December 1, 2002AJP Heart and Circulatory Physiology

Bradykinin-induced proinflammatory signaling mechanisms

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Population

Rat mesentery (single postcapillary venules)

Comparison

Bradykinin superfusion with or without various… vs Bradykinin alone

Design

Preclinical

Authors

SSSakuji ShigematsuBeppu Medical Center SIShuji IshidaKitasato University DGDean C. GuteLouisiana State University

Discussion

Member takes

Implication

Hypothesis-generating for bradykinin-driven microvascular inflammation; leaves open translation to human venular permeability disorders.

Structured PICO

Population

Rat mesentery (single postcapillary venules)

Intervention

Bradykinin superfusion with or without various inhibitors (bradykinin-B2 receptor antagonist, SOD mimetic, antioxidant, CYPE inhibitor, PKC inhibitor, immunoneutralizing P-selectin or ICAM-1, phalloidin)

Comparator

Bradykinin alone (implied control for inhibitor effects)

Outcome

Leukocyte/endothelial cell adhesive interactions (LECA) and venular protein leakage (VPL)surrogate

Bradykinin induces leukocyte adhesion and venular protein leakage in rat mesenteric venules through distinct B2-receptor-mediated signaling pathways involving CYPE, PKC, and oxidants.

Cite This Study

Shigematsu et al. (2002) studied this question.

synapsesocial.com/papers/6a7a0ca4dd2e05b79c320efa https://doi.org/10.1152/ajpheart.00538.2002

Topics

Dual antiplatelet therapy

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Bradykinin-induced proinflammatory signaling mechanisms

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Topics

Bradykinin-induced proinflammatory signaling mechanisms

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Topics

Also Consider