• 대한핵의학회:학술대회논문집
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• 1976.06a
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• pp.73-73
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• 1976

• 대한핵의학회:학술대회논문집
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• 1979.05a
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• pp.8.1-8.1
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• 1979

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.6
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• pp.771-778
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• 1998

To investigate interaction of angiotensin converting enzyme (ACE) inhibitor with local tissue renin- angiotensin system (RAS), changes in gene expression of the RAS components in various tissues in response to chronic administration of an ACE inhibitor, enalapril, were examined in Sprague-Dawley male rats. Enalapril was administered in their drinking water $(3{\sim}4\;mg/day)$ over 8 wk. Plasma and renal ACE activity increased significantly after 4 and 8 wk of enalapril treatment. Renin levels of the plasma and kidney of the enalapril-treated rats markedly increased after 4 wk and decreased thereafter, but still remained significantly higher than those of control rats. Kidney mRNA levels of renin markedly increased after 4 and 8 wk of enalapril treatment, but those of angiotensinogen and ANG II-receptor subtypes, $AT_{1A}$ and $AT_{1B}$, did not change significantly. The liver expressed genes for renin, angiotensinogen and $AT_{1A}$ receptor subtype, but $AT_{1B}$ receptor subtype mRNA was not detectable by RT-PCR. None of mRNA for these RAS components in the liver changed significantly by enalapril treatment. The hypothalamus showed mRNA expressions of renin, angiotensinogen, $AT_{1A}$ and $AT_{1B}$ receptor subtypes. $AT_{1A}$ receptor subtype mRNA was more abundant than $AT_{1B}$ receptor subtype in the hypothalamus as shown in the kidney. However, gene expression of the RAS components remained unchanged during 8-wk treatment of enalapril. In the present study, chronic ACE inhibition increased plasma and renal levels of ACE and renin, but did not affect mRNA levels of other RAS components such as angiotensinogen, ANG II receptor subtypes in the kidney. Gene levels of the RAS components in the liver and hypothalamus were not altered by chronic treatment of enalapril. These results suggest the differential expression of the RAS components in response to enalapril, and localized action and some degree of tissue specificity of enalapril.

• Journal of the Korean Society of Food Science and Nutrition
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• v.30 no.6
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• pp.1272-1277
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• 2001

This study was designed to investigate the effects of Korean Gu-Gi-Ja tea on plasma hormone such as renin and aldosterone water in cadmium administered rats. The cadmium administered rats were given 50 ppm and 100 ppm of CdCl$_2$.2$H_2O$ disolved in the distilled water. Sixty male Sprague-Dawley rats weighing 100$\pm$10 g were divided into 6 groups according to body weight. The control group was fed standard diet without cadmium. The experimental groups, which were fed standard diet containing 50 ppm and 100 ppm cadmium and Gu-Gi-Ja tea group. The results of this study were as follows; food intake, body weight gain and kidney weight content in cadmium administered groups were lower than those in Gu-Gi-Ja tea group. The contents of cadmium in kidney of the rats were determined by using ICP (Inductively Coupled Plasma Spectrcphotometer). In kidney accumulation of Gu-Gi-Ja tea groups were lower than those in cadmium administered group. Plasma levels of renin activity was increased by Cadmium administration group, compared with Gu-Gi-Ja tea and cadmium administred group. Plasma levels of aldosterone activity was increased by cadmium administration group, compared with Gu-Gi-Ja tea and cadmium administred group. This results suggested that Gu-Gi-Ja tea has a lowering effects on the accumulation of cadmium in kidney and it is believed that the Gu-Gi-Ja tea has some protective effects to cadmium administered lenin and aldosterone hormone in rats, but the mechanism of these effects was obscure.

• The Korean Journal of Physiology
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• v.19 no.2
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• pp.173-187
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• 1985

Renal compensatory adaptation caused by ablation of a part of renal mass has long been known in the field of the compensatory renal hypertrophy or hyperplasia. Many reports were found on the chronic mechanisms on the compensatory renal hyperfunction after exclusion of the contralateral kidney. However the mechanism(s) of the acute compensatory hyperfunction after contralateral exclusion has not yet been clarified. In the present experiment, we have tried to prove the possibility of the involvement of the renin-angiotensin system and/or prostaglandin system in the control mechanism of the acute compensatory renal hyperfunction after contralateral kidney exclusion. There were found different responses of the renal hyperfunction by contralateral renal pedicle or ureteral occlusion. Contralateral renal pedicle or ureteral occlusion caused a sustained increases of the urinary volume, sodium and potassium excretion, while the magnitude of the changes was different quantitatively by the maneuvers. Blood collection affected on the acute compensatory renal responses after ureteral as well as renal pedicle occlusion. Plasma prostaglandin $E_2$ level was not changed by the contralateral renal pedicle or ureteral occlusion. Urinary excretion of Prostaglandin $E_2$, the indices of renal prostaglandin biosynthesis, was not changed by the contralateral renal pedicle occlusion, but increased without significance by the contralateral ureteral occlusion. Acute renal compensatory responses after contralateral renal pedicle occlusion were blocked by the pretreatment of indomethacin. Plasma renin activity increased after contralateral ureteral occlusion, but the pattern of the increases was the same as in the time-control group. Plasma renin activity after contralateral renal pedicle occlusion did not change by the time sequence. SQ 20,881, an angiotensin I converting enzyme inhibitor, blunted the contralateral renal responses after the renal pedicle occlusion. Bilateral renal denervation abolished the contralateral renal responses after the renal pedicle occlusion. The above data suggest that there is no direct evidence to support the involvement of the renin-angiotensin system and/or prostaglandin system for the acute compensatory renal hyperfunction after contralateral kidney exclusion, and that the functional changes of the intact kidney may be caused by a humoral substances, or other mechanisms by afferent renal nerve activity originating from the treated kidney.

