It has been suggested that the mineralocorticoid action of glycyrrhizin is caused by a defect in the conversion of cortisol to cortisone through inhibition of the enzyme 11 beta-dehydrogenase (11 beta-DH). We investigated the functional significance of the inhibition of this enzyme as a mechanism of the mineralocorticoid action of glycyrrhizin. Eighteen healthy volunteers were divided into three groups of six and treated as follows: (1) 225 mg glycyrrhizin/day, (2) 0.1 mg 9 alpha-fluorocortisol (FC)/day and (3) 225 mg glycyrrhizin and 1.5 mg dexamethasone/day, all of which were given for 7 days. The administration of glycyrrhizin or FC induced a similar mineralocorticoid effect; specifically, suppression of plasma renin activity, hypokalaemia and kaliuresis. During the concomitant administration of glycyrrhizin and dexamethasone, however, these mineralocorticoid effects were significantly attenuated. During the administration of glycyrrhizin, urinary excretion of cortisol increased without change in the plasma levels of cortisol, while both plasma level and urinary excretion of cortisone decreased. Changes in cortisol metabolism were not observed during the administration of FC. These results demonstrated the functional significance of the inhibition of 11 beta-DH in the mineralocorticoid activity of glycyrrhizin in man.

SUMMARY The mechanism by which intracerebroventricularty administered aldosterone increases arterial pressure was investigated in trained, conscious dogs with cannulas chronically implanted in a lateral cerebral ventricle. In salt-replete and salt-depleted dogs, artificial cerebrospinal fluid with or without aldosterone (0.05 /ig/kg/hr) was infused intracerebroventricularly for 12 days by an osmotic minipump. A similar dose of aldosterone was infused subcutaneously for 12 days. Aldosterone infused intracerebroventricularly increased blood pressure significantly in both salt-replete and salt-depleted dogs. In salt-replete animals the hypertension was associated with increased total peripheral resistance without concomitant changes in blood volume, cardiac output, or in any of the neurohumoral parameters measured. We conclude that this type of hypertension is resistance-mediated from its outset and appears to be relatively independent of salt and water retention. The mechanism by which intracerebroventricularly administered aldosterone increases vascular resistance remains to be determined. (Hypertension 11: 750-753, 1988) KEY WORDS hemodynamics mineralocorticoid hypertension « centrally administered aldosterone H IGH affinity specific binding sites for mineralocorticoids have been described in various areas of the brain. 1 " 4 Quantitative autoradiography with intravenously injected [ 3 H]aldosterone has shown a wide distribution of specific binding sites in the brain, including the anterior hypothalamus, hippocampus, anterior pituitary, nucleus ventromedialis hypothalami, nucleus ambiguus, nucleus tractus solitarii, locus ceruleus, and area postrema.3 The functional importance of these binding sites was recently examined by Gomez-Sanchez in the rat.3 She found that a dose of aldosterone that was too small to produce changes in blood pressure when infused systemically produced elevations of blood pressure when infused into the lateral cerebral ventricle. The fact that the pressor effect could be blocked by the concomitant infusion of a specific aldosterone antagonist, prorenone, lent support to the concept that these mineralocorticoid binding sites in the brain are functional and that they could subserve a role in cardiovascular regulation.We have extended these observations by confirming

1. The effects of endothelin on systemic and renal haemodynamics and plasma concentrations of neuroendocrine hormones including plasma renin activity, aldosterone, adrenocorticotropic hormone, cortisol, catecholamines and arginine vasopressin were investigated in 18 conscious dogs. 2. Bolus injection of 4 pmol of endothelin/kg did not cause any significant changes in haemodynamics. Mean arterial pressure was elevated by both doses of 40 pmol/kg [91 +/- 2 to 99 +/- 2 mmHg (12.1 +/- 0.3 to 13.2 +/- 0.3 kPa), P less than 0.05] or 200 pmol/kg [93 +/- 2 to 107 +/- 3 mmHg (12.4 +/- 0.3 to 14.3 +/- 0.4 kPa), P less than 0.01], the latter dose increasing cardiac output (14%, P less than 0.05) and heart rate (9%, P less than 0.05), and the former reducing these parameters (14% and 8%, P less than 0.05, respectively). 3. In contrast with the various changes in systemic haemodynamics, renal blood flow transiently increased immediately after bolus injection in a dose-dependent manner (28%, P less than 0.05, 50%, P less than 0.01 and 110%, P less than 0.01 with 4, 40 and 200 pmol of endothelin/kg, respectively). This transient elevation of renal blood flow was followed by a gradual decrease (16%, P less than 0.05; 31%, P less than 0.01 and 36%, P less than 0.01) at 10 min. 4. All neurohormones were elevated in a dose-dependent manner.(ABSTRACT TRUNCATED AT 250 WORDS)

In recent years, remote sensing has been used to assessing water pollution distribution. In this study, water quality is analyzed using data collected by the Advanced Visible and Near Infrared Radiometer type-2 (AVNIR-2) of the Advanced Land Observing Satellite (ALOS) at various points in time. We carried out fuzzy regression analysis of the AVNIR-2 data and direct measurements of local water quality. The relationship between the water quality data and the AVNIR-2 data was analyzed by solving both the min and max problems. By comparing the maps of estimated water quality with actual distributions of water quality in the study area, we found that the method used in this study allows effective derivation of water quality conditions from AVNIR-2 data, which provides 10-m spatial resolution. Furthermore, by comparing the maps created using AVNIR-2 data collected at different times, we obtained results suggesting temporal changes in water quality. We also compared the results obtained using data collected by the optical sensor of the Landsat thematic mapper (TM) with 30-m resolution and those obtained using data collected by the active sensor of JERS-1 synthetic aperture radar (SAR), and examined the differences in classification results resulting from differences in resolution and sensors.

Plasma albumin leaks into urine as a result of glomerular hypertension and basement membrane injury, while urinary type IV collagen derives from mesangial matrix and glomerular basement membrane. The purpose of this study was to elucidate the pathophysiological significance of these urinary microproteins as an indicator of cardiovascular organ injuries in hypertension. In health-checkup participants without diabetes, proteinuria, or microhematuria, and who were not being treated for hypertension or any other disease at the time of enrollment, urinary albumin and type IV collagen were measured and their relations to organ injuries and cardiovascular risk factors were evaluated. Of 1,079 subjects (40-to 65-year-old; 256 men and 823 women) enrolled in the study, 120 (11.1 %) had untreated hypertension exceeding 140190 mmHg. Urinary albumin was positively correlated with both age (r=0.16, p<0.001) and systolic blood pressure (r=0.27, p<0.001). Urinary type IV collagen was not only positively correlated with age (r=0.12, p<0.001) and diastolic blood pressure (r=0.14, p<0.001) but also negatively correlated with blood hemoglobin (r=-0.12, p<0.001). Urinary albumin, but not type IV collagen, had a significant relation to electrocardiographic signs of left ventricular hypertrophy (p=0.012) and retinal arteriosclerosis on fundoscopy (p <0.001). Thus both albumin and type IV collagen would seem to have increased in association with age and hypertension in this cohort. It is suggested that urinary albumin is an indicator not only of renal injury, but also possibly of development of cardiac hypertrophy and arteriosclerotic changes. Urinary type IV collagen, on the other hand, may be associated with renal tissue injuries that affect erythrokinetics. (Hypertens Res 2000; 23: 459-466)