Affiliation:
1. From the Institute for Biodiagnostics, National Research Council, Winnipeg, Canada. National Research Council publication NRC 34759.
Abstract
Abstract
The aims of this study were to characterize the routes of influx of the K
+
congener, Rb
+
, into cardiac cells in the perfused rat heart and to evaluate their links to the intracellular Na
+
concentration ([Na
+
]
i
) using
87
Rb and
23
Na nuclear magnetic resonance (NMR) spectroscopy. The rate constant for Rb
+
equilibration in the extracellular space was 8.5 times higher than that for the intracellular space. The sensitivity of the rate of Rb
+
accumulation in the intracellular space of the perfused rat heart to the inhibitors of the K
+
and Na
+
transport systems has been analyzed. The Rb
+
influx rates were measured in both beating and arrested hearts: both procaine (5 mmol/L) and lidocaine (1 mmol/L) halved the Rb
+
influx rate. In procaine-arrested hearts, the Na
+
,K
+
-ATPase inhibitor ouabain (0.6 mmol/L) decreased Rb
+
influx by 76±24% relative to that observed in untreated but arrested hearts. Rb
+
uptake was insensitive to the K
+
channel blocker 4-aminopyridine (1 mmol/L). The inhibitor of Na
+
/K
+
/2 Cl
−
cotransport bumetanide (30 μmol/L) decreased Rb
+
uptake only slightly (by 9±8%). Rb
+
uptake was dependent on [Na
+
]
i
: it increased by 58±34% when [Na
+
]
i
was increased with the Na
+
ionophore monensin (1 μmol/L) and decreased by 48±9% when [Na
+
]
i
was decreased by the Na
+
channel blockers procaine and lidocaine. Dimethylamiloride (15 to 20 μmol/L), an inhibitor of the Na
+
/H
+
exchanger, slightly reduced [Na
+
]
i
and Rb
+
entry into the cardiomyocytes (by 15±5%).
31
P NMR spectroscopy was used to monitor the energetic state and intracellular pH (pH
i
) in a parallel series of hearts. Treatment of the hearts with lidocaine, 4-aminopyridine, dimethylamiloride, or bumetanide for 15 to 20 minutes at the same concentrations as used for the Rb
+
and Na
+
experiments did not markedly affect the levels of the phosphate metabolites or pH
i
. These data show that under normal physiological conditions, Rb
+
influx occurs mainly through Na
+
,K
+
-ATPase; the contribution of the Na
+
/K
+
/2 Cl
−
cotransporter and K
+
channels to Rb
+
influx is small. The correlation between Rb
+
influx and [Na
+
]
i
during infusion of drugs that affect [Na
+
]
i
indicates that, in rat hearts at 37°C, Rb
+
influx can serve as a measure of Na
+
influx. We estimate that, at normothermia, at least 50% of the Na
+
entry into beating cardiac cells is provided by the Na
+
channels, with only minor contributions (<15%) from the Na
+
/K
+
/2 Cl
−
cotransporter and the Na
+
/H
+
exchanger.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Cardiology and Cardiovascular Medicine,Physiology
Reference40 articles.
1. Horres CR Wheeler DM Piwnica-Worms D Lieberman M. Ion transport in cultured heart cells. In: Pinson A ed. The Heart Cell in Culture . Boca Raton Fla: CRC Press; 1987;1:77-108.
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