• The Korean Journal of Physiology
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• v.22 no.1
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• pp.41-53
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• 1988

The present study was undertaken to clarify the involvement of atrial natriuretic peptide in the development of hypertension in spontaneously hypertensive rats. Plasma concentration of immunoreactive atrial natriuretic peptide was higher in spontaneously hypertensive rats than in normotensive Sprague-Dawley and Wistar rats. Plasma renin concentration was lower in SHR than in normotensive rats, as observed in earlier experiments. Hydration-induced increase in urine flow and urinary excretions of sodium and potassium were smaller in SHR than in normotensive control rats. Intraarterial infusion of atrial natriuretic peptide resulted in increases in urine flow, urinary excretions of sodium and potassium in both hypertensive and normotensive rats. Renal response to atrial natriuretic peptide was markedly suppressed in SHR. Plasma renin and aldosterone concentration were suppressed by atrial natriuretic peptide in both SHR and normotensive rats. The responses were not significantly different in both groups. These results suggest that the renal responsiveness to atrial natriuretic peptide may be suppressed in SHR by some mechanisms still remaining obscure.

• The Korean Journal of Physiology
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• v.21 no.1
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• pp.13-22
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• 1987

Effects of synthetic atrial natriuretic peptide and furosemide on the cardiovascular and renal functions were examined in the freshwater turtle, Amyda japonica. Both atria and ventricle of turtle contained an immunoreactive atrial natriuretic peptide. Synthetic rat atrial natriuretic peptide (atriopeptin III) and turtle atrial extract caused a decrease in mean arterial blood pressure and the vasodepressor effect was dose-dependent. In hydrated turtles received either atriopeptin III or turtle atrial extract, no significant change in renal function was observed until 100 min except a slight natriuresis at 60 or 100 min after injection of 30 ug/kg atriopeptin III or atrial extract, respectively. However, furosemide, 2 mg/kg, caused marked diuresis, natriuresis and kaliuresis. In non-hydrated turtles, no significant change in renal function was observed until 6 hrs following injection of 30 ug/kg atriopeptin III. Plasma aldosterone decreased at 2 hr and increased at 24 hr after injection of atriopeptin III although plasma renin concentration did not change. But, furosemide caused persistent diuresis, natriuresis and kaliuresis. Additionally, plasma aldosterone and renin concentrations were significantly increased at 24 hrs after injection of furosemide. In conclusion, we suggest that the freshwater turtle may have an atrial natriuretic peptide in heart and vascular receptors for atrial natriuretic peptide, and that atrial natriuretic peptide is more important in the regulation of blood pressure rather than that of renal function in freshwater turtles. We also suggest that an increased plasma renin concentration caused by furosemide may not be due to the sodium concentration delivered to macula densa, but due to the dehydration caused by persistent diuresis and natriuresis.

• The Journal of Korean Medicine
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• v.18 no.2
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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.

• The Journal of Korean Medicine
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• v.18 no.1
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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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• 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.

• Journal of the korean academy of Pediatric Dentistry
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• v.28 no.1
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• pp.72-81
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• 2001

Dendroaspis natriuretic peptide (DNP), recently isolated from the venom of the green Mamba snake Dendroaspis angusticeps, is a 38-amino acid peptide containing a 17-amino acid disulfide ring structure similar to that of the natriuretic peptide family. The natriuretic peptide family was known to induce histamine release from human and rat mast cells, but there are no published data concerning the effects of DNP on histamine release from mast cells. The purpose of this study is to investigate whether DNP induces the histamine release from rat peritoneal mast cells (RMPCs) and to determine the mechanism of DNP-induced histamine release from RPMCs. After treatment of the various doses of DNP in RPMCs, the mast cell degranulation was observed with inverted microscopy and the histamine release was measured by radio-enzymatic assay. Calcium uptake and intracellular cyclic GMP level were measured by radioimmunoassays. DNP induced the mast cell degranulation. DNP released the histamine and increased the calcium uptake and the level of intracellular cyclic GMP of RPMCs, in a dose-dependent manner. The results indicate that DNP is capable of inducing histamine release from RPMCs by increasing of calcium uptake and intracellular cyclic GMP level.

• Journal of the korean academy of Pediatric Dentistry
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• v.28 no.3
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• pp.447-463
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• 2001

Dendroaspis natriuretic peptide (DNP), a fourth member of the natriuretic peptide isolated from the venom of the Dendroaspis angusticeps snake, has been reported to be present in human plasma and atrial myocardium and caused vasorelaxation and diuresis in experimental animals. However, it is uncertain whether they are present in peripheral organs other than the heart and its further physiological roles also remains to be clarified. To assess the possible physiological role of DNP in the salivary glands, I investigated the localization of DNP peptide in the rat salivary glands by immunohistochemistry and the binding sites for radiolabelled DNP in the rat salivary glands and oral mucosa using in vitro autoradiography. DNP immunoreactivity was widely distributed in the submandibular, sublingual and parotid glands, particularly in the ducts such as the intercalated and striated ducts, where atrial natriuretic peptide (ANP) was colocalized in consecutive sections, but not in acini. High density $^{125}I-DNP$ binding sites were localized in the epithelia of the tongue and hard palate, while low density binding sites for $^{125}I-DNP$ were also distributed in the submandibular, sublingual, and parotid glands. In the hard palate and tongue, the precise location of this binding was revealed on the basal and parabasal cells of the epithelia by emulsion microautoradiography. These results suggest that DNP may not only have a role in the salivary glands but also play a role in the regulation of growth in the oral epithelium, particularly in the hard palate and tongue.

• 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 Physiology
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• v.24 no.2
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• pp.261-268
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• 1990

It has long been suggested that the cardiac atrium is a low pressure volume receptor controlling body fluid volume and blood pressure. Recently, the cardiac atrium has been found to contain a family of powerful peptides. To clarify the relationship between high blood pressure and the biologically active atrial peptides, experiments were done to define the characteristics of atrial natriuretic peptide secretion in the isolated perfused atria of renal hypertensive rats. Higher concentrations of plasma atrial natriuretic peptide and renin activity were observed in the two-kidney, one clip hypertensive rat compared to the normotensive rat. Atrial volume changes in response to pressure elevations were attenuated in hypertensive rats compared to normotensive rats. Incremental response to atrial volume changes in ANP secretion was accentuated in hypertensive rats. These date suggest that the accentuated atrial natriuretic peptide response to volume changes of hypertensive rats may be a physiological or pathphysiological adaptation to the high blood pressure and may be, at least in part, responsible for the elevated levels of plasma atrial natriuretic peptide observed in hypertensive rats.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.6
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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.