patients.

To investigate the relationship between plasma neuropeptide Y (NPY) concentrations and blood pressure in haemodialysis (HD), we measured plasma immunoreactive neuropeptide Y (IR-NPY) concentrations and blood pressure before and after HD in 71 patients undergoing maintenance HD. Plasma IR-NPY concentrations were measured by radioimmunoassay after extraction with Sep-Pak C18 cartridges. We corrected the plasma IR-NPY values after HD by reference to the ratio of the plasma total protein levels before HD to the levels after HD, in order to exclude the influence of the haemoconcentration caused by HD. Plasma IR-NPY concentrations before and after HD in 71 patients undergoing maintenance HD were 413 +/- 94 pg/ml and 340 +/- 90 pg/ml (mean +/- SD), respectively. Plasma IR-NPY concentrations before HD in 28 hypertensive patients with HD (398 +/- 91 pg/ml) were not significantly different from those in 40 normotensive (427 +/- 98 pg/ml) and 3 hypotensive (372 +/- 21 pg/ml) patients with HD (P greater than 0.1). Plasma IR-NPY concentrations after HD in 9 patients whose systolic blood pressure fell more than 30 mmHg during HD (409 +/- 52 pg/ml) were significantly higher than those in the other patients (P less than 0.025). These findings suggest that the release of NPY is increased when the blood pressure falls during HD in patients undergoing maintenance HD.

Blood Pressure↗
PubMed1989

Neuropeptide Y- and somatostatin-like immunoreactivities in ganglioneuroma, ganglioneuroblastoma and neuroblastoma.

Neuropeptide Y (NPY)- and somatostatin (SS)-like immunoreactivities (LI) were investigated in tumor tissues of one ganglioneuroma (GN), 3 ganglioneuroblastomas (GNB) and one neuroblastoma (NB) by radioimmunoassay. NPY-LI was detected from all 5 tumor tissues (16.4-1247 pmol/g wet tissue). Sephadex G-50 column chromatography and reverse phase high performance liquid chromatography (HPLC) revealed that most of the NPY-LI in tumor extracts was eluted in an identical position to synthetic human NPY except one GNB (case 2). In this case, most of the NPY-LI was eluted in a higher molecular weight region than synthetic human NPY in Sephadex G-50 column chromatography and in a more hydrophobic position in HPLC. SS-LI was detected from 4 tumor extracts except one GNB (case 2) (21.3-787 pmol/g wet tissue). Sephadex G-25 column chromatography and reverse phase HPLC revealed that SS-LI in tumor extracts was eluted just after the void volume and then in the same positions as SS-28 and SS-14. These results suggest that NPY, SS-14 and SS-28 exist in tumor tissues of GN, GNB and NB, and most of the NPY-LI in one GNB was a higher molecular and more hydrophobic form of NPY-LI.

Chromatography, Gel↗
PubMed1988

Altered circadian blood pressure rhythm in patients with Cushing's syndrome.

The circadian blood pressure rhythm was compared in patients with Cushing's syndrome, essential hypertension, and primary aldosteronism. In patients with essential hypertension or primary aldosteronism, a clear nocturnal fall in systolic and diastolic blood pressure and heart rate was observed. This fall was seen in untreated subjects as well as in patients receiving combined treatment with a calcium antagonist, diuretic, converting enzyme inhibitor, alpha-blocker and beta-blocker, or sympatholytic drug. In these groups, there was a positive correlation between heart rate and systolic or diastolic blood pressure. On the other hand, in patients with Cushing's syndrome, there was no nocturnal fall in blood pressure but in some patients a rise was observed. In all patients there was a nocturnal fall in heart rate. Thus, there was no significant correlation between heart rate and blood pressure in these patients. Exogenous glucocorticoid eliminated the normal nocturnal fall of blood pressure in patients with chronic glomerulonephritis or systemic lupus erythematosus. These results suggest that the changed circadian blood pressure pattern in patients with Cushing's syndrome is not due to antihypertensive treatment or to the mineralocorticoid excess accompanying this disease, but it is attributable to excess glucocorticoid or the associated disturbance in the adrenocorticotropic hormone-glucocorticoid system (or both). This conclusion also implies that the normal circadian rhythm of blood pressure may be regulated at least in part by the adrenocorticotropic hormone-glucocorticoid system.

