• The Journal of Korean Medicine
• /
• v.17 no.1 s.31
• /
• pp.37-46
• /
• 1996

The aim of this experiments was to investigate the effect of Lycii Fructus water extracts on the blood pressure, plasma renin activity and plasma levels of atrial natriuretic peptide in two-kidney one clip Goldblatt hypertensive rats. Systolic blood pressure was decreased significantly after administration of Lycii Fructus water extracts. Plasma levels of atrial natriuretic peptide was increased significantly after adminstration of Lycii Fructus water extracts. Plasma renin activity was not changed after adminstration of Lycii Fructus water extracts. Thease results suggested that the depressor response after adminstration of Lycii Fructus water extracts were related with the changes of the plasma levels of atrial natriuretic peptide.

• The Korean Journal of Physiology
• /
• v.28 no.2
• /
• pp.225-231
• /
• 1994

The present study was undertaken to investigate the role of endogenous nitric oxide in renin release under different physiological conditions. In the first series of experiments, renin release was either inhibited by acute volume-expansion (VE) or stimulated by clipping one renal artery in the rat. VE was induced by intravenous infusion of saline (0.9% NaCl) up to 5% of the body weight over 45 min under thiopental (50 mg/kg, IP) anesthesia. VE caused a decrease of plasma renin concentration (PRC). With $N^G-nitro-L-arginine$ methyl ester $(L-NAME,\;5\;{\mu}g/kg\;per\;min)$ superadded to VE, PRC decreased further. The magnitude of increase in plasma atrial natriuretic peptide levels following VE was not affected by the L-NAME. In two-kidney, one clip rats, L-NAME-supplementation resulted in a decrease, and L-arginine-supplementation an increase of PRC. Plasma atrial natriuretic peptide levels were significantly lower in the L-arginine group than in the control. Blood pressure did not differ among the L-NAME, L-arginine, and control groups. In another series of experiments, the renin response to a blockade of NO synthesis was examined using in vitro preparations from isolated renal cortex. L-NAME significantly increased basal renin release, although it was without effect on the isoproterenol-stimulated release. These findings suggest that endogenous nitric oxide significantly contributes to the renin release. Since many factors may affect the renin release in vivo, an interaction between NO and renin under various pathophysiological states is to be further defined.

• Journal of Acupuncture Research
• /
• v.21 no.4
• /
• pp.1-18
• /
• 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 Physiology
• /
• v.22 no.2
• /
• pp.319-332
• /
• 1988

The regulations of renal function and renin release are influenced by neural, humoral and physical factors. During the last decade, considerable progress has been made in the identification and characterization of these extrinsic renal control systems. Mechanisms intrinsic to the kidney are also important for renal function. These include the autoregulation of blood flow, and the local control of renin secretion. Fundamental questions regarding the mechanism of these intrinsic controls remain unanswered. Recently, endogenous renal adenosine has been claimed to influence the tubuloglomerular feedback control and renin release. Two subclasses of adenosine receptors $A_1{\;}and{\;}A_2$ have been described. The present experiment was carried out to evaluate the effects of $N_6-cyclohexyladenosine$ $(CHA,{\;}A_1{\;}selective)$ and 5'-N-ethylcarbox-amide adenosine $(NECA,{\;}A_2{\;}selective)$ on the renal function and renin release in the unanesthetized rabbit. Intra-renal arterial infusion of NECA $(0.3{\sim}10.0n{\;}mole/min/rabbit)$ or CHA $(0.03{\sim}10.0n{\;}mole/min/rabbit)$ caused a prompt and dose-dependent decrease in urine volume, glomerular filtration rate (GFR), renal plasma flow (RPF), filtration fraction (FF), electrolyte excretion and free water clearance $(CH_2O)$, the effect being much more profound with CHA than with NECA. The NECA infusion resulted in a profound decrease of systemic blood pressure, but the CHA infusion did not. Both NECA and GHA infusions caused a prompt and dose-dependent decrease in renin secretion rate, again the effect being greater with CHA than with NEGA. These results suggest that both $A_1{\;}and{\;}A_2$ adenosine receptors may be involved in the intrinsic control of renal function and renin release, and that the $A_1$ receptors plays a more important role than the $A_2$ receptor in the regulation of renal fnction.

