• Journal of Chest Surgery
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• v.26 no.2
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• pp.102-107
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• 1993

Human atria play an important role in extracellular homeostasis through release of atrial natriuretic peptide. To evaluate the relationship between plasma level of atrial natriuretic peptide (ANP) and many changes which can develop during extracorporeal circulation, we studied 16 patients undergoing, 12 cardiac operation and 4 thoracic operation. Plasma level of ANP in cardiac patients group was significantly higher and more changeable than thoracic patients group. After aortic cross clamp release, blood was filled at right atrium and right atrial pressure was rapidly increased. At the same time, plasma level of ANP was rised suddenly. Increase of ANP level was correlated (p<0.05) with the increase of total bypass time, but was not correlated statistical with aortic cross clamp time. ANP level did not fall rapidly after aortic cross clamp while both atria were completely empty. This result was explained by intraoperative hypothermia at that time, which can inactivate plasmal endopeptidase and catalytic receptors of ANP. The ANP level of atrial fibrillation group in cardiac patients were generally higher than normal sinus group, but there was no statistical correlation.

• The Korean Journal of Physiology
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• v.24 no.1
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• pp.115-121
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• 1990

The interaction between a calcium channel blocker nifedipine and atrial natriuretic peptide (ANP) was examined in normotensive and renal hypertensive rats. The infusion of either ANP or nifedipine produced a significant decrease in mean arterial pressure (MAP). The combined infusion of ANP with nifedipine resulted in a greater fall of MAP than did the infusion of each drug alone. ANP significantly increased urinary volume and excretion of sodium, while nifedipine was without effects. The diuretic/natriuretic effects of ANP were potentiated by the combined infusion with nifedipine. The vasodepressor and renal effects of ANP or nifedipine were qualitatively similar between the normotensive and hypertensive rats. Nifedipine caused an upward and leftward shift of the ANP dose-relaxation curve of the phenylephrine-precontracted thoracic aortic rings isolated from the normotensive rats , suggesting that the vasodilation sensitivity to ANP is increased in the presence of nifedipine. These results indicate that nifedipine enhances the vasodepressor effect of ANP, the likely mechanisms being attributable to a contraction of effective intravascular volume as a consequence of potentiated renal excretion and a greater peripheral vasodilation.

• The Korean Journal of Zoology
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• v.34 no.1
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• pp.8-19
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• 1991

Atrial natriuretic peptide(ANP)의 유리기전에 대한 특성을 알아보고자, 흰쥐의 적출심장 관류모형을 사용하여 연구한 바 다음과 같은 결과를 얻었다. 1. 심방을 확장시켰을 때 ANP의 유리는 촉진되었다. 그러나 과용량을 부하하면 확장기간보다 회복기간에 ANP의 유리가 현저하게 증가하였다. 2. Epinephrine과 phenylephrine을 주입하면 ANP의 유리 량이 증가했으나, isoproterenol을 주입하면 심박수와 우심방 내압이 현저하게 증가했는데도 ANP의 유리량은 오히려 감소하였다 3. 미주신경을 자극하면 심박수의 현저한 감소에도 불구하고 ANP의 유리량은 증가하였다. 이상과 같은 결과에서 볼 때 결론적으로, 심방의 용량부하에 의해 심방근의 신장수용체가 자극을 받아 ANP의 유리가 촉진되는 것은 분명하고, 심방근이 확장할 때 보다는 확장 후 다시 원래의 길이로 환원될 때 ANP가 유리될 것으로 사료된다. 그리고 ANP의 유리에 대한 adrenergic조절은 o-receptor가 관련되어 있으며 심박수와 심방내압이 ANP의 유리를 변화시키는 데는 반드시 필수적인 인자가 아닌 것으로 여겨진다. 또한 특히 미주신경의 자극으로도 ANP의 유리가 조절될 수 있다는 것이 본 연구를 통해 새로이 발견되었다.