Adolescent↗
PubMed1988

Peptide histidine methionine may be a prolactin-releasing hormone in humans.

Peptide histidine isoleucine (PHI) was initially isolated from the porcine gastrointestinal tract and may be present in the brain. It has been suggested that PHI may be PRL-releasing hormone (PRH) because of its potent PRL-releasing activity and its existence in hypophysial portal plasma in rats. Vasoactive intestinal peptide and PHI are coded by the same gene, and human PHI has a C-terminal methionine instead of isoleucine [peptide histidine methionine (PHM)]. To investigate the possibility that PHM is a physiological PRH in humans, we measured the immunoreactive PHM concentration in human hypothalamic tissue and cerebrospinal fluid (CSF) using a specific RIA. We also examined in vivo the PRH activity of synthetic PHM. The human hypothalamus contained 19.3 +/- 6.2 (+/- SD; n = 5) pmol/hypothalamus, very similar to the content of GHRH or CRH. Immunoreactive PHM was also present in CSF; its levels in CSF were significantly lower in patients with prolactinomas than in control subjects. The CSF PHM levels in such patients increased after correction of hyperprolactinemia by long term bromocriptine therapy. The CSF PHM levels also were low in pregnant women. There was a significant negative correlation between plasma PRL and CSF PHM levels in all of these subjects. Gel filtration profiles of CSF extracts from normal subjects revealed two peaks of immunoreactive PHM: a high mol wt peak and one at the elution position of synthetic PHM. This profile resembled that of hyppothalamic extract. In contrast, only high mol wt material was detected in CSF from hyperprolactinemic subjects. Intravenous administration of synthetic PHM elicited a significant increase in plasma PRL in normal subjects; the responses to PHM were higher in women than in men. The presence of large amounts of immunoreactive PHM in the human hypothalamus suggests that PHM may participate in the regulation of anterior pituitary hormone secretion. Its specific PRL-releasing activity in vivo and the low CSF PHM levels of hyperprolactinemic subjects suggest that PHM may be a physiological PRH in humans.

Aged↗
PubMed1987

Suppression by glucocorticoid of the immunoreactivity of corticotropin-releasing factor and vasopressin in the paraventricular nucleus of rat hypothalamus.

The effect of glucocorticoid on the production of corticotropin-releasing factor (CRF) and vasopressin in the paraventricular nucleus of the hypothalamus (PVH) was examined immunocytochemically. Intraperitoneal administration of dexamethasone sulfate in a dose of 0.1 mg/day suppressed the immunoreactivity of CRF and vasopressin in the medial parvocellular divisions of the PVH of the rat subsequent to bilateral adrenalectomy. In the magnocellular divisions, suppression of vasopressin-immunoreactivity was not observed. These results suggest that the vasopressin in the medial parvocellular divisions plays a distinct role from that in the magnocellular divisions, the former having functional significance in the hypothalamo-hypophysio-adrenal axis.

Adrenalectomy↗
PubMed1987

Increased plasma immunoreactive neuropeptide Y concentrations in phaeochromocytoma and chronic renal failure.

To investigate the clinical usefulness of radio-immunoassay of neuropeptide Y (NPY), we measured plasma immunoreactive neuropeptide Y (IR-NPY) concentrations in normal subjects (n = 21), essential hypertensive patients (n = 33), patients with phaeochromocytoma (n = 7), patients with chronic renal disease with serum creatinine levels of less than 1.9 mg/dl (n = 5) and patients with chronic renal failure whose serum creatinine levels were greater than or equal to 1.9 mg/dl (n = 18, eight without haemodialysis and 10 undergoing maintenance haemodialysis), by radio-immunoassay. Plasma IR-NPY concentrations in patients with phaeochromocytoma (577 +/- 256 pg/ml, mean +/- s.d.) were significantly higher (P less than 0.001) than those in normal subjects (151 +/- 28 pg/ml), essential hypertensive patients (177 +/- 49 pg/ml) and patients with chronic renal disease with serum creatinine levels less than 1.9 mg/dl (198 +/- 71 pg/ml). Plasma IR-NPY concentrations in patients with chronic renal failure (without haemodialysis: 330 +/- 63 pg/ml; undergoing maintenance haemodialysis: 374 +/- 80 pg/ml) were also high. These results suggest that NPY is useful as one of the tumour markers of phaeochromocytomas. However, this study revealed that patients with chronic renal failure, without phaeochromocytoma also have increased plasma IR-NPY concentrations.

