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Kunihiko Hanew, Atsushi Utsumi, Akira Sugawara, Yasuyuki Shimizu and Kaoru Yoshinaga

Abstract.

The sources of TSH, which was excessively released by sulpiride (dopamine D2 receptor antagonist), were studied in 15 female patients with PRL-secreting adenoma (18-43 years). Sequential 3-day administration of sulpiride (100 mg, im) was given to 12 patients with prolactinoma and 6 normal female subjects (19-24 years). Patients with prolactinoma showed much greater TSH responses than normal subjects on the first day. However, TSH responses to sulpiride disappeared on the 2nd and 3rd day in both groups. In contrast, plasma PRL responses to the 1st sulpiride administration were smaller in patients with prolactinoma than in normal subjects, and the response disappeared following the 2nd administration in both groups. When TRH (500 μg, iv) was administered 120 min after the 3rd sulpiride injection, TSH and PRL increments were not different from those before the sulpiride injection in both patients with prolactinoma (N=6) and normal subjects (N=6) Further, combined administration of sulpiride and TRH in 5 patients with prolactinoma clearly enhanced the TSH and PRL responses compared with the single administration of each agent. These results suggest that there may be two readily releasable pituitary TSH and PRL pools, i.e. one dopamine-related and the other TRH-related, in patients with prolactinoma and normal female subjects.

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Kunihiko Hanew, Atsushi Sasaki, Toraichi Mouri and Kaoru Yoshinaga

Abstract.

The chronic effects of bromocriptine (CB-154) administration on pituitary somatotrophs and lactotrophs were investigated in 9 patients with acromegaly. Following therapy with CB-154 for 3 to 20 weeks, 6 of 9 cases showed a normalization of plasma GH (below 5 ng/ml) and a clinical improvement. These cases were termed 'CB-154-responders'. Plasma GH responses to TRH were observed in all cases of'CB-154-responders' before the therapy and were significantly suppressed during CB-154 therapy, although the response patterns expressed in logarithms were retained. When TRH was administered in 3 cases of acromegaly after acute administration of CB-154 and before chronic CB-154 therapy, the peak plasma GH responses were between those responses seen before and during CB-154 therapy. After iv infusion of arginine, 5 cases of 'CB-154-responders' showed an increase in plasma GH levels. These responses were also significantly suppressed during CB-154 therapy, while the response patterns were also preserved.

In these same patients, basal plasma prolactin was consistently suppressed to low levels (mean ± sem: 3.4 ± 0.9 ng/ml) in all 9 cases during CB-154 therapy and plasma prolactin responses to TRH almost disappeared after either acute or chronic administration of CB-154.

These findings demonstrate: 1) chronic CB-154 therapy in acromegalic patients gradually reduces the activity of the somatotrophs to synthesize and to release GH while it causes a rapid and marked suppression of lactotrophs; 2) the sites of action to CB-154 on the somatotrophs may be different from those to TRH and arginine (possibly GH-RF),while CB-154 and TRH appear to have a close relationship in regard to sites of action on the lactotrophs

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Makiko Yamamoto, Shintaro Saito, Toshiro Sakurada, Katsumi Yoshida, Kazuo Kaise, Nobuko Kaise and Kaoru Yoshinaga

ABSTRACT

The thiocyanate test was carried out in 18 patients with Hashimoto's disease. Thiocyanate was given orally several hours after the administration of tracer doses of 131I when the thyroid counts seemed to have reached a plateau. The per cent discharge of thiocyanate test was significantly higher in the groups with lower level of T4 (< 5.5 μg/100 ml), RSU (<25.5%) and BMR (<+2.5 %), and higher levels of TSH (> 10.0 μU/ml). A chi-square (ϰ2) test with Yates correction led to ϰ2 = 3.56 (1 df) with P=0.06 (per cent discharge vs T4, RSU, BMR and TSH). Then the per cent thiocyanate discharge was increased with the degree of hypothyroidism in patients with Hashimoto's disease. The correlation between the per cent discharge and 131I 24 h uptake was not significant. It was apparent that the iodide concentration mechanism was present even in the severe hypothyroid stage of Hashimoto's disease. This disproportion between the uptake of iodide and the iodide organification may result in the increase in unbound iodide. It is concluded that the hypothyroidism in Hashimoto's disease may not be caused by a defect in iodide organification, even if it correlated to the degree of hypothyroidism.

