Folia Endocrinologica Japonica

-Experiences at Hiroshima University School of Medicine-

Tohru UOZUMI

1995 Volume 71 Issue 7 Pages 1019-1036
Published: November 20, 1995
Released on J-STAGE: September 24, 2012

DOIhttps://doi.org/10.1507/endocrine1927.71.7_1019

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Hypothalamic-pituitary tumors are unique tumors which are present with various disorders of the cerebrum, cranial nerve, and endocrine system, and which critically ruin the patients' quality of life. However, during the past two decades, hypothalamic-pituitary tumor treatment has developed dramatically.
The curative method of the pituitary adenoma had not yet been introduced in the mid-1970s, but was accomplished several years after and spread rapidly through out the world. The main contributors which led to this development were the introduction of micro-neurosurgery (including transsphenoidal surgery), the development of new imaging modalities such as computed tomography (CT) and magnetic resonance imaging (MRI), and the introduction of newer, more effective medicine.
Other kinds of hypothalamic-pituitary tumor are also being cured by function-oriented surgery, drugs, and radiation therapy, which give the long-term useful life to patients. Regretably, there are some malignant tumors which still resist to any multidisciplinary remedy.
Efforts to prolong the useful lives of patients with malignant hypothalamic-pituitary tumors and also to improve the quality of life of patients with benign tumors should be continued. The most important point in managing hypothalamic pituitary tumors is to focus on “patient-oriented treatment” tailoring treatment to individual symptoms and needs.

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[title in Japanese]

1995 Volume 71 Issue 7 Pages 1037-1058
Published: November 20, 1995
Released on J-STAGE: September 24, 2012

DOIhttps://doi.org/10.1507/endocrine1927.71.7_1037

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Mechanism of Inhibition of Aldosterone Secretion by a Ca²⁺ Channel Blocker in Patients with Essential Hypertension and Patients with Primary Aldosteronism

Toyoharu YOKOYAMA, Kazuaki SHIMAMOTO, Osamu IIMURA

1995 Volume 71 Issue 7 Pages 1059-1074
Published: November 20, 1995
Released on J-STAGE: September 24, 2012

DOIhttps://doi.org/10.1507/endocrine1927.71.7_1059

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Three studies were conducted in order to investigate the suppressive effects of a calcium antagonist on aldosterone secretion and a possible mechanism. Study 1: A long-term (4 weeks) treatment with slow-release nifedipine (Nif), 40-60mg/day, was performed in 9 in-patients with essential hypertension (EHT). Mean arterial pressure (MAP), plasma renin activity (PRA), plasma angiotensin II levels (pAII) and plasma aldosterone concentration (PAC) were determined before and after Nif treatment. Study 2: In another 7 in-patients with EHT, Nif treatment (40-60mg, 7-10 days) was carried out to study its effect on aldosterone secretion in response to 2-hour ambulation, angiotensin II (AII) infusion (2.5ng/kg/min, for 1-hour) and ACTH injection (2.5mg i.v.). Study 3: The effects of Nif (40-60mg/day, for 7-10 days) on MAP, PAC, serum potassium, potassium clearance (Ck) and changes in PAC or plasma cortisol levels in response to ACTH injection (2.5mg i.v.) were studied in 6 in-patients with primary aldosteronism (PA).
In patients with EHT, MAP was reduced significantly at 1 week and 4 weeks after the administration of Nif. PRA and pAII increased significantly, though the increase of PAC was not significant. In the low-renin EHT group, PAC was reduced significantly (Study 1). The increase of PAC in response to 2-hour ambulation or AII infusion was inhibited by Nif, but no inhibition of aldosterone response to ACTH was observed (Study 2). In patients with PA, Nif lowered MAP, PAC, and Ck, and elevated serum potassium concentration significantly. On the other hand, Nif had no effect on the aldosterone or cortisol response to ACTH (Study 3).
These results indicated that the hypotensive effect of Nif is due in part to the inhibition of aldosterone secretion from the adrenal gland both in patients with EHT and in those with PA. Regarding the mechanism of the inhibition of aldosterone secretion by Nif, these data suggest that in patients with EHT, inhibition of the aldosterone response to AII is the most important factor, although it was not clear from this study whether Nif inhibits the potassium-induced aldosterone release or not. In patients with PA, ACTH-induced aldosterone secretion was not inhibited by Nif and the reduction of PAC is not likely via inhibition of AII action since the reninangiotensin system is markedly suppressed. Reduced cytosolic calcium concentration in the adenomatous tissue by Nif may have something to do with the lowered aldosterone synthesis in PA.

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The Significance of Platelet Alpha₂-Adrenoceptor and Sympathetic Nerve Activity in The Hypertensive Mechanism under Essential Hypertension

-With Special Reference to Pressor Response to Norepinephrine-

Niro SAWAI, Kazuaki SHIMAMOTO, Atushi MIYAMOTO, Hideyo OHSHIKA, Osamu ...

1995 Volume 71 Issue 7 Pages 1075-1088
Published: November 20, 1995
Released on J-STAGE: September 24, 2012

DOIhttps://doi.org/10.1507/endocrine1927.71.7_1075

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Although many studies have examined the metabolism of catecholamines and cardiovascular responsiveness to norepinephrine in essential and various experimental hypertension, the role of sympathetic nervous system in the pathogenesis of hypertension has not been elucidated. In this study, therefore, the role of sympathetic nerve activity related to platelet alpha₂-adrenoceptor was investigated to clarify the mechanism in which sympathetic nervous system augments the blood pressure elevation in patients with essential hypertension (EHT).
Tritiated yohimbine binding was used to estimate platelet membrane alpha2-adrenoceptor characteristics in 27 hospitalized patients with mild to moderate EHT and 27 normotensive subjects (NT) receiving a regular diet containing 120mEq/day of sodium and 75mEq/day of potassium.
In this study, mean arterial pressure (MAP) and plasma norepinephrine concentration (pNE) was significantly higher in EHT than those in NT. Total binding sites (Bmax) and dissociation constant (Kd) for ³H-yoshimbine in EHT was also significantly higher than those in NT.
There was a significant positive correlation between Bmax and age in NT, but not in EHT. A significant positive correlation was observed between the pressor response to infused norepinephrine (NE-R:increments in MAP induced by i.v. infused 0.2μg/kg/min of NE) and Bmax both in NT and EHT. On the other hand, no significant correlation was found between NE-R and Kd in NT and EHT. In addition, Bmax was correlated inversely with PNE in both NT and EHT.
These findings suggest that down-regulation mechanism exists in platelet alpha₂-adrenoceptor number responded to PNE levels. Moreover, the increased density of alpha-adrenoceptor might have something to do with the augmented NE-R in EHT, indicating an important pathophysiological role of this receptor in the hypertensive mechanisms in EHT.

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