• 한국환경독성학회:학술대회논문집
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• 한국환경독성학회 2002년도 추계국제학술대회
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• pp.165-165
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• 2002

Hypertension is considered to be caused by a complicated combination of genetic and environmental factors. Atrial natriuretic peptide (ANP) has been to suppress renin activity and inhibit the synthesis and release of aldosterone. Therefore, Abnormalities of this peptide caused by genetic variation may be influence the blood pressure. The aim of present study was to examine the relationship between hypertension and Sca I RFLP of ANP gene in Korean population. The genotype distribution of this RFLP was significantly different between normotensives and hypertensives (P<0.05). However, this genetic marker was not significantly associated with any anthropometric parameters or plasma lipid concentrations in our study group. Therefore, our result suggest that Sca I RFLP of ANP gene may be useful as genetic marker in the ethiology of hypertension in Korean population, independent of any cardiovascular risk. factors studied.

• 대한흉부심장혈관외과학회:학술대회논문집
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• 대한흉부외과학회 1996년도 제 28차 추계학술대회 및 총회 대한흉부외과학회
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• pp.6-6
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• 1996

• Toxicological Research
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• 제22권2호
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• pp.69-74
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• 2006

Hypertension leads to major health problems in many industrialized countries, and multiple etiologic factors are involved in the pathogenesis of this disorder. The genetic components of the natriuretic peptide system might be involved in the pathogenesis of hypertension. In this regard, the atrial natriuretic peptide (ANP) gene has been proposed as a candidate hypertension gene. Therefore, we investigated the G1837A and C-664G polymorphisms of the ANP gene in 143 Korean normotensives and 118 hypertensives. There were no significant differences in the genotype and allele frequencies between the two groups. Although the frequencies in each of these polymorph isms were not significantly different between normotensives and hypertensives, our results provide additional ethnic information for linkage analysis and associated studies of this disorder with cardiovascular disease.

• The Korean Journal of Physiology and Pharmacology
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• 제26권6호
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• pp.469-478
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• 2022

WNT signaling plays an important role in cardiac development, but abnormal activity is often associated with cardiac hypertrophy, myocardial infarction, remodeling, and heart failure. The effect of WNT signaling on regulation of atrial natriuretic peptide (ANP) secretion is unclear. Therefore, the purpose of this study was to investigate the effect of Wnt agonist 1 (Wnta1) on ANP secretion and mechanical dynamics in beating rat atria. Wnta1 treatment significantly increased atrial ANP secretion and pulse pressure; these effects were blocked by U73122, an antagonist of phospholipase C. U73122 also abolished the effects of Wnta1-mediated upregulation of protein kinase C (PKC) β and γ expression, and the PKC antagonist Go 6983 eliminated Wnta1-induced secretion of ANP. In addition, Wnta1 upregulated levels of phospho-transforming growth factor-β activated kinase 1 (p-TAK1), TAK1 banding 1 (TAB1) and phospho-activating transcription factor 2 (p-ATF2); these effects were blocked by both U73122 and Go 6983. Wnta1-induced ATF2 was abrogated by inhibition of TAK1. Furthermore, Wnta1 upregulated the expression of T cell factor (TCF) 3, TCF4, and lymphoid enhancer factor 1 (LEF1), and these effects were blocked by U73122 and Go 6983. Tak1 inhibition abolished the Wnta1-induced expression of TCF3, TCF4, and LEF1 and Wnta1-mediated ANP secretion and changes in mechanical dynamics. These results suggest that Wnta1 increased the secretion of ANP and mechanical dynamics in beating rat atria by activation of PKC-TAK1-ATF2-TCF3/LEF1 and TCF4/LEF1 signaling mainly via the WNT/Ca²⁺ pathway. It is also suggested that WNT-ANP signaling is implicated in cardiac physiology and pathophysiology.

• 대한한의학회지
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• 제20권2호
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• pp.141-145
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• 1999

The aim of this experiment was to investigate the effects of a mixture of Scutellariae Radix, Coptidis Rhizoma and Coptidis Rhizoma water extracts on the blood pressure, plasma renin activity, plasma levels of aldosterone and atrial natriuretic peptide (ANP) in spontaneously hypertensive rats (SHR). The results of this study were as follows: 1. Systolic blood pressure decreased significantly after the administration of a mixture of Scutellariae Radix, Coptidis Rhizoma, and Coptidis Rhizoma water extract 0.2 ml/200g. 2. Plasma renin activity and plasma levels of ANP were not changed after the administration of a mixture of Scutellariae Radix, Coptidis Rhizoma and Coptidis Rhizoma water extracts, 3. Plasma levels of aldosterone was increased significantly after the administration of a mixture of Scutellariae Radix, Coptidis Rhizoma and Coptidis Rhizoma water extracts 0.1 ml/200g.

