• Korean Journal of Pharmacognosy
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• v.14 no.4
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• pp.145-148
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• 1983

Angiotensins and bradykinin play important roles in blood pressure regulation and in other physiological and pathological conditions. The present work is aimed to investigate potential antagonists against either angiotensin or bradykinin from plant sources. Each methanol extract of selected 25 plants was solvent fractionated to three fractions. The effects of total of 75 plant samples against the contractions induced by angiotensin I or bradykinin in rat ileum were measured. The results are summarized.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.6
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• pp.615-621
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• 1999

In spite many evidences has supported the cardioprotective effect of bradykinin, its direct effects at the cell level are still under question. We investigated the both effects of bradykinin (BK) on $Ca^{2+}-related$ ionic currents using whole cell voltage clamp technique in rabbit cardiomyocytes and on the intracellular $Ca^{2+}$ transient using calcium sensitive fluorescence dye, indo-1AM. Simultaneously with recording intracellular $Ca^{2+}$ transients, cell contractility was estimated from the changes in length of the electrical stimulated rat cardiac myocytes. L-type $Ca^{2+}$ current decreased by bradykinin at the entire voltage range. Inward tail current increased initially up to its maximum about 4 min after exposing myocytes to BK, and then gradually decreased again by further exposure to BK. This tail current decreased remarkably at washing BK off but slowly recovered ca. 20 min later. The change in cell contractility was similar to that in tail current showing initial increase followed by gradual decrease. Removal of BK brought remarkable decrease in contractility, which was recovered $15{\sim}20$ min after cessation of electrical stimulation. Bradykinin increased $Ca^{2+}$ transient initially but after some time $Ca^{2+}$ transient also decreased coincidentally with contractility. From these results, it is suggested that bradykinin exerts directly its cardioprotective effect on the single myocytes by decreasing the intracellular $Ca^{2+}$ level followed by an initial increase in $Ca^{2+}$ transient.

• BMB Reports
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• v.29 no.6
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• pp.549-554
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• 1996

Phosphoinositide turnover in response to platelet-derived growth factor, epidermal growth factor, and bradykinin was evaluated in NIH 3T3 cells. Platelet-derived growth factor and bradykinin induced a significant increase in incorporation of $^{32}P$ into phosphatidylinositol (PI), phosphatidylinositol 4-monophosphate (PIP), and phosphatidylinositol 4.5-bisphosphate ($PIP_2$) in serum-starved NIH 3T3 cells. However, epidermal growth factor increased incorporation of $^{32}P$ into these phosphoinositides by only a small amount. Stimulation with platelet-derived growth factor, not bradykinin, caused a rapid elevation of PI and PIP kinase activities that were maximally activated within 10 min. The maximal levels of their elevation in cells with plateletderived growth factor stimulation were 3.2-fold for PI kinase, and 2.1-fold for PIP kinase. Short term pretreatment of NIH 3T3 cells with phorbol 12-myristate 13-acetate, activator of protein kinase C. caused an approximately 60% decrease in platelet-derived growth factor-induced PI kinase activities, indicating the feedback regulation of phosphoinositide turnover by protein kinase C. These results suggest that although the enhancement of phosphoinositide turnover is a rapidly occurring response in platelet-derived growth factor- or bradykinin-stimulated NIH 3T3 cells, phosphoinositide kinases may be associated with initial signal transduction pathway relevant to platelet-derived growth factor but not to bradykinin.

• Journal of Life Science
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• v.17 no.7 s.87
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• pp.905-909
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• 2007

The dual-function protein redox factor-1 (Ref-1) is essential for base excision repair of oxidatively damaged DNA and also governs the activation of many redox-sensitive transcription factors. We examined the role of Ref-1 in regulation of nitric oxide (NO) synthesis employing adenoviral-mediatedoverexpression of Ref-1 in bradykinin-stimulated endothelial cells. Intracellular NO was detected with the NO-sensitive fluorophore DAF-2. Overexpression of Ref-1 potentiates bradykinin-stimulated NO production in endothelial cells. And, cells ifected with AdRef-1 showed higher fluorescence intensity compared with uninfected or AdD1312-infected cells. In parallel with this, over expression of Ref-1 also stimulated endothelial NO synthase (eNOS) enzyme activity, compared with unifected or AdD1312-infected cells, in bradykinin-stimulated cells as well as in unstimulated cells. These results suggest that Ref-1 implicates in endothelium-dependent vasorelaxation resulting from NO production in vascular system.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.128-128
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• 2003

Bradykinin modulates the sympathetic system in various ways. It can stimulate sympathetic neurotransmission directly through presynaptic receptors (Llona et al., 1991) and indirectly via its hypotensive or nociceptive effects which activate central and ganglionic mechanisms (Kuo and Keeton, 1991; Dray et al., 1988). However, it has been found that bradykinin can also liberate prostaglandins in peripheral tissues, thereby attenuating the release of catecholamines(Starke et al., 1977). (omitted)