• The Korean Journal of Physiology
• /
• v.19 no.2
• /
• pp.173-187
• /
• 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 and Pharmacology
• /
• v.1 no.2
• /
• pp.151-159
• /
• 1997

In an attempt to investigate whether hemorrhage affects the gene expression of the renin-angioteusin system (RAS) components in the brain and peripheral angiotensin-generating tissues, changes in mRNA levels of the RAS components in response to hemorrhage were measured in conscious unrestrained rats. Wistar rats were bled at a rate of 3 ml/kg/min for 5 min, and then decapitated 7 h after hemorrhage. Levels of mRNA for renin, angiotensinogen and angiotensin $II-AT_1$ receptor subtypes ($AT_{1A}$ and $AT_{1B}$) were determined with the methods of northern blot and reverse transcriptase-polymerase chain reaction (RT-PCR). Hemorrhage produced a profound hypotension with tachycardia, but blood pressure and heart rate recovered close to the basal level at 7 h. Plasma and renal renin levels were significantly increased at 7 h. Hemorrhage induced rapid upregulation of gene expression of both $AT_{1A}$ and $AT_{1B}$ receptor subtypes in the brainstem and hypothalamus, downregulation of them in the adrenal gland and liver. However, renin mRNA level increased in the brainstem, decreased in the liver, but was not changed in the hypothalamus, kidney and adrenals after hemorrhage. Angiotensinogen mRNA level was not significantly changed in any of the tissue except a slight increase in the liver. The kidney and liver did not show any significant change in gene expression of the RAS components. These results suggest that gene expression of the RAS in central and peripheral tissues are, at least in part, under independent control and the local RAS in each organ plays specific physiologic role.

• Childhood Kidney Diseases
• /
• v.28 no.2
• /
• pp.51-58
• /
• 2024

Patients with chronic kidney disease (CKD) bear a significant financial burden and face numerous complications and higher mortality rates. The progression of CKD is associated with glomerular injury caused by glomerular hyperfiltration and oxidative stress. Factors such as uncontrolled hypertension, elevated urine protein levels, anemia, and underlying glomerular disease, contribute to CKD progression. In addition to conservative treatment, several medications are available to combat the progression of CKD to end-stage kidney disease. Renin-angiotensin-aldosterone system blockers could slow the progression of CKD by reducing glomerular hyperfiltration, lowering blood pressure, and decreasing inflammation. Mineralocorticoid receptor antagonists inhibit the mineralocorticoid receptor signaling pathway, thereby attenuating inflammation and fibrosis. Sodium-glucose cotransporter 2 inhibitors exhibit protective effects on the kidneys and against cardiovascular events. Tolvaptan, a selective vasopressin V2-receptor antagonist, decelerates the rate of increase in total kidney volume and deterioration of kidney function in patients with rapidly progressive autosomal dominant polycystic kidney disease. The protective effects of AST-120 remain controversial. Due to a lack of evidence regarding the efficacy and safety of these medications in children, it is imperative to weigh the benefits and adverse effects carefully. Further research is essential to establish the efficacy and safety profiles in pediatric populations.