• The Korean Journal of Physiology and Pharmacology
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• 제10권3호
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• pp.149-154
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• 2006

Selective inhibition of phosphodiesterase (PDE) 5 opened a new therapeutic approach for cardiovascular disorders. Therefore, the effect of PDE5 inhibition on the cardiac function should thoroughly be defined. The purpose of the present study was to define the effects of sildenafil, a selective inhibitor of PDE5, on the atrial cGMP efflux, atrial dynamics, and the release of atrial natriuretic peptide (ANP). By perfusing rabbit left atria to allow atrial pacing, changes in atrial stroke volume and pulse pressure, transmural extracellular fluid translocation, cGMP efflux, and ANP secretion were measured. SIN-I, an NO donor and soluble (s) guanylyl cyclase (GC) activator, and C-type natriuretic peptide (CNP), an activator of particulate (p) GC activator, were used. Sildenafil increased basal levels of cGMP efflux slightly but not significantly. Sildenafil in a therapeutic dose increased atrial dynamics (for atrial stroke volume, $2.84{\pm}1.71%$, n=12, vs $-0.71{\pm}0.86%$, n=21; p<0.05) and decreased ANP release ($-9.02{\pm}3.36%$, n=14, vs $1.35{\pm}3.25%$, n=23; p < 0.05), however, it had no effect on the SIN-1- or CNP-induced increase of cGMP levels. Furthermore, sildenafil in a therapeutic dose accentuated SIN-1-induced, but not CNP-induced, decrease of atrial pulse pressure and ANP release. These data indicate that PDE5 inhibition with sildenafil has a minor effect on cGMP levels, but has a distinct effect on pGC-cGMP- and sGC-cGMP-induced contractile and secretory function.

• 한국동물학회:학술대회논문집
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• 한국동물학회 1994년도 한국생물과학협회 학술발표대회
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• pp.184.2-184
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• 1994

No Abstract, See Full Text

• Animal cells and systems
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• 제6권3호
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• pp.253-261
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• 2002

Although cardiac distribution of specific receptors for atrial natriuretic peptide (ANP) was mainly observed in the ventricular endocardium, the modulation of ANP receptors in relation to cardiac development is not defined. The present study was undertaken to investigate ANP receptor modulation in rat during development. In the developmental stages examined (fetus, after postnatal 3-days, 1-, 2-, 3-, 4-, and 8-week-old Sprague Dawley rats) specific ANP binding sites were localized in the right and left ventricular endo-cardia by quantitative in vitro receptor autoradiography using (equation omitted)-rat ANP as labeled ligand. The specific bindings to endocardium were much higher in the right than the left ventricle. The binding affinities of ANP were much higher in the right than the left ventricular endocardium. The difference of these binding affinities among various developmental stages was not observed in the right ventricle, whereas the binding affinity in left ventricle was gradually increased with aging and reached the peak value at 8 weeks. No significant difference in maximal binding capacities of endocardial bindings was observed in the right and left ventricular endocardia during developmental stages. Also, cGMP production via activation of particulate guanylyl cyclase-coupled receptor subtypes in the ventricular membranes was gradually decreased with close relationship to aging. Therefore, the present study show that the endocardial ANP receptor is modulated with close relationship to cardiac development in the left ventricle rather than the right ventricle, and may be involved in regulating myocardial contractility in left heart.

• 대한임상검사과학회지
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• 제37권2호
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• pp.88-95
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• 2005

Even though the echocardiograph has been recognized as the method of choice among various diagnostic tools to detect congestive heart failure (CHF), there were some limitations in relation to the consumption of time, labor and process. We analyzed results of N-terminal probrain-type natriuretic peptide (NT-proBNP) and various parameters of the echocardiographic findings to clarify the diagnostic usefulness of NT-proBNP in detecting patients with CHF. We analyzed the sera from total of 242 cases from in-patients and out-patients, which were requested from the cardiovascular section of department of Internal Medicine at Chungnam National University Hospital from March 2003 to May 2004. The procedures were performed in order as shown below; sampling, NT-proBNP analysis, data acquisition and data analysis. All data including personal information and echocardiographic findings ware acquired by medical record review. When classifying the study population into six groups according to the degree of left ventricular ejection fraction (LVEF), the serum level of NT-proBNP was higher in the group with 51-60% of LVEF (P=0.023). There were low correlation between the serum level of NT-proBNP and various parameters of the echocardiographic findings with LVESD (r=0.1513), LVEDD (r=0.0831), LVEF (r=0.2035), IVST (r=0.03) and LVPWT (r=0.0728), respectively. When comparing NT-proBNP with atrial and/or ventricular enlargement, the patient group with both left atrial and left ventricular enlargement (p=0.186) or only left atrial (p=0.105) or only left ventricular enlargement (p=0.256) showed higher level of NT-proBNP without statistical significance than patient group with no enlargement. Searching the optimal cutoff of the serum level of NT-proBNP, the sensitivity (98.9%) and the specificity (100%) was highest at the cutoff of 300 pg/mL than any other cutoffs. These findings suggested that the analysis of NT-proBNP in serum might detect the patients with CHF earlier than with the echocardiograph, especially in patients with asymptomatic or mild symptomatic CHF. In conclusion, NT-proBNP test was proved to be clinically useful to diagnose CHF patients.

• The Korean Journal of Physiology
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• 제28권2호
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• pp.225-231
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• 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.