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Inhibition of nNOS Changes Cerebrovascular Responses to Acute Hypertension
Author(s) -
Talman William T.,
Dragon Deidre Nitschke
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a294-a
Subject(s) - medicine , phenylephrine , autoregulation , basal (medicine) , acetylcholine , vasodilation , blood pressure , cerebral arteries , nitric oxide , cerebral blood flow , nitric oxide synthase , anesthesia , cerebral autoregulation , cerebral circulation , endocrinology , cardiology , insulin
Interruption of parasympathetic nitroxidergic nerves to cerebral blood vessels or systemic administration of a nitric oxide synthase (NOS) inhibitor attenuates breakthrough of cerebrovascular autoregulation during acute hypertension. We hypothesized that neuronal NOS (nNOS) in parasympathetic fibers participated in the cerebrovascular effect and tested the hypothesis by administering the selective nNOS inhibitor propyl‐L‐arginine (PLA) or vehicle control into a cranial window. We first assessed the influence of PLA on cerebrovascular responses to acetylcholine (ACh; 10 −5 M), which promotes synthesis of NO through endothelial NOS. We then increased mean arterial pressure (MAP) with intravenous phenylephrine (PE) while monitoring the diameter of cerebral arteries (41 ± 3 μm basal diameter). There was no significant change in dilatation in response to ACh before (7 ± 1 %) vs. after (5 ± 2 %) PLA. Basal MAP did not differ between groups. Vascular diameters increased significantly (p<0.05) less in animals that received the nNOS inhibitor (18 ± 6 μm) than in control rats (70 ± 15 μm) despite there being no significant difference in the change in MAP between groups. These findings further support our hypothesis that parasympathetic nitroxidergic innervation of cerebral blood vessels may participate in regulating cerebrovascular tone during hypertension. Support: VA Merit Review and NIH R01 HL59593.