Adrenal Gland Neoplasms↗
PubMed1987

Immunoreactive corticotropin-releasing hormone in human plasma during pregnancy, labor, and delivery.

We previously reported that immunoreactive corticotropin-releasing hormone (CRH) is present in human placenta and third trimester maternal plasma, and that such material is very similar to rat CRH and the predicted structure of human CRH. We suggested that maternal plasma immunoreactive CRH may be of placental origin. To further investigate this possibility, we measured plasma immunoreactive CRH in women during pregnancy, labor, and delivery and 1 and 2 h postpartum, and in nonpregnant women. Umbilical cord plasma and placental CRH concentrations were also measured. In the first trimester of pregnancy, the mean maternal plasma level was 5.9 +/- 1.0 pg (+/- SEM)/ml (n = 24), not significantly different from that in 10 nonpregnant women (5.8 +/- 0.8 pg/ml). Plasma CRH concentrations progressively increased during pregnancy (second trimester, 35.4 +/- 5.9 pg/ml (n = 39); early third trimester (28-34 weeks), 263 +/- 41 pg/ml (n = 14); late third trimester (35-40 weeks), 800 +/- 163 pg/ml (n = 20)]. There was a significant correlation between maternal plasma CRH levels and weeks of pregnancy. Plasma CRH concentrations were further elevated (2215 +/- 329 pg/ml; n = 9). During early labor, peaked at delivery (4409 +/- 591 pg/ml; n = 28), and declined rapidly after delivery [1 h postpartum, 1042 +/- (353 pg/ml (n = 13); 2 h postpartum, 346 +/- 91 pg/ml (n = 13)]. There was a significant correlation (r = 0.562; P less than 0.01) between matched maternal plasma and placental CRH concentrations. The mean umbilical cord plasma CRH level (50.6 +/- 6.1 pg/ml; n = 28) was much lower than that in the mother at the time of delivery. Umbilical venous plasma CRH levels were significantly greater than those in simultaneously obtained umbilical arterial plasma (70.8 +/- 11.3 and 41.8 +/- 4.9 pg/ml, respectively; n = 11). There was a significant correlation (r = 0.384; P less than 0.05) between maternal and fetal CRH concentrations. Gel filtration of plasma obtained from women during the third trimester, at delivery, and early postpartum and placental extracts revealed two major peaks of immunoreactive CRH: a high mol wt peak and one at the elution position of rat CRH. In contrast, only rat CRH-sized material was detected in plasma from nonpregnant women and umbilical cord plasma. Maternal plasma immunoreactive CRH-sized material stimulated ACTH release from anterior pituitary tissue in a dose-dependent manner and was equipotent with rat CRH.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1987

Immunoreactive corticotropin-releasing hormone present in human plasma may be derived from both hypothalamic and extrahypothalamic sources.

