• The Korean Journal of Physiology
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• 제20권1호
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• pp.89-102
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• 1986

It has long been suggested that the change of renin-angiotensin system is responsible for the increased arterial blood pressure in the experimental hypertension. But the exact nature of the cause and maintenance of early and late Phase of renal hypertension is still controversial. Increased renin-angiotensin system has been suggested. To clarify the altered renin-angiotensin system in the early phase of two kidney one clip Goldblatt hypertension(2K1C GH), experiments were carried out in the rats of 3,7, and 14 days of 2K1C GH rats, sham-operated, and control rats. Responses of the plasma renin activity to the intravenous infusion of L-isoproterenol were dose-dependent. Responses of the plasma renin activity to the intravenous L-isoproterenol in 2K1C GH rats were not different from sham-operated control rats. Hypotensive responses of the 2K1C GH rats were not different from sham-operated rats. Suppression by intravenous infusion of angiotensin II of plasma renin activity showed a dose-dependent manner. Suppression by angiotensin ll of plasma renin activity was attenuated or abolished in the early phase of 2K1C GH rats. Intravenous infusion of arginine vasopressin(AVP) showed a dose-dependent suppression of plasma renin activity, Attenuated responses by AVP of plasma renin activity were noticed in the early phase of 2K1C GH rats. These results suggest that the altered renin-angiotensin system in the early phase of the two kidney one clip Goldblatt hypertension may be caused by failure of the short loop negative feedback control mechanism.

• The Korean Journal of Physiology
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• 제19권2호
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• pp.189-202
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• 1985

Enhanced activity of renin-angiotensin-aldosterone system has been suggested as a cause of the high blood pressure in certain forms of experimental hypertension. In spontaneously hypertensive rats, however, increased activity of the system has not been found, and even suppressed renin angiotensin system has been reported in the spontaneously hypertensive rat. In the present experiments it was attempted to explore the possible alteration of the short loop negative feedback control in the hypertensive rat. Experiments have been done in the anesthetized spontaneously hypertensive rats(SHR) as well as in normotensive Wistar and Sprague Dawley rats as control. Responses of the plasma renin activity to the intravenous L-isoproterenol were dose dependent, in both SHR and normotensive control rats. Hypotensive responses to smaller do sea of L-isoproterenol were more accentuated in SHR than in the normotensive control rats. Angiotensin If given intravenously suppressed plasma renin activity in a dose dependent fashion in both groups. However, these suppressive responses were significantly attenuated in SHR as compared with the normotensive control rats. Treatment with angiotensin I-converting enzyme inhibitor did not correct the attenuated responses of the plasma renin activity to angiotensin II in SHR. Intravenous infusion of arginine vasopressin also produced a dose-dependent suppression of plasma renin activity in both groups. The responses to arginine vasopressin were also significantly attenuated to the normotensive control rats. In the sodium-depleted SHR, arginine vasopressin did not suppress plasma renin activity, whereas the suppressive responses to arginine vasopressin in the normotensive control rats were not different from the untreated control rats. These data suggest that there may be a derangement in the short loop negative feedback control of the renin-angiotensin system in spontaneously hypertensive rat.

• The Korean Journal of Physiology
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• 제25권1호
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• pp.61-67
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• 1991

In order to determine possible relationships between the renin-angiotensin system and nephron heterogeneity, we compared the response of renin release and the angiotensin-converting enzyme (ACE) activity from different areas of the rat kidney. We used the renal cortical slices from the capsular surface to the juxtamedullary junction. Slices from outer one-third of the cortex were designated as outer cortical slices (OC), middle one-third as midcortical slices (MC), and inner one-third as inner cortical slices (IC). The renal renin content markedly decreased from OC and MC to IC. The basal lenin release was higher in OC than in MC or IC. On the contrary the percent change of renin release in response to L-isoproterenol was significantly higher in MC than in OC or IC. By TMB-8, the renin release in MC by $231{\pm}21%$ was higher than OC by $171{\pm}19%$ or IC by $$162{\pm}19. Angiotensin II suppressed renin release in OC and MC by $68{\pm}2,\;71{\pm}4%$ respectively, but only $40{\pm}7%$ in IC. The ACE activity was higher in IC than in OC, MC, medulla and papilla. The present data indicate that renin content and basal lenin release gradulally decreased from outer (OC) to inner (IC) cortex. The renin release in response to beta-adrenergic agonist, L-isoproterenol and intracellular calcium antagonist, TMB-8 were higher in MC than in OC and IC, but angiotensin II suppressed renin release less in IC than in OC and MC. It is suggested that juxtaglomerular cells of outer, mid-and inner cortices show a difference in renin release response to the stimuli.

