• Biomolecules & Therapeutics
• /
• v.9 no.2
• /
• pp.96-103
• /
• 2001

These studies were investigated about influence of SKP 450, a $K^{+}$ channel opener, on the pressor actions induced by norepinephrine, angiotensin II and carotid artery occlusion in rats. Before these studies, effect of SKP 450 itself on blood pressure was examinated. SKP 450 produced the depressor action in proportionaly to dose of 0.3, 1.0 and 3.0 $\mu$g/kg given intravenously and this depressor action was weakened by pretreatment of glibenclamide, a $K^{+}$ channel blocker. The pressor action induced by norepinephrine, an alpha-adrenergic agonist, was blocked 1 hr after administation of SKP 450 in a dose of 3.0 $\mu\textrm{g}$/kg, i.v. and directly after in a dose of 6.0 $\mu\textrm{g}$/kg, i.v.. The pressor action induced by angiotensin II was blocked immediatly after treatment of SKP 450 in a dose of 3.0 $\mu\textrm{g}$/kg, i.v.. The pressor action caused by carotid artery occlusion was not affected by SKP 450 of 3.0 $\mu\textrm{g}$/kg, i.v., whereas markedly blocked by SKP 450 of 6.0 $\mu\textrm{g}$/㎦, i.v.. The potentiated-pressor actions of norepinephrine and angiotensin II by pretreatment of chlorisondamine, a autonomic ganglionic blocking agent, were also blocked by administration of SKP 450 in a dose of 6.0 $\mu\textrm{g}$/kg, i.v.. The weakened-pressor action of carotid artery occlusion by pretreatment of chlorisondamine was more weakened by SKP 450 6.0 $\mu\textrm{g}$/kg, i.v.. The results suggest that hyperpolarization formed through $K^{+}$ channel opening in cell membrane inhibits the pressor action induced norepinephrine ; angiotensin II ; and carotid artery occlusion.usion.

• 대한핵의학회:학술대회논문집
• /
• 1976.06a
• /
• pp.66.2-67
• /
• 1976

• Applied Biological Chemistry
• /
• v.49 no.4
• /
• pp.293-297
• /
• 2006

Angiotensin converting enzyme(ACE) is a zinc-containing dipeptidase widely distributed in mammalian tissues and is thought to play a significant role in blood pressure regulation by hydrolyzing angiotensin I to the potent vasoconstrictor, angiotensin II. Recently, the presence of ACE in pig ovary was reported and the ACE from pig kidney was isolated and characterized. However no nucleotide sequence of the ACE gene from pig is yet known. We report here the cloning of the ACE cDNA from pig kidney by using the reverse transcriptase-polymerase chain reaction. The complete amino acid sequence deduced from the cDNA contains 1309 residues with a molecular mass of 150 kDa, beginning with a signal peptide of 33 amino acids. Amino acid sequence analysis showed that pig kidney ACE is also probably anchored by a short transmembrane domain located near the C-terminus. This protein contains a tandem duplication of the two homologous amino acid peptidase domain. Each of these two domains bears a putative metal-binding site (His-Glu-Met-Gly-His) identified in mammalian somatic ACE. The alignment of pig ACE amino acid sequence with human, rabbit, and mouse reveals that both two domains have been highly conserved during evolution.

• Archives of Pharmacal Research
• /
• v.20 no.5
• /
• pp.389-395
• /
• 1997

We investigated the interaction between nitric oxide and the renin angiotensin system in regulating isolated pulmonary arterial tension and pulmonary arterial pressure (PAP) in renal hypertensive rats (RHR) made by complete ligation of left renal artery. Losartan induced a depressor response that was smaller in RHR than in normotensive rats (NR) (3.3 and 7.0 mmHg, respectively, at 3.0 mg/kg, p<0.05), and the response was significantly reduced by $N^{G}$-nitro-Larginine methyl ester (L-NAME). Angiotensin II elevated the PAP (7.6 and 10.8 mmHg at $0.1 {\mu}g/kg$; 20.3 and 23.6 mmHg at $1.0{\mu}g/kg$, respectively) and contracted the isolated pulmonary artery ($pD_2$: 8.79 and 8.71, respectively) from both NR and RHR with similar magnitude, and these effects were significantly enhanced by L-NAME in NR, but not in RHR. Acetylcholine lowered the PAP slightly less effectively in RHR than in NR (3.8 and 6.0 mmHg at 10 .mu.g/kg, respectively) and relaxed the pulmonary artery precontracted with norepinephrine in both rats with similar magnitude ($E_max$: 60.8 and 63.6%, respectively), and the effect being completely abolished after pretreatment.with L-NAME or removal of endothelial cells. These results suggest that nitric oxide interacts with renin angiotensin system to control the pulmonary vascular tension and pulmonary arterial circulation of RHR.R.

