A Neuro-Immune Approach In Understanding Acute Kidney Injury
Abstract
Acute kidney injury (AKI) is a significant health concern. The primary causes of AKI are
ischemia, sepsis and nephrotoxicity. Acute kidney injury is mediated by both adaptive and innate
immune systems. The role of the nervous system in the activation of immune response and vice-
versa is becoming a topic of interest in acute kidney injury. The two systems have a different
mode of action. While the nervous system is static, its functions are executed by nerve fibers
everywhere in the body. The immune system, on the other hand, is largely migratory in its
responses using the blood, lymphatic vessels, and lymphoid organs to recruit mediators to sites
of interest.
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CGRP does not directly influence the basal blood
pressure, but it is dependent upon factors such as angiotensin II, glucocorticoids, nerve growth
factor, and sympathetic nerve reflexes. CGRP receptors cause vascular relaxation through direct
action on smooth muscle cells via increasing the cAMP levels [18, 19 pp2]. CGRP also
downregulates the expression of acetylacholinestrase at the transcription level [35 pp 1].
Kidney is the second largest known site for CGRP clearance [8147781]. But kidney does not
solely account for degradation of CGRP, other more generalized degradative systems such as
endothelial-bound enzymes of blood vessels are suspected to be involved [Braslis,1988].
Its vasodilatation effects depend on other processes such as RAAS, oxidative stress and other
inflammatory molecules. The feature that distincts CGRP from other vasodilators is its long
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duration of action. CGRP is involved in increase in inflammation; increase the number of
circulating cells and chemotactic factors, neuronal plasticity and synapse formation
[17002803][pgi pr]. CGRP is a key regulatory neuropeptide with important roles in immune
outcome and inflammatory mediators such as