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Division of Hypertension and Vascular Research, Department of Internal Medicine, Henry Ford Hospital, Detroit, Michigan 48202
Nitric oxide (NO) plays an essential
role in the maintenance of cardiovascular and renal homeostasis.
Endogenous NO is produced by three different NO synthase (NOS)
isoforms: endothelial NOS (eNOS), inducible NOS (iNOS), and neuronal
NOS (nNOS). To investigate which NOS is responsible for NO production
in different tissues, NOS knockout (
/) mice have been generated for
the three isoforms. This review focuses on the regulation of
cardiovascular and renal function in relation to blood pressure
homeostasis in the different NOS/ mice. Although regulation of
vascular tone and cardiac function in eNOS/ has been extensively
studied, far less is known about renal function in these mice.
eNOS/ mice are hypertensive, but the mechanism responsible for
their high blood pressure is still not clear. Less is known about
cardiovascular and renal control in nNOS/ mice, probably because
their blood pressure is normal. Recent data suggest that nNOS plays
important roles in cardiac function, renal homeostasis, and regulation
of vascular tone under certain conditions, but these are only now
beginning to be studied. Inasmuch as iNOS is absent from the
cardiovascular system under physiological conditions, it may become
important to blood pressure regulation only during pathological
conditions related to inflammatory processes. However, iNOS is
constitutively expressed in the kidney, where its function is largely
unknown. Overall, the study of NOS knockout mice has been very useful
and produced many answers, but it has also raised new questions. The appearance of compensatory mechanisms suggests the importance of the
different isoforms to specific processes, but it also complicates interpretation of the data. In addition, deletion of a single gene may
have physiologically significant effects in addition to those being
studied. Thus the presence or absence of a specific phenotype may not
reflect the most important physiological function of the absent gene.
endothelial nitric oxide synthase; neuronal nitric oxide synthase; inducible nitric oxide synthase; knockout mice; blood pressure
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