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To the Editor:We read with great interest the recent article by Bowers et al1 dealing with the role of calcitonin gene-related peptide (CGRP) in hypertension-induced renal damage. The results of their study demonstrated that the deoxycorticosterone (DOC)-salt hypertensive α-CGRP knockout (KO) mice displayed markedly enhanced and progressive renal damage and expression of inflammatory markers in the immunohistochemical investigation. In addition, they indicated that the DOC-salt hypertensive α-CGRP KO mice exhibited elevated urinary biomarkers of oxidative stress and a marked reduction in kidney function compared with the DOC-salt wild-type mice. The authors proposed that sensory nerves, via α-CGRP, might be renoprotective against hypertension-induced damage.Several studies have reported that enhanced activity of sympathetic nervous system might actively participate in the pathogenesis of renal damage in hypertension.2,3,4 In a study we presented previously, the change in norepinephrine (NE) release induced by α-CGRP was investigated in rat central nervous system.5 In an in vitro study, we showed …

Calcitonin Gene-Related Peptide and Sympathetic Nervous System in Hypertension-Induced Renal Damage