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.25 no.1
• /
• pp.39-45
• /
• 1996

The study was performed to investigate the effects of administration of aluminum compound in Kidney metabolism and plasma hormone of rats. Seventy frve male Sprague-Dawley strains rats were divided into five groups consisting of the control, 250ppm AlCl$_3$group, 500ppm AlCl$_3$ group, 250ppm $Al_2$(SO$_4$)$_3$group, 500ppm $Al_2$(SO$_4$)$_3$group and kept on the diet for 2 weeks. The body weight gain was increased by the administration of AlCl$_3$ but decreased by the administration of $Al_2$(SO$_4$)$_3$as compared to the control. The urinary excretion of sodium and creatinine were increased and free water clearance and urine volume were decreased significantly after AlCl$_3$adminstration group as compared to the control. The water balance, free water clearance, excretion of sodium and creatinine were increased and the excretion of chlorine was decreased after $Al_2$(SO$_4$)$_3$ administration as compared to the control. Plasma renin activity was increased and plasma aldosterone content was compared to the control. Plasma renin activity was increased and plasma aldosterone content was significantly decreased after adminstration of aluminum compounds as compared to the control.

• The Korean Journal of Physiology and Pharmacology
• /
• v.6 no.2
• /
• pp.127-130
• /
• 2002

The present study was aimed to investigate whether the adriamycin-induced nephrosis is associated with an altered regulation of local renin-angiotensin system (RAS) in the kidney. Rats were subjected to a single injection of adriamycin (2 mg/kg body weight, IV) and kept for 6 weeks to allow the development of nephrosis. They were then divided into two groups, and supplied with and without cilazapril, an angiotensin converting enzyme (ACE) inhibitor, in drinking water (100 mg/l) for additional 6 weeks. Another group without adriamycin-treatment served as control. The mRNA expression of renin, ACE, type 1 and type 2 angiotensin II receptors (AT1R, AT2R), and transforming growth factor $(TGF)-{\beta}1$ was determined in the cortex of the kidney by reverse transcription-polymerase chain reaction. Adriamycin treatment resulted in heavy proteinuria. Accordingly, the mRNA expression of renin, ACE, and AT1R was increased in the renal cortex, while that of AT2R was decreased. Co-treatment with cilazapril attenuated the degree of proteinuria. While not affecting the altered expression of renin, cilazapril decreased the expression of ACE to the control level. Cilazapril further increased the expression of AT1R, while it restored the decreased expression of AT2R. The expression of $(TGF)-{\beta}1$ was increased by the treatment with adriamycin, which was abolished by cilazapril. An altered expression of local RAS components may be causally related with the development of adriamycin-induced nephrosis, in which AT1R is for and AT2R is against the development of nephrosis.

• The Korean Journal of Physiology
• /
• v.23 no.1
• /
• pp.51-66
• /
• 1989

Mammalian cardiocytes secrete atrial natriuretic peptides (ANPs) into plasma, which cause marked natriuresis, diuresis, vasorelaxation and inhibition of hormone secretions. Aging influences the ability of the kidney both to conserve and to excrete sodium; i.e., in old animals, the excretory capacity of sodium is reduced and the time required to excrete sodium load is prolonged. Therefore, it is possible that animals differing in ages may respond differently to ANP. In the present study, we determined whether the renal, hormonal and vascular effects of ANP may be influenced by aging in conscious rabbits. The plasma renin concentration decreased with aging but plasma ANP concentration was significantly lower only in 24-month-old rabbits. Plasma aldosterone concentration and atrial ANP content did not change by aging. In 1-month-old rabbits, ANP (atriopeptin III, 3 ug/kg) administered intravenously caused hypotension and decreased in plasma renin and aldosterone concentrations, but did not cause diuresis and natriuresis. In 2 to 5 month-old rabbits, ANP caused hypotension, decreases in Plasma renin and aldosterone concentrations and marked renal effects. However, in 24-month-old rabbits, all the above effects of ANP was blunted. With hydration of physiological saline at a rate of 15 ml/kg/h for 2hr, urine volume and glomerular filtration rate did not change but the electrolyte excretion as well as fractional excretion of sodium significantly increased. The plasma concentrations of active renin and aldosterone were decreased but plasma inactive renin and ANP concentrations were increased. The changes in renal function and plasma level of hormone showed no differences in different ages. These results suggest that the peripheral vascular receptors to ANP may develop earlier than those in the kidney, and the attenuated vascular and renal responses to ANP in the old age may be due to age-related modifications in renal function and blood vessel.