• Proceedings of the Korean Biophysical Society Conference
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• 1998.06a
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• pp.31-31
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• 1998

The role of a phosphoinositide-specific phospholipase C, PLC-deltal, in the bradykinin receptor-mediated signaling pathway was investigated using a clone of stably overexpressed PLC-deltal in rat pheochromocytoma (PC12) cells. Stimulation with bradykinin induced significantly higher [Ca$\^$2＋/]i rise in PLC-deltal-overexpressed cells (PC12-D1) than in the wild type (PC12-W) and the vector-transfected (PC12-V) cells.(omitted)

• Archives of Pharmacal Research
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• v.29 no.3
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• pp.241-248
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• 2006

Angiotensin converting enzyme (ACE) inhibitors have cardioprotective effects in different species including human. This cardioprotective effect is mainly due to the inhibition of bradykinin (BK) degradation rather than inhibition of the conversion of angiotensin I to angiotensir. II. Bradykinin, a nonapeptide, has been considered to be the potential target for various enzymes including ACE, neutral endopeptidase 24.11, carboxypeptidase M, carboxypeptidase N, proline aminopeptidase, endopeptidase 24.15, and meprin. In the present study, the coronary vascular beds of Sprague Dawley rat isolated hearts were perfused (single passage) with Krebs solution alone or with different concentrations of BK i.e. $2.75{\times}10^{-10},\;10^{-7},\;10^{-6}\;and\;10^{-5}M$ solution. Percent degradation of BK was determined by radioimmunoassay. The degradation products of BK after passing through the isolated rat-hearts were determined using RP-HPLC and mass spectroscopy. All the four doses of BK significantly decreased the perfusion pressure during their passage through the hearts. The percentage degradation of all four doses was decreased as the concentration of drug was increased, implying saturation of a fixed number of active sites involved in BK degradation. Bradykinin during a single passage through the hearts degraded to give [1-7]-BK as the major metabolite, and [1-8]-BK as a minor metabolite, detected on HPLC. Mass spectroscopy not only confirmed the presence of these two metabolites but also detected traces of [1-5]-BK and arginine. These findings showed that primarily ACE is the major cardiac enzyme involved in the degradation of bradykinin during a single passage through the coronary vascular of bed the healthy rat heart, while carboxypeptidase M may have a minor role.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.1
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• pp.99-105
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• 2001

It is well known that the inflammation of somatic tissues, bladder and colon can alter the sensitivity of primary afferents innervating these tissues. To see if uterine afferents also show altered sensitivity, we examined their responses to the algesic agent bradykinin before and after induction of uterine inflammation. Inflammation was induced by injecting the mustard oil into the uterine lumen of adult female rats. After induction of inflammation, the response latency to bradykinin did not change, but the duration and peak of the response and integrated impulse discharges during the response period increased significantly. Furthermore, after inflammation, the level of resting discharges of the afferents was much higher. These results are consistent with the idea that the inflammation can sensitize the uterine afferents.

• The Korean Journal of Pharmacology
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• v.26 no.2
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• pp.161-166
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• 1990

Infusion of bradykinin (BK) into the renal arteries increases sodium excretion. However, it is not clear whether natriuresis results from the renal hemodynamic effects or from the direct effect on renal tubular sodium transport. Therefore, we examined the effects of BK on the transport-dependent oxygen consumption in the distal tubule (DT) and cortical collecting tubule (CCT) of deoxycorticosterone-treated rats. BK inhibited oxygen consumption in a dose-dependent way with a maximal reduction at $0.1\;{\mu}M$ BK. The inhibitory effect of BK was not present in the absence of sodium or in the presence of ouabain (1 mM). These data imply that the inhibitory effect of BK is restricted to the sodium transport-dependent oxygen consumption. We also investigated the relationship between the effect of BK on oxygen consumption and arachidonic acid metabolism. Mepacrine $(10\;{\mu}M)$, an inhibitor of membrane phospholipases, prevented the inhibitory effect of BK, but indomethacin (0.5 mM) didn't. These results suggest that BK decreases the sodium transport-related oxygen consumption in the rat DT and/or CCT, and that it may be mediated by products of enzymes other than cyclooxygenase.

• Korean Journal of Microbiology
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• v.50 no.4
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• pp.281-284
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• 2014

Immune defense responses against Pseudomonas aeruginosa infection play an important role in maintaining homeostasis in the human body. Previously, we reported that expression of the bradykinin receptor (BR) is induced in response to P. aeruginosa infection. However, the factors responsible for the induction was uncertain. Here, we found that the type III secretion system (T3SS) is responsible for the induction of BR expression, and nucleoside diphosphate kinase (Ndk), as a novel T3SS effector, mediates the upregulation. The Ndk-mediated expression of BR was not induced by fliC mutant treatment, indicating the involvement of flagellin, one of the well-known pathogen-associated molecular patterns (PAMPs). Taken together, this study demonstrated that Ndk cooperates with flagella in the development of defense responses against P. aeruginosa infection.