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Nitric oxide release in rat skeletal muscle capillary
1John P. Robarts Research Institute, University of Western Ontario, London, Canada.
The American Journal of Physiology
|May 1, 1996
Summary
This study reveals that nitric oxide (NO) is released from capillary endothelial cells (EC), influencing capillary blood flow and leukocyte adhesion. Bradykinin (BK) stimulates NO release, potentially causing vasodilation in microvasculature.
Area of Science:
- Physiology
- Microcirculation Research
- Endothelial Cell Biology
Background:
- Nitric oxide (NO) is a known vasodilator in large vessels, released by endothelial cells (EC).
- NO release from the capillary bed, the largest source of EC, has not been previously examined.
- Understanding capillary NO release is crucial for comprehending microvascular regulation.
Purpose of the Study:
- To investigate the release and function of nitric oxide (NO) in the capillary bed.
- To determine the effect of NO synthase inhibition on capillary blood flow and leukocyte adhesion.
- To examine the role of NO in mediating responses to vasodilators like bradykinin (BK).
Main Methods:
- Intravital microscopy was employed to observe the microvasculature of rat extensor digitorum longus muscle.
- NG-nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor, was locally applied to capillaries, arterioles, and venules.
- Red blood cell (RBC) velocity and flux, arteriolar and venule diameter, and leukocyte adhesion were measured.
- The effects of bradykinin (BK) on microvascular parameters were assessed with and without L-NAME pretreatment.
Main Results:
- Local application of L-NAME to capillaries significantly reduced RBC velocity and flux, increased hemoconcentration, and elevated leukocyte adhesion.
- L-NAME did not alter feeding arteriole or draining venule diameter when applied locally.
- Bradykinin (BK) application increased capillary RBC velocity and arteriolar diameter, a response abolished by L-NAME pretreatment.
- L-NAME applied to arterioles or venules did not affect capillary RBC velocity.
Conclusions:
- Nitric oxide (NO) is released from capillary endothelial cells (EC) under basal conditions and in response to bradykinin (BK).
- Basal NO release modulates capillary blood flow by affecting hemoconcentration and leukocyte adhesion.
- Stimulated NO release, as induced by BK, may contribute to remote vasodilation and increased microvascular blood flow.