K+/H+ antiport in heart mitochondria

Area of Science:

• Mitochondrial physiology
• Membrane transport

Background:

• Divalent cations like Mg2+ are crucial for mitochondrial function.
• Mitochondrial dysfunction can lead to altered ion permeability and swelling.

Purpose of the Study:

• To investigate ion transport mechanisms in divalent cation-depleted heart mitochondria.
• To explore the role of a potential K+/H+ antiport in mitochondrial swelling and cation exchange.

Main Methods:

• Heart mitochondria were depleted of divalent cations using A23187 and EDTA.
• Mitochondrial swelling and 42K+ (potassium-42) exchange were measured under various conditions (e.g., different K+ salts, presence of uncouplers, pH changes).
• Effects of inhibitors (Mg2+, quinine, dicyclohexylcarbodiimide) and hypotonic conditions were assessed.

Main Results:

• Divalent cation-depleted mitochondria swelled in K+ acetate or K+ nitrate with uncouplers.
• These mitochondria exhibited passive 42K+ exchange with external K+, Na+, or Li+, independent of respiration.
• Both swelling and exchange were inhibited by Mg2+ and activated at alkaline pH. Swelling was inhibited by dicyclohexylcarbodiimide, while exchange was not.
• Mg2+-depleted mitochondria showed increased permeability to H+, anions, and cations.

Conclusions:

• Observed swelling and cation exchange are consistent with a Mg2+- and H+-sensitive K+/H+ antiport.
• However, the data do not provide definitive proof for the K+/H+ antiport's involvement.
• Generalized membrane permeability changes likely contribute to ion movement in these depleted mitochondria.