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(Hypertension. 1995;26:1177-1180.)
© 1995 American Heart Association, Inc.

Articles

Regulation of Neuronal Calcitonin Gene–Related Peptide Expression

Role of Increased Blood Pressure

Scott C. Supowit; Huawei Zhao; Donna H. Wang; Donald J. DiPette

From the Departments of Internal Medicine (Division of General Internal Medicine and Hypertension Section) and Human Biological Chemistry and Genetics, University of Texas Medical Branch, Galveston.

Abstract Calcitonin gene–related peptide (CGRP) is a potent vasodilator neuropeptide. We have previously demonstrated that CGRP mRNA levels are increased in dorsal root ganglia, and immunoreactive CGRP content is elevated in the spinal cord in mineralocorticoid-salt hypertension. Dorsal root ganglia neuronal cell bodies synthesize CGRP and send axons peripherally to blood vessels and centrally to spinal cord sites involved in blood pressure regulation. This increased synthesis of a potent vasodilator is a compensatory response to attenuate the increase in blood pressure; however, it is not known if neuronal CGRP is regulated simply by the elevated blood pressure or by changes in other parameters. To determine if elevation of blood pressure in normal rats induced by the administration of a potent vasoconstrictor can increase neuronal CGRP mRNA, 7-week-old male Sprague-Dawley rats were treated for 2 weeks with either angiotensin II (n=6) or vehicle (n=6) by using implanted osmotic minipumps. After the treatment period, the angiotensin II–treated rats displayed a marked increase in systolic blood pressure (angiotensin II, 217±18 versus control, 131±3 mm Hg, P<.001), and decrease in plasma renin activity (angiotensin II, 3.7±3.5 versus control, 35.9±14.2 ng · mL^-1 · h^-1, P<.05). However, dorsal root ganglia CGRP mRNA content did not significantly differ between the two groups of rats. These results demonstrate that a marked increase in blood pressure, by itself, does not increase neuronal CGRP mRNA accumulation. We propose that in mineralocorticoid-salt hypertension there are specific changes in as yet unidentified factor(s) that modulate neuronal synthesis and release of CGRP independent of blood pressure elevation.

Key Words: calcitonin gene–related peptide • RNA • hypertension, experimental • angiotensin II • genes

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