• 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
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• 제30권1호
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• pp.33-41
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• 1996

The present study was aimed to investigate the role of endothelium-derived nitric oxide (NO) in the control of renin release and to examine if NO is implicated in the development of two-kidney, one clip (2K1C) hypertension. Male Sprague-Dawley rats $(150{\sim}200\; g)$ were constricted at the left renal artery. They were then supplemented with $N^{G}-nitro-L-arginine\;methyl\;ester\;(L-NAME,\; 5mg/100\;mL)$ or with L-arginine hydrochloride (400 mg/100 mL) in the drinking water. The control group was supplied with normal tap water. The sham-clipped rats were operated as in 2K1C rats except for that no clip was made. The kidneys were taken to examine in vitro release of renin at days 7 and 14 following clipping the renal artery. Northern blot analysis was also done to assess the expression of renin gene in the kidney. In sham-clipped rats, L-NAME caused a sustained increase of the blood pressure, whereas L-arginine was without effect. Neither L-NAME nor L-arginine-supplementation significantly affected the development of hypertension in 2K1C rats. Plasma renin concentration (PRC) measured on day 28 did not significantly differ among the L-NAME, L-arginine and control groups either in 2K1C or in sham-clipped rats. Renin contents (RRC) in the clipped kidney were increased, while those in the contralateral kidney were decreased. The release of renin in vitro from cortical slices was also enhanced in the clipped kidney, whereas it was attenuated in the contralateral. Comparing the RRC and in vitro release, the latter was more rapidly decreased than the former in the contralateral kidney. The renin mRNA levels in the contralateral kidney were almost at their nadir at days 7 and 14 in 2K1C rats. It is suggested that NO does not affect the development of 2K1C hypertension in which the renin-angiotensin system has been activated. The data also confirm that RRC and renin gene expression are increased in the clipped kidney and suppressed in the contralateral kidney in 2K1C rats.

• The Korean Journal of Physiology
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• 제23권2호
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• pp.253-261
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• 1989

장기적으로 소금량을 다르게 섭취시킴에 따라서, 체내의 Na 대사에 관여하는 호르몬인 aldosterone, atrial natriuretic peptide (ANP) 및 renin 분비와 신장의 배설 반응에 나타나는 변화를 정상 혈압쥐 Wistar와 spontaneously hypertensive rat (SHR)에서 비교하고자 실험하였다. 생후 7주의 숫쥐인 Wistar와 SHR에게 저염과 고염 식이 (각각 2, 25 mmol Na/100 g diet)를 6주간 먹였다. 그 후 ether 마취하에서 대퇴 동맥과 정맥 및 방광에 관을 삽입한 후, restraining cage에 넣었다. 수술회복 후 안정시 뇨와 혈액을 채취한 후, 0.9% saline을 30분동안 체중의 3%되게 정맥주입(혈장량 증가)하고 뇨와 혈액을 채취하였다. 혈장의 호르몬을 방사면역법으로 측정하였다. Wistar와 SHR의 저염, 고염 식이군의 성장률에는 유의한 차이가 없었다. Wistar 저염과 고염군의 평균 동맥혈압은 각각 113과 110 mmHg로 차이가 없었으며, SHR의 동맥압은 141과 149mmHg로 고염군이 높았다. 저염식이군에서 혈장 aldosterone농도는 고염군보다 월등히 높았고, ANP 농도는 차이가 없었으며, renin은 고염군보다 낮았다. 혈장량 증가 이후 혈장 aldosterone은 모든 군에서 $30{\sim}40%$정도 감소하였고, renin은 $30{\sim}60%$정도 감소하였다. 혈장량 증가 이후 ANP는 증가하였는데 고염군에서의 증가도가 저염군에서보다 월등히 높았다. 혈장량 증가 이전의 Wistar군의 혈장 aldosterone과 renin의 대조치 값은 SHR보다 유의하게 높았고, ANP 농도는 차이가 없었다. 그러나 혈장량 증가 이후의 Wistar와 SHR의 aldosterone과 renin의 감소정도는 유의한 차이가 없었으나, ANP의 증가도는 Wistar가 SHR보다 높은 경향을 보였다. 호르몬들 중에서 혈장 aldosterone과 renin사이에는 양의 대수함수 관계가 있으며, 기울기는 고염군이 저염군보다 유의하게 높았다. 혈장량 증가 이후에 나타나는 뇨량과 소금 배설률의 증가 정도는 고염군과 저염군 사이에 차이가 없었다. 그러나 SHR이 Wistar보다 더 심한 이뇨와 Na 배설항진 반응을 보였다. 이상의 결과는 소금 섭취량에 따라서 aldosterone, ANP 및 renin의 분비 조절이 다르며, 정상 혈압과 고혈압쥐 사이에서도 차이가 있음을 시사해 주고 있다.

• 대한한의학회지
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• 제18권2호
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• pp.267-272
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• 1997

The aim of the present experiments was to investigate the effect of Yukmijihwangtang water extracts on the plasma renin activity and plasma levels of atrial natriuretic peptide and aldosterone in rats. The results of this study were as follows: 1. Plasma renin activity decreased significantly after the administration of Yukmijihwangtang water extracts 1.5ml/kg. 2. Plasma levels of atrial natriuretic peptide (ANP) decreased significantly after the administration of Yukmijihwangtang water extracts. 3. Plasma levels of aldosterone increased significantly after the administration of Yukmijihwangtang water extract.