• The Korean Journal of Physiology
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• v.25 no.1
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• pp.69-79
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• 1991

To evaluate the acute and chronic effects of potassium on aldosterone response to different amounts of sodium intake, two series of experiments were conducted. In the first series of experiments, when the plasma K level was increased acutely by KCI infusion $(20\;{\mu}g/kg/min\;for\;20 min)$, plasma aldosterone concentration increased in both low Na and high Na groups. However, the aldosterone response to K infusion was significantly greater in the low Na than in the high Na groups. In the second series of experiments, rats fed a high K diet chronically showed a significantly higher plasma K level than those fed a low K diet. However, plasma Na level was maintained relatively constant independent of the Na intake. Both the plasma renin activity (PRA) and aldosterone levels were inversely related to the Na intake. There was a highly positive correlation between aldosterone level and PRA over a wide range of sodium intakes. However, the slope of the correlation line was distinctly steeper in the K-repleted than in the K-depleted rats. The above results indicate that the adrenotropic action of acute K load was augmented in the presence of high plasma renin levels. However, when plasna K level was elevated chronically by a high-K diet, aldosterone secretion was markedly stimulated, although the plasma lenin levels were suppressed.

• Journal of Ginseng Research
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• v.18 no.2
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• pp.137-147
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• 1994

• The Korean Journal of Nuclear Medicine
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• v.13 no.1_2
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• pp.23-29
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• 1979

To evaluate the renin-angiotensin-aldosterone system in diabetes mellitus, basal plasma renin activity (PRA) and its response to intravenous furosemide were determined in 40 diabetic subjects. The diabetics were divided into 4 groups according to the pressence of nephropathy and/or hypertension. Uncomplicated diabetics (Group I) were taken as control group and the results of the ether groups were compared to this group. In diabetics with nephropathy alone (Group II), and with nephropathy and hypertension (Group III), basal PRA values were $0.63{\pm}0.59ng/ml/hr.,\;and\;0.79{\pm}0.62ng/ml/hr.,$ respectively, both significantly lower than control group. ($1.53{\pm}1.09ng/ml/hr.$). (p<0.05) In both of the above groups, the responses to intravenous furosemide tended to be blunted. On the other hand, in diabetics with hypertension only (Group IV), the basal and stimulated PRA were not significantly different from control. Above results suggests that nephropathy may be one of the factors which suppress renin activity in diabetes mellitus.

• Journal of Acupuncture Research
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• v.21 no.4
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• pp.1-18
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• 2004

Objective : This study was performed to investigate the effects of aqua-acupuncture of Jibaikjihwangtang in two-kidney one clip Goldblatt hypertensive rats and spontaneously hypertensive rats. Methods : we injected aqua-acupuncture solution into Shin-Soo ($BL_{23}$) which corresponds to human acupuncture point in two-kidney one clip Goldblatt hypertensive rats and spontaneously hypertensive rats. Systolic blood pressure, renin activity, aldosterone and atrial natriuretic peptide (ANP) plasma levels were tested. Results : Systolic blood pressure decreased significantly after aqua-acupuncture of jibaikjihwangtang. Acupuncture group in two-kidney one clip Goldblatt hyper-tensive rats had deference with control group. In plasma levels of atrial natriuretic peptide, acupuncture group of spontaneously hypertensive rats increased meaningfully but to two-kidney one clip Goldblatt hypertensive rats it was decreased meaningfully. In Serum Aldosterone density, the acupuncture group of spontaneously hypertensive rats had significant alteration than control group, but the acupuncture group of two-kidney one clip Goldblatt hypertensive rats had decreased alteration than control group. Conclusion : According to these results, after Aqua-Acupuncture of Jibaikjihwangtang blood pressure decreased significantly and data suggest that blood pressure reduction activity connected with renin activity reduction in renal hypertensive rat.

• The Korean Journal of Pharmacology
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• v.20 no.2
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• pp.1-6
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• 1984

It has been generally recognized that the secretion of aldosterone is mainly regulated by angiotensin II in animals and humans, however, potassium and ACTH are also proposed as other humoral factors involved in the aldosterone secretory process. Recently, stress, anesthesia, adrenergic stimulation, low sodium intake or water deprivation stimulate plasma renin activity, while high sodium intake and deoxycorticosteroid have been reported to cause suppression of renin activity in animals. It seems that overall response of aldosterone secretory mechanisms reflects complex interactions both intrarenal and extrarenal components. Furosemide has been widely used to investigate the control of renin secretion by the kidney, and the relationship between diuretics and the disposition of endogenous aldosterone were reported (Oh, 1984). The sequential with 10 min interval samples of plasma were collected following administration of furosemide(1 mg/kg), aspirin(10 mg/kg), respectively. And also similar experiment was performed in the propranolol (10 mg/kg) pretreated rabbits. The results were as follows : 1) The concentration of plasma aldosterone was average of $426.I{\sim}485.5pg/ml$ in normal rabbits. Plasma concentrations of aldosterone rised significantly after injection of furosemide during 50 min, and the rise of plasma aldosterone was blocked by the propranolol pretreatment 2) Significant fall in the plasma level of aldosterone after injection of aspirin was noted. This result indicates that the increased secretion of aldosterone induced by furosemide administration is mediated through ${\beta}-receptors$, and the possible role of prostaglandin is substantiated.