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Microvascular leakage in mouse pial venules induced by bradykinin
1Department of Medical Physiology, College of Medicine, Texas A&M University, College Station 77843, USA.
Abstract:
The actions of bradykinin on pial venule leaky site formation were measured intra-vitally in two inbred strains of mice (BALB/c and SJL/J). Pial venules were visualized using an open cranial window microscopy technique and the microvascular leaky site formation was assessed visually using a fluorescein-dextran (70 kDa) INDICATOR. The SJL/J strain was found to be very sensitive to bradykinin-induced microvascular leakage. Pial venule leaky site formation was observed after exposure to 10 pM of bradykinin. In contrast, the BALB/c strain was found to be refractory to bradykinin-induced leakage. Pial arterioles were dilated in response to bradykinin in both strains of mice. These results support the concept that genetically controlled differences in vascular sensitivity and localization of inflammatory peptides play important roles in the generation of vasogenic oedema and inflammation in CNS trauma and disease.
Insights
Mice strains show different responses to bradykinin, a peptide linked to inflammation. SJL/J mice are sensitive to bradykinin-induced microvascular leakage, while BALB/c mice are not, highlighting genetic differences in vascular inflammation.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Bradykinin (BK) is a peptide implicated in inflammation and edema.
- Vascular permeability changes are crucial in central nervous system (CNS) trauma and disease.
- Genetic factors may influence individual responses to inflammatory mediators.
Purpose of the Study:
- To investigate the differential effects of bradykinin on pial venule permeability in two inbred mouse strains.
- To explore the role of genetic background in bradykinin-induced microvascular leakage.
- To understand the implications for vasogenic edema and CNS inflammation.
Main Methods:
- Intravital microscopy was used to visualize pial venules in BALB/c and SJL/J mice.
- An open cranial window technique allowed for in vivo observation.
- Fluorescein-dextran (70 kDa) was used as an indicator for microvascular leakage.
Main Results:
- SJL/J mice exhibited significant pial venule leaky site formation at 10 pM bradykinin.
- BALB/c mice were refractory to bradykinin-induced microvascular leakage.
- Bradykinin caused pial arteriole dilation in both mouse strains.
Conclusions:
- Genetically controlled differences in vascular sensitivity to bradykinin exist between mouse strains.
- These differences in vascular response and inflammatory peptide localization may influence CNS edema and inflammation.
- Understanding these genetic variations is important for developing treatments for CNS trauma and disease.