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Kazuhiro Iitake, Tokihisa Kimura, Kuniaki Matsui, Kozo Ota, Masaru Shoji, Minoru Inoue and Kaoru Yoshinaga

Abstract. Changes in plasma ADH levels and plasma aldosterone levels (PA) were studied in patients with end-stage renal disease (N = 40). The patients were divided into two groups according to their plasma renin activity (PRA) into a low renin (LR, n = 9) and a high renin group (HR, n = 31). The metabolic clearance rate (MCR) of plasma ADH was also investigated in 4 patients and 5 normal volunteers. Additionally, it was examined whether plasma ADH, aldosterone and renin were permeable through the dialysis membrane. Pre- and post-dialysis plasma ADH levels in LR were similar to those in the HR group. However, pre- and post-dialysis PA in the HR group were significantly greater than those in the LR group. Post-dialysis PRA was significantly increased in HR compared to pre-dialysis, but not in LR. Pre- and post-dialysis plasma osmolality was increased in both groups, but effective plasma osmolality (EPosm) was within the normal range. There was a significant correlation between EPosm and plasma ADH level both before and after haemodialysis, but the majority of the abnormally high values of ADH compared to the normal values was found within the normal range of EPosm. The patients exhibited high blood pressure and a rise in body weight, and haemodialysis caused a significant fall in body weight and blood pressure in both groups. MCR of ADH was significantly lower in the patients than that in normal subjects. Plasma ADH proved to be permeable through the dialysis membrane in all cases, but aldosterone in only a few cases. Renin was not permeable.

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Osamu Murakami, Kazuhiro Takahashi, Masahiko Sone, Kazuhito Totsune, Makoto Ohneda, Keiichi Itoi, Kaoru Yoshinaga and Toraichi Mouri

The presence of three regulatory peptides, corticotropin-releasing hormone, neuropeptide Y and endothelin-1, was studied by radioimmunoassay in the tumor tissue of an ACTH-secreting bronchial carcinoid. A 36-year-old female was admitted to hospital because of moon face, central obesity and hypertension. High levels of plasma ACTH and cortisol and urinary 17-OHCS and 17-KS were found. One mg dexamethasone did not suppress plasma ACTH and cortisol levels, but 8 mg did so slightly. Corticotropin-releasing hormone (100 μg. iv) stimulated plasma ACTH levels (0 min; 34.8 pmol/l; 30 min; 41.1 pmol/l). The computerized tomography showed the presence of a tumor in the right lung. This lung tumor was removed surgically and has been shown by microscopical examination to be a bronchial carcinoid with ACTH-positive cells. The tumor tissue concentrations of corticotropinreleasing hormone, neuropeptide Y and endothelin-1 were 3.34 pmol/g wet weight, 8.07 pmol/g wet weight and 0.92 pmol/g wet weight, respectively, although plasma concentrations of these three peptides were not elevated. Reverse phase high performance liquid chromatography showed that immunoreactive peptides in the tumor tissue were mainly eluted in the position of the standard peptides. These findings indicate that this case of ACTH-secreting bronchial carcinoid had high levels of corticotropin-releasing hormone, neuropeptide Y and endothelin-1 in its tumor tissue and suggested that these peptides may act locally, in a paracrine or autocrine manner, in the tumor.

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Kunihiko Hanew, Atsushi Utsumi, Akira Sugawara, Yasuyuki Shimizu, Satoru Tazawa and Kaoru Yoshinaga

Abstract.

The relation between pituitary magnetic resonance imaging (MRI) findings and anterior pituitary function was studied in 36 patients with classic idiopathic GH deficiency. These patients were divided into three groups based on MRI findings which were compared with those of 14 normal short children; i.e. normal stalk (N=6), narrowed stalk (N=20), and transected stalk (N=10). The transected and narrowed stalk groups showed significantly delayed TSH responses to TRH compared with the normal stalk group and with the normal short children. Further, the mean maximal TSH increment in the narrowed and transected stalk group was slightly greater than that in normal short children. In contrast, there were no differences in basal plasma GH and PRL levels and their responses to GHRH and TRH among the three groups. When the patients were divided into normal anterior pituitary and atrophic pituitary groups regardless of stalk changes or when they were divided into groups of stalk changes (narrowing and transection) with and without pituitary atrophy, no differences in GH, TSH and PRL dynamics between the groups were observed. These results indicate that pituitary thyrotrope functions, but not somatotrope and lactotrope functions, in patients with idiopathic GH deficiency are more closely correlated to stalk changes than to anterior pituitary changes observed on MRI.

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Kozo Ota, Tokihisa Kimura, Meiichi Ito, Minoru Inoue, Masaru Shoji, Susumu Shinoda, Michio Nagashima, Kuniaki Matsui, Kazuhiro Iitake and Kaoru Yoshinaga

Abstract. In order to study the effect of atrial tachycardia on the release of atrial natriuretic peptide (ANP), AVP, and methionine enkephalin (M-Enk), plasma concentrations of these peptides in the right ventricle were determined in patients with various arrhythmias (N = 10) during cardiac catheterization and incremental atrial pacing. Each pacing (100 per min, the maximum rate for 1:1 atrioventricular conduction, and 200 per min) lasted 4 to 5 min. Plasma ANP was significantly increased from 53.1 ± 12.2 in the resting condition to 168.9 ± 59.9 pmol/l at a pacing rate of 200 beats per min (P < 0.05); plasma AVP tended to decrease, but not significantly, and plasma M-Enk did not change at all. Pulse pressure in the right atrium (PPRA) and mean right atrial pressure (MRAP) tended to increase during the pacing, and at the rate of 200 beats per min PPRA was significantly higher than at the rate of 100 beats per min. Mean arterial blood pressure, plasma osmolality, and plasma sodium and potassium concentrations did not change significantly. There were significant correlations between plasma ANP and PPRA, MRAP and heart rate. These results indicate that atrial pacing stimulates ANP release with a rise in right atrial pressure, but does not influence M-Enk and AVP releases.