• The Korean Journal of Physiology and Pharmacology
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• 제24권4호
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• pp.319-328
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• 2020

High fructose intake induces hyperglycemia and hypertension. However, the mechanism by which fructose induces metabolic syndrome is largely unknown. We hypothesized that high fructose intake induces activation of the renin-angiotensin system (RAS), resulting in hypertension and metabolic syndrome. We provided 11-week-old Sprague-Dawley rats with drinking water, with or without 20% fructose, for two weeks. We measured serum renin, angiotensin II (Ang II), and aldosterone (Aldo) using ELISA kits. The expression of RAS genes was determined by quantitative reverse transcription polymerase chain reaction. High fructose intake increased body weight and water retention, regardless of food intake or urine volume. After two weeks, fructose intake induced glucose intolerance and hypertension. High fructose intake increased serum renin, Ang II, triglyceride, and cholesterol levels, but not Aldo levels. High fructose intake increased the expression of angiotensinogen in the liver; angiotensin-converting enzyme in the lungs; and renin, angiotensin II type 1a receptor (AT1aR), and angiotensin II type 1b receptor (AT1bR) in the kidneys. However, expression of AT1aR and AT1bR in the adrenal glands did not increase in rats given fructose. Taken together, these results indicate that high fructose intake induces activation of RAS, resulting in hypertension and metabolic syndrome.

• 대한약리학회지
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• 제30권1호
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• pp.75-86
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• 1994

선천성 고혈압 흰쥐(SHR)와 정상혈압 흰쥐에서 교감신경성 신경전달에 미치는 부신수질 및 renin-angiotensin계의 역할을 알아보기 위해, 부신수질을 제거하거나 angiotensin 변환 효소 억제제를 장기간 처치한 뒤 중추신경계가 파괴된 상태에서 절전신경을 자극했을 때 나타나는 승압반응과 대동맥의 catecholamine농도 및 angiotensin 변환 효소 활성도의 변화를 비교 검토하였다. 부신수질을 제거하더라도 중추신경계를 파괴하기 전후의 혈압에는 영향을 주지 못했으며, 절전 신경 자극에 의한 승압반응은, 자극 주파수에 의존적으로 증가하였으며 prazosin 전처치로서 거의 완전히 억제되었다. 정상혈압 흰쥐에서와는 달리, 선천성 고혈압 흰쥐에서는 부신수질을 제거했을 때는 절전신경 자극에 의한 승압반응이 부신수질을 제거하지 않는 군(이하 대조군)에 비하여 유의하게 약화되었다. SHR에서 부신수질 제거로 부신 catecholamine 함량은 현저히 감소되었고, 혈청의 angiotensin 변환 효소 활성도는 감소되는 경향을 나타내었다. 그러나 혈장 및 대동맥 절편의 catecholamine 함량, 대동맥 절편의 angiotensin 변환 효소의 활성도는 대조군과 유의한 차이가 없었다. 그러나 WKY에서는 부신수질이 제거된 군에서 대동맥 절편의 angiotensin 변환 효소의 활성도와 catecholamine함량이 대조군에 비해 유의하게 증가되어 있었다. Enalapril처치에 의해서 선천성 고혈압 흰쥐 평균 혈압은, 부신 catecholamine 함량 및 대동맥 절편의 angiotensin 변화 효소의 활성도와 함께 현저히 저하되어 정상혈압 흰쥐와 유사하였다. 그리고 선천성 고혈압 흰쥐에서 부신수질의 제거로 절전신경 자극에 의한 승압반응이 대조군에 비하여 약화되는 현상은 enalapril을 처치하였을 때는 관찰되지 않았다. 이상의 결과로 미루어보아 교감신경성 신경전달을 항진시키는 부신수질의 작용은 renin-angiotensin계의 활성화에 의존적이었으며, 부신수질의 제거로 정상혈압 흰쥐에서는 renin-angiotensin계가 보상적인 조절이 일어났으나, 선천성 고혈압 흰쥐에서는 보상적인 조절이 일어나지 않았다.

• The Korean Journal of Physiology and Pharmacology
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• 제10권6호
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• pp.343-347
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• 2006

The present study was designed to investigate the effects renin-angiotensin-aldosterone system (RAAS), endothelin (ET) and local natriuretic peptide (NP) system for glomerulopathy induced in the experimental bilateral ureteral obstructive rats. Sprague-Dawley male rats ($200{\sim}220g$ body weight) were bilaterally obstructed by ligation of the proximal ureters for 24 hours. Control rats were treated in the same ways, except that no ligature was made. The glomeruli were isolated from cortex by graded sieve methods, and the mRNA expressions of local renin-angiotensin system (RAS), aldosterone synthase (CYP11B2), endothelin-1 (ET-1) and NP system were determined by real-time polymerase chain reaction. Following the bilateral ureteral obstruction, the mRNA expressions of renin, angiotensin converting enzyme 1 as well as ET-1 were increased, while that of angiotensin converting enzyme 2 was not changed. The expressions of CYP11B2 and angiotensin II receptors were not changed. C-type natriuretic peptide (CNP) expression was increased, while its receptors (natriuretic peptide receptor-B) were not changed. We suggest that the upregulation of local RAS and ET playa role in the progressive glomerular injury, and that the enhanced CNP activity also plays a compensatory role in obstructive uropathy in the glomerulus.