Immunoreactive CRH concentrations were determined in human plasma using an immunoaffinity chromatographic extraction procedure and sensitive RIA. Immunoreactive CRH was detectable in the plasma of all normal subjects (mean +/- SD, 6.2 +/- 2.4 pg/mL; n = 15). Basal (0800-1000 h) plasma immunoreactive CRH levels were significantly lower in patients with Cushing's syndrome due to adrenal (2.8 +/- 1.1 pg/mL; n = 4) or pituitary adenomas (2.9 +/- 0.8 pg/mL; n = 5), in patients with hypothalamic hypopituitarism (3.2 +/- 0.9 pg/mL; n = 5), and in glucocorticoid-treated patients (3.9 +/- 1.9 pg/mL, n = 8). Basal plasma CRH levels were also low in patients with acromegaly (2.8 +/- 0.8 pg/mL; n = 14) and insulin-treated diabetic patients whose pituitary-adrenal function was normal (3.6 +/- 1.0 pg/mL; n = 12). In normal subjects plasma CRH levels increased after insulin-induced hypoglycemia; this response was abolished by the prior administration of dexamethasone. In contrast, basal plasma CRH levels were not affected by prior administration of metyrapone or dexamethasone. No evidence for diurnal variation in plasma immunoreactive CRH was found in normal subjects. In addition, in normal subjects oral glucose administration elicited a significant increase in plasma CRH (basal, 7.3 +/- 0.9 pg/mL; peak 30 min after glucose, 16.7 +/- 5.8 pg/mL; n = 5; P less than 0.05) without concomitant changes in ACTH. Gel filtration of extracts of pooled plasma from normal subjects revealed a major component of immunoreactive CRH in the position of synthetic rat CRH. Immunoreactive CRH-sized material had the same retention time as authentic rat CRH in a reverse phase high pressure liquid chromatography system. The content of immunoreactive CRH in human placenta, pancreas, and adrenal gland was much larger than that in hypothalamus. These findings suggest that immunoreactive CRH is present in peripheral plasma; the increase in plasma immunoreactive CRH after insulin-induced hypoglycemia may reflect stimulation of hypothalamic CRH release; the increase in plasma immunoreactive CRH after glucose administration may reflect extrahypothalamic CRH release; and the lack of diurnal variation in plasma immunoreactive CRH together with the lack of suppression of CRH by dexamethasone suggest that basal plasma CRH is of extrahypothalamic origin.

Adolescent↗
PubMed1987

Distribution, plasma concentration, and in vivo prolactin-releasing activity of peptide histidine methionine in humans.

The distribution of immunoreactive peptide histidine methionine (PHM) in human tissues and its plasma concentrations were examined using a specific RIA and gel filtration chromatography. The effects of synthetic PHM on anterior pituitary hormone secretion also were studied. Immunoreactive PHM was found in all tissues studied; high concentrations were found in the gastrointestinal tract, lung, and parotid gland. Subsequent but smaller amounts of PHM were found in the hypothalamus, pituitary stalk, olfactory lobe, and cerebral cortex. The distribution of immunoreactive PHM in human tissues was very similar to that of vasoactive intestinal polypeptide (VIP), and PHM and VIP were in equimolar concentrations. Immunoreactive PHM was also detectable in plasma of normal subjects, and similar plasma concentrations were found in patients with prolactinomas. Molecular sieve chromatography of extracts of nonneural tissues and plasma extracts revealed only one peak, eluting in the position of synthetic PHM. Two peaks of immunoreactive PHM were found in brain tissue; one coeluted with synthetic PHM, and the other eluted in the high mol wt region. Bolus injections of synthetic PHM significantly increased plasma PRL levels in a dose-dependent manner. However, PHM did not alter plasma GH, TSH, ACTH, LH, or FSH levels. These results indicate that PHM is distributed widely in human tissues, and posttranslational processing of the VIP-PHM precursor molecule may be different in different tissues. The finding of equimolar distributions of PHM and VIP is consistent with the notion that these two peptides are synthesized from a common precursor. The presence of immunoreactive PHM in human hypothalamic and pituitary stalk tissue and its specific in vivo PRL-releasing activity suggest that PHM may play an important role in the regulation of PRL secretion.

Aged↗
PubMed1987

Potentiation of peptide histidine methionine (PHM) on corticotropin-releasing hormone (CRH) induced ACTH secretion in humans.

The effects of rat corticotropin-releasing hormone (CRH) and of synthetic peptide histidine methionine (PHM) on ACTH release were studied in vivo in humans. PHM alone did not alter the basal plasma ACTH or cortisol levels, but it strongly potentiated CRH-induced ACTH secretion. These results, together with our previous observation that PHM immunoreactivity is present in human hypothalamus and pituitary stalk, suggest that PHM may play a physiological role in the regulation of ACTH secretion in humans.

Adrenocorticotropic Hormone↗