Nihon Naibunpi Gakkai zasshi最新文献

From reviewing the activity of the Japan Endocrine Society over the last 30 years, the author can point out that the overall number of researchers has increased, the relative ratio of researchers from internal medicine has increased, and the society has become oriented toward clinical research. Newly independent conferences and societies on several special endocrinological fields have evolved from the Society, which might have brought about the decrease in the relative ratio of researchers from these fields. One of the important characteristics of endocrinology is that it has developed on the basis of mutual understanding among different medical fields. Therefore, the Japan Endocrine Society should manage to convey the information from related fields to the members of the society in the annual conference and in its journal. Future, endocrinology would become a more clinically oriented bioscience, and it may include a part of immunology and neurology in addition to conventional endocrinology, in order to understand the physiological and pathological whole body reaction.

The Japan Endocrine Society as it ought to be is discussed. 1. Paradigms of endocrine research. The recent rapid progress of molecular biology brought about breakthroughs in endocrine research. The cloning of hormone cDNA, as well as their receptors, enables us to study the mechanisms of intracellular signal transduction in detail. Genomic DNA might be considered the basic structure of a signal transduction system (endocrine system). In other words, endocrine research at present is performed by a paradigm that reduces components of a system in its minimum elements-genomic DNAs. It might, however, be naive of endocrinologists to believe that they can completely understand the endocrine phenomena merely by analyzing the minimum elements of the system (DNA). It might be necessary to reconstruct the systems from minimum elements to the system of the whole body. 2. What the Japan Endocrine Society should be. The Japan Endocrine Society should be reorganized in order to meet with the rapid progress of science. The board of regents of the Japan Endocrine Society appointed a committee in 1993 to discuss the society as it ought to be. The board of regents has decided as follows. 1) The autumn meeting of the society will be abolished in 1998. 2) In place of the autumn meeting, meetings of related societies (such as the thyroid branch of the society and the neuroendocrine branch of the society) will be held in the autumn.

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), 40-60 mg/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 (40-60 mg, 7-10 days) was carried out to study its effect on aldosterone secretion in response to 2-hour ambulation, angiotensin II (AII) infusion (2.5 ng/kg/min, for 1-hour) and ACTH injection (2.5 mg i.v.). Study 3: The effects of Nif (40-60 mg/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 (2.5 mg 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 renin-angiotensin 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.

In order to continue the advances of basic endocrinology, further development of molecular endocrinology and neuroendocrinology is necessary. In molecular endocrinology, investigations of the action mechanisms of hormones in non-typical target tissues, such as those of estrogen in bone, in cholesterol metabolism and in the immune system, may yield lucrative results. In these studies, estrogen action by non-classical pathways should also be investigated. In the investigation of brain functions, the role of neuroendocrinology seems to be important since signal transduction pathways in both the nervous and endocrine systems are similar. For these further developments of basic endocrinology, creative investigations by young and impartial investigators should be particularly accelerated.

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 alpha 2-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 alpha 2-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 0.2 micrograms/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 alpha 2-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.