Bradykinin and nitric oxide in infectious disease and cancer

Maeda, Hiroshi; Akaike, Takaaki; Wu, Jun; Noguchi, Yoichiro; Sakata, Yoshifumi

doi:10.1016/0162-3109(96)00063-x

Cited by 67 publications

(29 citation statements)

References 23 publications

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“…1a and Table 1) and in patients with diabetic foot infection (Fig. 1b and Table 1 Inflammation induced by bacterial invasion into previously healthy peripheral soft tissues alters the microenvironment as a consequence of plasma protein extravasation and edema formation (7). In patients with long-lasting diabetes mellitus, the microenvironment in peripheral tissues is already altered by peripheral neuropathy as well as by macro-and microangiopathy (3).…”

mentioning

confidence: 99%

Penetration of Fosfomycin into Inflammatory Lesions in Patients with Cellulitis or Diabetic Foot Syndrome

Legat¹,

Maier

Dittrich

et al. 2003

Antimicrob Agents Chemother

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mentioning

confidence: 99%

Penetration of Fosfomycin into Inflammatory Lesions in Patients with Cellulitis or Diabetic Foot Syndrome

Legat¹,

Maier

Dittrich

et al. 2003

Antimicrob Agents Chemother

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“…Bradykinin is known also to act at BK B 2 receptors in the kidney (Maeda et al, 1996) and in mesenteric vascular beds (Peredo et al, 1997) to stimulate formation of eicosanoids and nitric oxide. Stimulation of phospholipase A 2 and formation of arachidonic acid in the signal transduction pathway for BK accounts for the prostaglandin production in these preparations.…”

Section: Discussionmentioning

confidence: 99%

Metabotropic Signal Transduction for Bradykinin in Submucosal Neurons of Guinea Pig Small Intestine

Gao

Liu

et al. 2004

J Pharmacol Exp Ther

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Intracellular recording methods with "sharp" microelectrodes were used to study signal transduction mechanisms underlying the excitatory action of bradykinin (BK) in morphologically identified neurons in the small intestinal submucosal plexus. Exposure to BK evoked slowly activating membrane depolarization and enhanced excitability associated with increased input resistance in AH-type and decreased input resistance in S-type neurons. Preincubation with pertussis toxin did not affect the BK-evoked responses. Pretreatment with the cyclooxygenase inhibitors indomethacin or piroxicam suppressed or abolished the BK-evoked responses. Application of prostaglandin (PG) E 2 or PG analogs evoked BK-like depolarizing responses in the submucosal plexus with a potency order of PGE 2 Ͼ PGE 1 Ͼ 17-phenyl trinor-PGE 2 Ͼ PGI 2 Ͼ sulprostone Ͼ PGF 2␣ . Depolarizing responses to bradykinin or PGE 2 in S-type neurons were suppressed in the presence of the phospholipase C inhibitor U73122 [(1-6-The inositol-1,4,5-trisphosphate receptor antagonist 2-aminoethoxydiphenylborane and the calmodulin inhibitor W-7, but not ryanodine, suppressed both bradykinin-and PGE 2 -evoked responses. KN-62, an inhibitor of calmodulin kinases, or GF109203X, a specific protein kinase C inhibitor, suppressed both BK-and PGE 2 -evoked depolarizing responses. Selective protein kinase A inhibitors did not alter BKor PGE 2 -evoked depolarizing responses in S neurons. The results suggest that BK stimulates synthesis and release of PGE 2 , which acts at EP 1 receptors to evoke depolarizing responses in submucosal neurons. The postreceptor transduction cascade includes activation of phospholipase C, inositol-1,4,5-trisphosphate production, intraneuronal Ca 2ϩ mobilization, activation of protein kinase C and/or calmodulin kinases, and phosphorylation of cationic channels.Exposing neurons in the guinea pig small intestinal myenteric or submucosal plexus to bradykinin (BK) in vitro evokes slowly activating depolarization of the membrane potential and enhanced excitability characterized by increased firing frequency during intraneuronal injection of depolarizing current pulses in both AH-and S-type neurons and the appearance of anodal break excitation at the offset of hyperpolarizing current pulses in AH neurons (Hu et al., 2003(Hu et al., , 2004. The depolarizing responses are associated with increased input resistance (i.e., decreased conductance) in AH neurons and with decreased input resistance (i.e., increased conductance) in S neurons. Selective BK B 2 receptor antagonists, but not BK B 1 antagonists, suppress the actions of BK in both myenteric and submucosal plexuses (Hu et al., 2003(Hu et al., , 2004. Binding studies with a fluorescently labeled, selective BK B 2 receptor antagonist reveal expression of BK B 2 receptors on a majority of the ganglion cells in the myenteric and submucosal plexuses. RT-PCR and Western blot analysis confirms the expression of BK B 2 receptor mRNA and protein in both plexuses (Hu et al., 2003(Hu et al., , 2004.Inhibition...

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“…13) Nitric oxide (No) No, synthesized from l-arginine by No synthase (NoS), is a well-known vasoactive agent that increases vascular permeability in tumors. [46][47][48] Because of such vasoactivity, No may increase the EPR effect against nanocarriers by widening the endothelial gaps of tumor-feeding arteries. In one such case, in humans, treatment with the No-releasing agent isosorbide dinitrate enhanced the opening of the tumor-feeding artery, and more drug entered the tumor.…”

Section: Increased Blood Flow In Tumors Diphtheria Toxinmentioning

confidence: 99%

Alteration of Tumor Microenvironment for Improved Delivery and Intratumor Distribution of Nanocarriers

Ishida

Kojima

2013

Biological & Pharmaceutical Bulletin

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Nanocarrier-based cancer chemotherapeutics are thought to increase therapeutic efficiency and reduce the side effects of associated chemotherapeutic agents by altering the agents' pharmacokinetics and tissue distribution following intravenous administration. In spite of these favorable properties, nanocarrier-based cancer chemotherapeutics are not always effective because of their heterogeneous intratumoral localization. Homogeneous distribution of nanocarriers in a tumor would improve the efficacy of nanocarrier-based cancer chemotherapeutics. In this article, we describe and discuss some trials that attempt to manipulate the barriers in the tumor microenvironment that hinder extravasation through the tumor vasculature and penetration of nanocarriers in solid tumors. Alterations of the tumor microenvironment that relate directly to the intratumoral distribution of nanocarriers may be potential strategies to improve the delivery of nanocarrierbased cancer chemotherapeutics.

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Bradykinin and nitric oxide in infectious disease and cancer

Cited by 67 publications

References 23 publications

Penetration of Fosfomycin into Inflammatory Lesions in Patients with Cellulitis or Diabetic Foot Syndrome

Penetration of Fosfomycin into Inflammatory Lesions in Patients with Cellulitis or Diabetic Foot Syndrome

Metabotropic Signal Transduction for Bradykinin in Submucosal Neurons of Guinea Pig Small Intestine

Alteration of Tumor Microenvironment for Improved Delivery and Intratumor Distribution of Nanocarriers

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