• The Korean Journal of Physiology
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• 제20권2호
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• pp.236-248
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• 1986

Alterations of renin-angiotensin system have been suggested as one of the mechanisms increasing arterial blood pressure in experimental and clinical hypertension. But the exact nature of high blood pressure in the early and late phase of renal hypertension is still controversial. To clarify the nature of renin release in both unclipped and clipped kidney of two kidney one clip Goldblatt lypertensive rat, experiments have been done in kidney slices, which were obtained from the rats of 3 and 7 days of operation. Basal rate of renin release was suppressed in unclipped kidney slices compared to clipped kidney Norepinephrine increased renin release from unclipped kidney slices, but not from clipped kidney slices. Suppressions by angiotensin Il and arginine vasopressin of renin release were attenuated in the clipped kidney slices compared to unclipped and sham-operated kidney slices. Increases by verapamil and trifluoperazine of renin release were attenuated in the clipped kidney slices compared to unclipped and sham-operated kidney slices. These results suggest that the negative feedback control mechanism of the renin-angiotensin system by angiotensin Il and arginine vasopressin is attenuated in the clipped kidney of two kidney one clip Goldblatt hypertensive rat, and that one of the altered mechanisms may be caused by certain regulatory changes of intracellular calcium and/or calcium-calmodulin complex in the juxtaglomerular cells.

• The Korean Journal of Physiology and Pharmacology
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• 제2권1호
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• pp.55-62
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• 1998

${\alpha},\;{\beta}-Adrenergics$, and calcium channels were known to be related to inducing cardiac hypertrophy. Recently, it was reported that the cardiac renin-angiotensin system (RAS) was an important factor in ventricular hypertrophy. The present study was aimed to investigate the effects of ${\alpha},\;{\beta}-adrenergic$, and calcium channel blockers that might be involved in the regulation of cardiac RAS. The reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the expression of renin gene in the perfused rat heart. Changes in angiotensin converting enzyme (ACE) activity and cyclic AMP (cAMP) content which were thought to play a role in inducing cardiac hypertrophy were measured in the perfused rat heart. The expression of renin gene was not only increased by isoproterenol with metoprolol-pretreatment but also increased by vasopressin treatment in the presence of calcium channel blocker, nifedipine or verapamil. Either prazosin alone or norepinephrine with prazosin-pretreatment significantly increased the ACE activity. However, isoproterenol with metoprolol-pretreatment significantly decreased the ACE activity. On the other hand, the ACE activity was not changed by vasopressin, nifedipine, or verapamil treatments. The content of cAMP was significantly increased by either isoproterenol or vasopressin treatment. According to these results, renin gene expression was associated with ${\beta}2$ - adrenoceptor and calcium channel. ACE activity was associated with ${\alpha}-\;and{\beta}2$ - adrenoceptor. In conclusion, ${\beta}2$ - adrenoceptor was important in cardiac renin gene expression and ACE activity and ${\alpha},\;{\beta}$ -adrenergic, and calcium channel blockers might be involved in the regulation of cardiac RAS in a complicated way.

• The Korean Journal of Physiology and Pharmacology
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• 제3권3호
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• pp.315-320
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• 1999

Molecular regulation of the renin-angiotensin system (RAS) was investigated in deoxycorticosterone acetate (DOCA)-salt hypertension. The expression of renin, angiotensinogen and angiotensin II receptor genes in the kidney and liver was determined by Northern blot analysis in rats which were made DOCA-salt hypertensive over the period of 2 or 4 weeks. Along with the hypertension, renin mRNA was decreased in the remnant kidney. The expression of angiotensinogen gene was not significantly altered in the kidney, but was significantly decreased in the liver. The expression of angiotensin II receptor gene was increased in the kidney, while it remained unaltered in the liver. The duration of hypertension did not affect the altered gene expression. It is suggested that the components of RAS are transcriptionally regulated in DOCA-salt hypertension in a tissue-specific manner.

• 대한핵의학회:학술대회논문집
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• 대한핵의학회 1973년도 제12차 학술대회
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• pp.62.2-62.2
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• 1973