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Changes of Sodium and ATP Affinities of Renal
Na,K-ATPase During and After Nitric Oxide-Deficient Hypertension
N. VRBJAR, V. JAVORKOVÁ, O.
PECHÁŇOVÁ1
Department of Biochemistry, Institute for
Heart Research and 1Institute of Normal and Pathological
Physiology, Slovak Academy of Sciences, Bratislava, Slovak
Republic
Received October 2, 2001
Accepted February 11, 2002
Summary
The aim of this study was to assess the molecular basis of renal
Na,K-ATPase disturbances in response to NO-deficient
hypertension induced in rats by NO-synthase inhibition with 40
mg/kg/day NG-nitro-L-arginine methyl ester (L-NAME) for four
weeks. After 4-week administration of L-NAME, the systolic blood
pressure (SBP) increased by 30 %. Three weeks after terminating
the treatment, SBP recovered to control value. When activating
the Na,K-ATPase with its substrate ATP, a 36 % increase in Km
and 29 % decrease in Vmax values were observed in NO-deficient
rats. During activation with Na+, the Vmax was decreased by 20 %
and the KNa was increased by 111 %, indicating a profound
decrease in the affinity of the Na+-binding site in NO-deficient
rats. After spontaneous recovery from hypertension, the Vmax
remained at the level as in hypertension for both types of
enzyme activation. However, in the presence of lower
concentrations of substrate which are of physiological relevance
an improvement of the enzyme activity was observed as documented
by return of Km for ATP to control value. The KNa value for Na+
was decreased by 27 % as compared to hypertension, but still
exceeded the corresponding value in the control group by 55 %
thus resulting in a partial restoration of Na+ affinity of
Na,K-ATPase which was depressed as a consequence of NO-dependent
hypertension.
Key
words
Sodium pump · Nitric oxide · Hypertension · L-NAME · Kidney
Reprint
requests
N. Vrbjar, Institute for Heart Research, Department of
Biochemistry, Slovak Academy of Sciences, Dúbravská cesta 9, 842
33 Bratislava, Slovak Republic, FAX: +421 2 5477 6637, E-mail:
usrdnorb@savba.sk
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