• 대한한의학회지
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• 제18권1호
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• pp.449-455
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• 1997

The aim of the present experiments was to investigate the effect of Yukmijihwangtang water extracts on the plasma renin activity and plasma levels of atrial natriuretic peptide and aldosterone in rats. The results of this study were as follows: 1. Plasma renin activity decreased significantly after the administration of Yukmijihwangtang water extracts 1.5 ml/kg. 2. Plasma levels of atrial natriuretic peptide (ANP) decreased significantly after the administration of Yukmijihwangtang water extracts. 3. Plasma levels of aldosterone increased significantly after the administration of Yukmijihwangtang water extract.

• 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.

• The Korean Journal of Physiology and Pharmacology
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• 제2권6호
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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.

• 생명과학회지
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• 제18권2호
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• pp.187-192
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• 2008

본 연구는 수분 및 글리세를 섭취가 renin activity, 직장온도, 혈중 전해질 농도에 미치는 효과에 대하여 알아보기 위해 수분 섭취 그룹과 글리세롤 섭취 그룹으로 나누어 측정한 결과는 다음과 같다. renin activity의 경우, 안정시와 비교하여 운동 후 40분에 수분 섭취 그룹과 글리세를 섭취 그룹에서 유의한 증가를 보였다(p<0.01). Osmolality의 경우, 수분 섭취 그룹에서 차이를 보이지 않았으나, 글리세를 섭취그룹에서는 안정 시와 비교하여 운동 후 40분에 차이를 보였다(p<0.05). 직장온도의 경우, 수분 섭취 그룹과 글리세를 섭취 그룹 모두 운동 시간에 따라 점진적으로 증가하는 것을 볼 수 있었다. Na과 K의 경우, 수분 섭취 그룹에서 차이를 보이지 않았으나 글리세를 섭취 그룹에서 차이를 보였다(p<0.05). Ca과 Mg의 경우, 두 그룹 모두 그룹과 운동시기 간에 유의한 차이를 보이지 않았다.

• 대한핵의학회지
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• 제12권1호
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• pp.1-8
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• 1978

To find out a convenient and reliable method of. detecting low renin status, we employed intravenous furosemide injection as a stimulatory maneuver. The results thus obtained were compared with those from the postural stimuli and basal plasma renin activity (PRA) in relation to sodium excretion. Intravenous furosemide test was performed in 66 control subjects and 44 patients with essential hypertension. The results were as follow; 1) Mean PRA in control subjects rose from $2.5{\pm}1.95$ ng/ml/hr (basal) to $4.5{\pm}2.51,\;5.2{\pm}2.49\;and\;4.2{\pm}2.44$ ng/ml/hr at 1, 2 and 3hrs after IV injection. One-hour response is more convenient in clinical practice. 2) Postural stimuli by assuming an upright posture for 3 hrs gave rise to considerable increase in PRA ($4.0{\pm}2.92\;from\;2.4{\pm}1.85$), but we found it less convenient than stimulation with furosemide. 3) The increase in PRA was much less marked in patients with essential hypertension as a whole ($2.9{\pm}2.75$). Hyporesponsiveness to furosemide stimuli was found in 34.1%. Of these hypo responders, a third had a normal basal PRA, indicating the need for this kind stimulatory procedure. 4) Younger age group showed greater renin responsiveness than older age group after furosemide stimuli. Likewise mean age of low renin patients ($52.9{\pm}5.38$ years old) was significantly higher than that of high and normal renin patients ($44.1{\pm}13.78$ years old).

• The Korean Journal of Physiology and Pharmacology
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• 제1권1호
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• pp.45-53
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• 1997

In humans and many animal models with chronic progressive renal diseases, angiotensin-converting enzyme (ACE) inhibitor markedly attenuates the progression of nephropathy. Several studies have reported augmented gene expression and redistribution of renal renin in partial nephrectomized rats. Although precise mechanism(s) is not known, the renin-angiotensin system (RAS) may play an important role in the progression of renal diseases. Thus, this study was undertaken to examine the gene expression of renal renin, angiotensinogen, and $AT_1$ subtypes ($AT_{1A}$ and $AT_{1B}$) in rats with diabetic nephropathy, and the influences of lipopolysaccharide (LPS)-induced septicemia on the gene expression. Four weeks after streptozotocin (STZ) treatment (55 mg/kg, i.p.), rats were randomly divided into LPS-treated (1.6 mg/kg, i.p.) and control rats. At 6 hours after LPS treatment, the rats were killed and the kidney was removed from each rat. Northern blot and reverse transcription-polymerase chain reaction (RT-PCR)techniques were used to detect mRNA expression. STZ treatment markedly attenuated body weight gain and significantly increased blood glucose level. Renal renin content (RRC) was significantly decreased in the STZ-treated rats compared to that in control rats. The renal ACE activity between STZ-treated and control rats was not significantly different. Renal renin mRNA level was prominently increased, while angiotensinogen and $AT_{1A}$ mRNA levels were slightly decreased in STZ-treated rats compared to those in controls. $AT_1$B mRNA level did not differ in both groups. Acute LPS treatment did not show any significant changes of mRNA levels of intrarenal RAS components in both groups. These results suggest that intrarenal RAS components were differentially regulated in STZ-treated diabetic rats. Further studies are required to evaluate the relationship between intrarenal RAS and other vasomodulatory systems.