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Cerebral arteriolar regulation by eNOS and nNOS during hypotension and reduced oxygen tension
Author(s) -
Bauser Holly D.,
Bohlen Glenn
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.a278-a
Subject(s) - oxygen tension , microcirculation , chemistry , vasodilation , autoregulation , anesthesia , medicine , oxygen , cerebral blood flow , blood pressure , endocrinology , cardiology , organic chemistry
Prior studies indicate decreased blood flow and impaired regulation of blood flow in the brain when NOS is blocked. The signal neural and endothelial cells use to activate NOS during hypotension may involve decreased oxygen. We tested the hypothesis that hypotension causes a decline in perivascular PO2 despite autoregulation of blood flow. The in vivo parietal cortex microcirculation of rats was observed while measuring NO and oxygen with microelectrodes. The perivascular PO2 declined in proportion to arterial pressure while the arteriolar wall [NO] and diameter increased. To determine if a simple decrease in PO2 at a normal arterial pressure stimulated increased NO and caused dilation, the bath PO2 was lowered from ~ 40 mmHg to ~10 mmHg. Decreasing periarteriolar oxygen tension was associated with dilation and increased vessel wall [NO]. To determine the role of nNOS in oxygen sensing, blockade by N‐(4S) −4‐amino−5‐[2‐(2‐aminoethyl)‐phemylamino]‐pentyl‐N‐nitroguanidine was used. Arteriolar dilation to lowered oxygen tension was strongly suppressed. The involvement of the Na+/Ca2+ exchanger was tested during decreased PO2 using KB‐R7943. After blockade, the periateriolar NO concentration did not increase at lowered PO2. These results suggest that the Na+/Ca2+ exchanger acting through endothelial and neuronal NOS generates NO in the brain when O2 availability declines. (Supported by NIH HL‐20605)