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Makiko Yamamoto, Kazuro Kaise, Hirofumi Kitaoka, Katsumi Yoshida, Nobuko Kaise, Hiroshi Fukazawa, Toshiro Sakurada, Shintaro Saito and Kaoru Yoshinaga

Abstract.

A 36 year old man with a diffuse goitre, signs of mild hypothyroidism, strikingly low levels of T4 (0.9 μg/dl) and T3 (24 ng/dl), elevated TSH (140 μU/ml) and elevated microsomal haemagglutination antibody (MCHA, 1:409 600), subsequently became non-goitrous and euthyroid with a decreased titre of antimicrosomal antibody without any medication. At the time of surgical biopsy, serum levels of T4 and T3 had risen to the normal range (4.6 μg/dl and 73 ng/dl, respectively), serum TSH had decreased to 30 μU/ml and the titre of MCHA to 1:25 600. Thyroid specimens showed Hashimoto's thyroiditis. The activity of thyroid peroxidase (TPO) was normal. The latest examination, 1 year and 3 months after initial evaluation, showed that the patient remained euthyroid with no goitre, that serum thyroid hormones were within the normal range (T4 7.7 μg/dl and T3 97 ng/dl), and that TSH was not detectable. The titre of MCHA decreased strikingly to 1:400.

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Kozo Ota, Tokihisa Kimura, Kuniaki Matsui, Kazuhiro Iitake, Masaru Shoji, Minoru Inoue, Kazutoshi Sato, Masahiro Ohta, Tadasu Yamamoto and Kaoru Yoshinaga

Abstract

To assess the central effect of hypertonic NaCl on the release of vasopressin (AVP) and methionine enkephalin-like substances into the blood and cerebrospinal fluid, and on blood pressure, ventriculocisternal perfusion (0.25 ml/min, 60 min) was performed in anesthetized dogs with artificial cerebrospinal fluid (CSF), either isotonic (300 mosmol/kg) or hypertonic (600 and 1200 mosmol/kg). The effect of central administration of a V1-AVP antagonist on the central osmotic challenge was also studied. In dogs, given 600 mosmol/kg, CSF osmolality increased with a concomitant rise in mean arterial pressure and plasma AVP concentrations. Plasma osmolality, heart rate, CSF AVP and plasma and CSF methionine enkephalin-like substances showed no significant change. In dogs, given 1200 mosmol/kg, the CSF osmolality increase was accompanied by a rise in mean arterial pressure, heart rate, plasma AVP and CSF AVP. Plasma osmolality and plasma and CSF methionine-enkephalinlike substances did not change significantly. A V1-AVP antagonist given centrally attenuated the rise in mean arterial pressure induced by osmotic challenge. In dogs, given 300 mosmol/kg, no parameters changed significantly except for a gradual fall in heart rate. These results suggest that central osmotic stimulation by hypertonic NaCl increases blood pressure, heart rate and the release of AVP, but not methionine enkepholin-like substances, into the blood and CSF, and a V1-blocker given centrally attenuates the pressor response.

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Kazutoshi Sato, Tokihisa Kimura, Kozo Ota, Masaru Shoji, Minoru Inoue, Masahiro Ohta, Tadasu Yamamoto, Takeharu Funyu, Kaoru Yoshinaga and Keishi Abe

To assess whether increases in circulating atrial natriuretic hormone (ANH) in response to the plasma volume expansion, besides the volume receptor-mediated mechanisms, attenuate the arginine vasopressin (AVP) response to increased plasma osmolality and whether changes in plasma AVP and ANH affect renal solute excretion under hypertonic plasma volume expansion, hypertonic saline (0.95 mol/l saline) alone, hypertonic saline with 6% dextran (6D-HS) and hypertonic saline with 9% dextran (9D-HS) were administered into anesthetized dogs. In the control study, 0.15 mol/l NaCI alone was administered. Plasma AVP and ANH and cardiovascular and renal functions were determined. Hypertonic saline and 9D-HS also were administered into the vagotomized and sham operated dogs, and the same parameters were determined. Mean blood pressure and heart rate never changed in all the groups, but central venous pressure and plasma volume increased markedly in 6D-HS and 9D-HS groups. In the control and hypertonic saline groups, central venous pressure increased slightly but plasma volume never changed. Plasma AVP increased in the order of hypertonic saline, 6D-HS and 9D-HS, but plasma ANH increased in reverse order. Vagotomy restored the AVP response to 9D-HS to 75% of its response to hypertonic saline, with a marked rise in plasma ANH. Urine sodium and potassium excretion and urine flow increased in hypertonic saline, 6D-HS and 9D-HS groups, but these increases were comparable among the groups. In the control group, these parameters never changed. These results suggest that the volume receptor-mediated vagal neural and ANH responses to the plasma volume expansion may have an effect on the suppression of the AVP response to osmotic stimuli, and increased plasma ANH release never potentiated the natriuresis under the hypertonic plasma volume expansion.