• KSBB Journal
• /
• v.14 no.5
• /
• pp.600-605
• /
• 1999

For the production of angiotensin I converting enzyme inhibitory peptides as a material for antihypertensive functional foods from animal blood produced in slaughterhouse, the optimum condition for enzymatic hydrolysis to yield a peptide fraction of the highest activity were investigated with a respect of industrial production. Among several industrially-usable enzymes tested, $Alcalase^？$ produced hydrolysates of the highest activity from total plasma and purified albumin. $IC_50$ values of albumin hydrolysate and its third fraction separated by gel chromatography were 0.5 and 0.02 mg/mL, respectively. The fraction was found to be obtained by a simple ultrafiltration using a membrane of MW cutoff 1,000. The possibility for the industrial production of antihypertensive peptides from animal blood plasma protein was suggested.

• BMB Reports
• /
• v.35 no.3
• /
• pp.251-254
• /
• 2002

The genetic factors that contribute to the development of coronary artery disease (CAD) are poorly understood. It is likely that multiple genes that act independently or synergistically contribute to the development of CAD and the outcome. Recently, an insertion/deletion (I/D) polymorphism of the human angiotensin I-converting enzyme (ACE) gene, a major component of the renin-angiotensin system (RAS), was identified. The association of the ACE gene D allele with essential hypertension and CAD has been reported in the African-American, Chinese, and Japanese populations. However, other studies have failed to detect such an association. It has been suggested that these inconsistencies may be due to the difference in backgrounds of the population characteristics. In the present study, we investigated the I/D polymorphism of the ACE gene in 103 subjects of both sexes, consisting of 59 normal controls and 44 patients with hypertension. The allele and genotype frequency were significantly different between the hypertensive and control groups (p < 0.01). Among the three ACE I/D variants, the DD genotype was associated with the highest value of the mean systolic blood pressure [SBP] and mean diastolic blood pressure [DBP] (p = < 0.05) in men, but not in women. In the overall population, the mean SBP and DBP was highest in DD subjects, intermediate in I/D subjects, and the least in II subjects.

• The Korean Journal of Zoology
• /
• v.34 no.2
• /
• pp.142-147
• /
• 1991

Angiotensin I-converting enzyme (ACE) activity has been characterized in the rice eel, Monopterus albus. Peak activity of ACE in plasma from the rice eel was shown at around pH 10, which was more alkaline compared to that of mammals. Chloride requirements for the optimal ACE activity were different from species to spedes. ACE inhibitors, EDTA, teprotide (SQ 20, 881), and captopril (SQ 14, 225) showed dose-dependent inhibitions of ACE activity in plasma from the rice eel as well as mammals. ACE activity in the rice eel was increased by CoCI2, and the enzyme activity was more unstable at high temperature as compared to mammals The highest activity of ACE among the various tissues in the rice eel was found in the brain.

• Bulletin of the Korean Chemical Society
• /
• v.25 no.12
• /
• pp.1791-1800
• /
• 2004

Angiotensin I, a model decapeptide, was glycosylated and partially hydrolyzed with HCl (6 N, 80 $^{\circ}C$, 4 h), aminopeptidase, and carboxypeptidase Y. A single peptide mass map obtained from truncated peptides in the partial acid hydrolysate of angiotensin and its glycosylation product mixture by matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry enabled sequencing of angiotensin by a combinatorial procedure. MALDI-TOF and electrospray ionization (ESI) tandem mass spectrometric results indicate that both the N-terminal amino group of aspartic acid and the guanidinium group of the second residue arginine are glycosylated.

• Tuberculosis and Respiratory Diseases
• /
• v.55 no.5
• /
• pp.478-487
• /
• 2003

Background : There have been several studies showing that the angiotensin II and angiotensin converting enzyme(ACE) contributes to the apoptosis of alveolar epithelial cells in idiopathic interstitial pneumonia and the activation of fibroblasts during the process of pulmonary fibrosis. These results suggest that the pulmonary fibrosis can be inhibited by the angiotensin II receptor antagonist(AGIIRA). This study was performed to identify the therapeutic effect of AGIIRA in idiopathic pulmonary fibrosis(IPF). Method : Thirteen patients with IPF, who were diagnosed with an open lung biopsy(6 patients) and furfilling the ATS criteria(7 patients) between March 1999 and October 2001 at the Gachon medical center, were enrolled in this study. Of these patients, eight patients were treated with a regimen including AGIIRA(AT group), and five were treated without AGIIRA(NT group). The pulmonary function tests and dyspnea(ATS scale) were measured at diagnosis and 1 year after treatment. All the data was collected to analyze the therapeutic effect of AGIIRA on the patients with IPF. Results : The AT group contained 8 patients(M:F=4:4) and the NT group contained 5 patients(M:F=3:2). There was no significant difference in the serum angiotensin II level between the two groups($202.5{\pm}58.5$ vs $163.7{\pm}47.3pg/ml$, p>0.05). The AT group showed an upward trend in TLC(+3%), FVC(+4%), FEV1(+3%) and DLco(+2%) compared to the NT group(TLC(-14%), FVC(-3%), FEV1(-4%) except for DLco(+5%)). The dyspnea score in the AT group improved significantly but not in the NT group. Conclusion : These results suggest that the angiotensin II receptor antagonist may have an effect on stabilizing IPF.

• Bulletin of the Korean Chemical Society
• /
• v.31 no.5
• /
• pp.1377-1380
• /
• 2010