MINIREVIEW
The Potential Role of Nitric Oxide in the Hypertrophic
Growth of the Left Ventricle
F. Šimko1, J. Šimko2
1Department of Pathophysiology, Faculty of Medicine,
Comenius University and 2Department of Genetics and
Center of Human genetics, Faculty Hospital, Bratislava, Slovak
Republic
Received July
30, 1999
Accepted September 21, 1999
Summary
Left ventricular hypertrophy (LVH) is the result of interaction
between a chronic hemodynamic overload and non-hemodynamic
factors. There are several lines of evidence presented in this
work suggesting that nitric oxide (NO) may participate in the
hypertrophic growth of the myocardium. First, endothelial NO
production was shown to be decreased in several types of
hemodynamically overloaded circulation both in animals and
humans. Second, compounds stimulating NO production were able to
diminish the extent or modify the nature of LVH in some models
of myocardial hypertrophic growth. Third, arterial hypertension
can be induced by inhibition of nitric oxide synthase activity.
This NO-deficient hypertension is associated with the
development of concentric LVH, myocardial fibrosis and protein
remodeling of the left ventricle. The mechanism of LVH
development in NO-deficient hypertension is complex and involves
decreased NO production and increased activation of the
renin-angiotensin-aldosterone system. Cardiovascular protection
via ACE inhibition in NO-deficient hypertension may be induced
by mechanisms not involving an improvement of NO production. In
conclusion, the hypertrophic growth of the LV appears to be the
result of interaction of vasoconstrictive and growth stimulating
effects of angiotensin II on the one hand and of vasodilating
and antiproliferative effects of nitric oxide on the other.
Key
words
Nitric oxide · Cardiac hypertrophy · Angiotensin II · L-NAME
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F. Šimko, M.D., Ph.D., Associate Professor, Department of Pathophysiology, Faculty of
Medicine, Sasinkova 4, 813 72 Bratislava, Slovak Republic, e-mail: simko@medik.fmed.uniba.sk.
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