• The Korean Journal of Physiology
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• v.24 no.1
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• pp.131-144
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• 1990

It is well known that the atrial natriuretic peptide (ANP) has a prepro-hormone of 151 amino-acids which loses their hydrophobic signal peptide to form 126 amino acid prohormone. The whole prohormone is released and then cleaved by proteases into more than one circulating forms. Recently, Winters et al. (1988a, b) reported that high concentrations of N-terminal fragments of prepro-ANP $(26{\sim}55),\;(56{\sim}92)\;and\;(104{\sim}123)$ were detected in human plasma. However, their physiological roles have not been established. The present study was conducted to determine whether the N-terminal fragments of pro-ANP have any effect on the renal function and to compare the effect with those of G-terminal fragments of pro-ANP The results indicate that intrarenal arterial infusions of prepro-ANP $(26{\sim}41),\;(26{\sim}55),\;(56{\sim}92)\;and\;(104{\sim}123)$ induced no significant changes in renal function. Whereas ${\alpha}-human$ ANP $(prepro-ANP,\;124{\sim}151)$ and pro-ANP caused a significant increase in urine volume, renal plasma flow, glomerular filtration rate, urinary excretions of sodium, chloride and potassium, and fractional excretion of sodium. These results suggest that the N-terminal fragments of pro-ANP are ineffective, while the C-terminal fragments retain the natriuretic and diuretic activities.

• Korean Journal of Veterinary Research
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• v.37 no.4
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• pp.735-744
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• 1997

심방근 세포는 심방이뇨호르몬을 합성, 저장 그리고 분비하며, 세포내외 이온의 농도, 수분균형 및 혈압 등을 조절하는 것으로 알려져 있다. 또한 심방근의 인장자극에는 Atrial Natriuretic Peptide(ANP)를 2단계(분비, 유리)의 과정으로 이루어져 있으며, 이에 따른 심방이뇨호르몬의 분비 조절기전에 대하여서는 명확히 알려져 있지 않다. 따라서 본 연구는 백서의 심방근 적출관류 모델을 이용하여 protein kinase C와 ANP 조절의 상관관계를 밝히고 분비와 유리의 과정중 어떠한 과정을 이용하여 분비자극에 영향을 주는지를 관찰하기 위하여 본 실험을 실시하였다. PKC 활성제인 PMA(phorbol 12-mystrate 13-acetate)는 ANP의 유리를 현저하게 증가시켰으며, PKC 억제제인 H-7(1-(5-isoquinoline sulfonyl)-2-methyl piperazine dihydrochlo-ride)에 의해 유리를 억제시켰다. PMA와 H-7을 동시에 처리한 경우 PMA에 의하여 증가된 ANP의 유리가 H-7에 의하여 차단됨을 관찰할 수 있었다. 따라서 백서의 관류 심방에서의 ANP 분비 증가는 PKC 활성화에 의하여 이루어지며, ANP분비의 2단계중 ANP 유리에 영향을 줌을 알 수 있었다.

• The Korean Journal of Physiology
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• v.23 no.1
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• pp.67-78
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• 1989

Since the atrial receptor was suggested to be involved in the control of extracellular fluid volume, it has been shown that the granularity of atrial cardiocytes can be changed by water and salt depletion, and that an extract of atrial tissue, when injected intravenously into anesthetized rats, causes a large and rapid increase in renal excretions of sodium and water. The immunoreactive atrial natriuretic peptide (ANP) has been found in the plasma of patients suffering from various cardiovascular diseases. A high level of ANP in the plasma has been reported in essential hypertension. Several studies on the effects of ANP on renal function and arterial blood pressure have presented contradictory results showing attenuated or accentuated responses. Thus, involvement of the ANP in the development of hypertension remains unresolved. Present study was undertaken to investigate whether the ANP is involved in the development of hypertension in two-kidney one-clip Goldblatt hypertensive rats. The plasma concentration of immunoreactive ANP appeared to be significantly elevated in hypertensive rats as compared with normotensive Goldblatt operated and sham-operated rats. Plasma renin concentration was higher in hypertensive rats than in normotensive rats, as observed in earlier experiments. Intravenous infusions of ANP resulted in increases of urine flow and urinary excretions of sodium and potassium in both hypertensive and normotensive rats. The renal response to ANP was markedly accentuated in Goldblatt hypertensive rats. The plasma concentration of ANP showed a linear relationship with the arterial blood pressure. Infusions of ANP reduced blood pressure both in hypertensive and normotensive rats. These results suggest that in Goldblatt hypertensive rats an elevation of ANP level in the plasma may not be a cause, but instead a consequence of hypertension, and that the renal responsiveness to the ANP is accentuated by some unknown mechanisms.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.3
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• pp.235-241
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• 2000

