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Neural mechanisms in nitric-oxide-deficient hypertensionNitric oxide is hypothesized to be an inhibitory modulator of central sympathetic nervous outflow, and deficient neuronal nitric oxide production to cause sympathetic overactivity, which then contributes to nitric-oxide-deficient hypertension. The biochemical and neuroanatomical basis for this concept revolves around nitric oxide modulation of glutamatergic neurotransmission within brainstem vasomotor centers. The functional consequence of neuronal nitric oxide in blood pressure regulation is, however, marked by an apparent conflict in the literature. On one hand, conscious animal studies using sympathetic blockade suggest a significant role for neuronal nitric oxide deficiency in the development of nitric-oxide-deficient hypertension, and on the other hand, there is evidence against such a role derived from 'knock-out' mice lacking nitric-oxide synthase 1, the major source of neuronal nitric oxide.
Document ID
20040142100
Acquisition Source
Legacy CDMS
Document Type
Reprint (Version printed in journal)
Authors
Sander, M.
(University of Texas Southwestern Medical Center Dallas, United States)
Victor, R. G.
Blomqvist, C. G.
Date Acquired
August 22, 2013
Publication Date
January 1, 1999
Publication Information
Publication: Current opinion in nephrology and hypertension
Volume: 8
Issue: 1
ISSN: 1062-4821
Subject Category
Life Sciences (General)
Distribution Limits
Public
Copyright
Other
Keywords
Review, Tutorial
NASA Discipline Cardiopulmonary
Non-NASA Center
Review

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