Table 2.
Diabetes-Related Traditional Chronic Complication | Role of Dopamine | Effect | Rationale for Treatment (Dopamine Agonists or Levodopa) |
---|---|---|---|
Retinopathy [45,46,47,48,49,50,51,52,53,54,55] | Impaired intraretinal metabolism (deficiency) | Defective photoreceptor adaptation to light | Yes |
Chronic renal disease [56,57,58,59,60] | Impaired renal metabolism (glomerular filtration-depended reduction) | Dysregulation in water and natrium resorption; promotion of glomerular hyperfiltration; micro- and macroalbuminuria | Scanty evidence or negative results |
Neuropathy [64,65,66] | Defective axonal transport; impaired metabolism (accumulation due to inadequate conversion to noradrenaline?) | Implication for painful neuropathy | No (dopamine antagonists) |
Stroke [72,73,74,75,76,77,78] | Impaired cerebral metabolism (deficiency) | Loss of motivation, motor impairment, and pathogenic role in post-stroke neuropsychiatric disorder | Scanty evidence or negative results |
Cardiovascular diseases [61,62,63,64,65,66,67,68,69,70] | Impaired cardiac metabolism (accumulation due to inadequate conversion to noradrenaline?); striatal deficiency | Increased risk of heart failure, impaired coronary vasodilatation, cardiac autonomic neuropathy | Scanty evidence or negative results |
Table 2 summarizes the leading evidence indicating the role of dopamine in the pathophysiology of traditional diabetes-related chronic complications.