We examined the expression of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) mRNAs upon isoproterenol (Iso)-induced cardiac hypertrophy in rats. Then, we tried to investigate the effects of sympatholytics to see if they can modulate the expression of ANP and BNP. In this study, RT-PCR technique was used to characterize the expression of ANP and BNP in right atrium (RA) and left ventricle (LV) of the hypertrophied rat heart. Histologic findings indicated that stimulation of ${\beta}-adrenoceptors$ with Iso for 5 days was sufficient to induce cardiac hypertrophy in rats. A continuous stimulation with Iso for 7 days resulted in an increase of the ANP and BNP expression in the LV and BNP expression in the RA. The increased expressions of ANP and BNP in the LV were slightly inhibited, and the increased expressions of BNP in the RA were markedly inhibited by a continuous treatment with propranolol, metoprolol, and clonidine for 7 days. Overall, our data present a differential expression of the natriuretic peptides in Iso-induced cardiac hypertrophy, and that the mechanisms involved in this differential ANP and BNP gene expression could be mediated via sympathetic nervous system.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.4
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• pp.283-289
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• 2000

Natriuretic peptides comprise a family of three structurally related peptides; atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). The present study was performed to investigate the effect of ANP on the proliferation and activity of ROS17/2.8 and HOS cells which are well-characterized osteoblastic cell lines. ANP dose-dependently decreased the number of ROS17/2.8 and HOS cells after 48-hour treatment. ANP generally increased the alkaline phosphatase activity of ROS17/2.8 and HOS cells after 48 hr treatment, regardless of the fact that basal activity of alkaline phosphatase was much lower in HOS cells compared to that of ROS17/1.8 cells. ANP increased the NBT reduction by ROS17/2.8 and HOS cells. ANP showed the variable but no significant effect on the nitric oxide production by ROS17/2.8 and HOS cells. ROS17/2.8 and HOS cells produced and secreted gelatinase into culture medium, and this enzyme was thought to be the gelatinase A type with the molecular weight determination. The gelatinase activity produced by ROS17/2.8 cells was increased by the treatment of ANP. However, the enzyme activity was not affected by ANP treatment in the HOS cell culture. In summary, ANP decreased the proliferation and increased the alkaline phosphatase activity and NBT reduction of osteoblasts. These results indicate that ANP is one of the important regulators of bone metabolism.

• Korean Journal of Veterinary Research
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• v.36 no.1
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• pp.65-74
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• 1996

Atrial Natriuretic Peptide(ANP) is a hormone with potent natriuretic, diuretic and relaxing properties of vascular smooth muscle. Specific chemical modulator responsible for the ANP secretion has not yet been found. Although atrial stretch of stretch-release is to be a major stimulus for the secretion of ANP, the precise mechano-molecular transduction mechanism responsible for its evoked secretion remains to be elucidated. It is interested to clarify the effect of superoxide anion in the stretch-induced ANP secretion. In order to investigate the effectg of $H_2O_2$ in the regulation of ANP secretion, a perfused model of left atrium of rats was used. The results obtained were as follows; 1. The ANP secretion and the extracellular fluid(ECF) translocation were accentuated by the effect of repetitive atrial distension-reduction volume at atrial pressure($4cmH_2O$). 2. The dilution curve showed to be in parallel between pure atriopeptin III (AP III) and perfusated buffer. 3. $H_2O_2(5{\times}10^{-4}M)$ accenturated a strectch-release induced increase of the ANP secretion. The amount of released ANP was significantly(p<0.01) increased. These results suggest that the superoxide anion may be involved in the regulatory mechanism of mechanically activated ANP release.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.1
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• pp.79-82
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• 1997

The present study was aimed to explore an interaction between endothelium-derived nitric oxide (NO) and atrial natriuretic peptide (ANP) systems in normotensive and hypertensive states. Rats were made two-kidney, one clip (2K1C) hypertensive and supplemented with either $N^G-nitro-L-arginine$ methyl ester (L-NAME, 5 mg/100 ml drinking water) or L-arginine hydrochloride (400 mg/100 ml drinking water). One group supplied with normal tap water served as control. Sham-clipped rats were also divided into the L-NAME, L-arginine, and control groups. The plasma levels and atrial contents of ANP were determined at day 28 following clipping the renal artery. In 2K1C rats, the plasma level of ANP was higher and the atrial content was lower than in the sham-clipped control. L-Arginine increased the atrial content of ANP in association with a decreased plasma ANP, whereas L-NAME significantly affected neither parameter. The increase of blood pressure in 2K1C rats was not affected by L-arginine or L-NAME. In sham-clipped rats, the plasma level of ANP was significantly increased by L-NAME along with an increase in blood pressure. On the contrary, L-arginine did not affect the blood pressure or plasma ANP. The atrial content of ANP was significantly altered neither by L-arginine nor by L-NAME. These results suggest that NO plays a tonic inhibitory role on the ANP release with concomitant increases of the atrial tissue content. In addition, hypertension is suggested to modify the release and tissue storage of ANP.