The neural control of the kidneys is through the sympathetic nervous system, efferent renal sympathetic nerves innervation and neuroeffector junctions have been identified along the renal vasculature, the tubules, the granular cells of juxtaglomerular apparatus (Kate etal, 2004; Edward etal, 2011). The action of sympathetic system is via the release the norepinephrine at sympathetic nerve terminals into the interstitial space. A moderately high levels of nerve stimulation has more effect on efferent arteriole than afferent thereby the RBF fall more than the GFR in consistent with efferent arteriolar constriction, however at maximal nerve stimulation afferent vasoconstriction predominates and leads to drastic reductions in both RBF and GFR
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Dopaminergic nerve fibers have been reported to terminate in the kidney, however the physiologic significance of these nerves is unclear (Sterns, 2013). Dopamine is synthesized within the kidney in the proximal tubule via the decarboxylation of circulating L-3,4-dihydroxyphenylalanine (L-DOPA) by the enzyme L-amino acid decarboxylase and discharged into membrane into the lumen, where it bind to and activate specific dopaminergic receptors (Carey, 2001) . It acts locally to exert its actions in a paracrine and autocrine fashion and the major effects is increase in renal blood flow and natriuretic response. Dopamine receptors are classified into the D1 and the D2 subtype families, dopamine D1 receptor stimulation results in renal vasodilatation and natriuresis while dopamine D2 receptors may play a synergistic role in the dopamine modulated natriuresis (Cheung and Barrington, 1996).
L-DOPA is derives from the amino acids L-phenylalanine and L-tyrosine and increased availability of these by protein diet intake will enhance intrarenal dopamine synthesis, thus it was hypothesised that the amino acid-induced glomerular hyperfiltration might due to increased dopamine secretion. In line with this, studies in human has demonstrated an increase in dopamine secretion after a high protein meal (WILLIAMS etal. 1986;