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(Hypertension. 1998;31:719-720.)
© 1998 American Heart Association, Inc.

Letters to the Editor

Central Nervous System Is Not Involved in Initiation of the Pressor Effect of 7-Nitroindazole in Urethane-Anesthetized Rats

Yuri Zagvazdin; Anton Reiner; ; Ibrahim F. Benter

Department of Anatomy and Neurobiology, University of Tennessee, Memphis, Tenn
Department of Pharmacology, Southern College of Optometry, Memphis, Tenn

To the Editor:

We read with interest the article by Sander et al¹ ; it provided a valuable update on the controversies concerning the role of the inhibition of neuronal nitric oxide synthase (NOS) acting within the central sympathetic nervous system (CNS) in the systemic hypertension caused by NOS inhibition. Some authors have suggested that neuronal NO is involved in the tonic restraint of sympathetic vasoconstrictor outflow from the CNS. Removal of such restraint by inhibition of neuronal NOS should, in principle, lead to sympathetic activation and increased systemic blood pressure. After careful analysis of published studies in this area and their own work, Sander et al concluded that central inhibition of NOS does not contribute to the onset of hypertension after systemic NOS inhibition in conscious animals, but it does contribute to the long-term maintenance of such hypertension in conscious rats. Sander et al noted that support for a neurogenic component in NOS-induced hypertension was, however, evident in studies of anesthetized animals. The authors did not clarify whether this effect was on initiation or maintenance of hypertension or both. Some studies in anesthetized rats that were not noted by Sander et al, however, did not support a neurogenic component in the hypertension induced by L-arginine–derived NOS inhibitors.^{2 3 4} On the other hand, the rapid pressor effect of diphenyleneiodonium, an NOS inhibitor that is chemically distinct from N^G-substituted arginine analogs, does appear to be CNS-dependent in anesthetized rats.⁵ The basis of these conflicting data on the role of a . . . [Full Text of this Article]

Mikael Sander; Jim Hansen; ; Ronald G. Victor

Molecular Cardiology Laboratories, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Tex