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(Hypertension. 2005;46:e23.)
© 2005 American Heart Association, Inc.

Hypertension Electronic Pages

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

Division of Cardiology, Department of Medicine, Wakayama Medical University, Wakayama, Japan

An extract of the first 250 words of the full text is provided, because this article has no abstract.

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 -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 -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 -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 -CGRP was investigated in rat central nervous system.⁵ In an in vitro study, we showed that -CGRP inhibited the stimulation-evoked NE release in a dose-dependent manner.⁵ It was also demonstrated that a dihydropyridine-sensitive calcium (Ca) channel agonist Bay K 8644 significantly reversed the inhibitory effect of -CGRP on NE release, indicating that -CGRP might partially interact with dihydropyridine-sensitive Ca channels and modulate intracellular Ca mobilization. Furthermore, we showed that the inhibitory action of -CGRP on NE release was significantly attenuated in spontaneously hypertensive rats compared with normotensive rats.⁶ In the peripheral tissues, Ohhashi and Jacobowitz⁷ observed that -CGRP reduced the electrical stimulation–induced contraction of rat vas deferens, suggesting that -CGRP . . . [Full Text of this Article]

Mark C. Bowers

Texas A&M University System Health Science Center, College of Medicine, Scott and White Health System, Department of Medicine, Temple, Texas

Khurshed A. Katki

Texas A&M University System Health Science Center, College of Medicine, Scott and White Health System, Department of Medicine, Temple, Texas

Arundhati Rao

Scott and White Health System, Department of Pathology, Temple, Texas

Michael Koehler

Texas A&M University System Health Science Center, College of Medicine, Scott and White Health System, Department of Medicine, Temple, Texas

Parag Patel

Scott and White Health System, Department of Pathology, Temple, Texas

Alvin Spiekerman

Scott and White Health System, Department of Pathology, Temple, Texas

Donald J. DiPette

Texas A&M University System Health Science Center, College of Medicine, Scott and White Health System, Department of Medicine, Temple, Texas

Scott C. Supowit

Texas A&M University System Health Science Center, College of Medicine, Scott and White Health System, Department of Medicine, Temple, Texas