Left ventricular hypertrophy (LVH) is accompanied by a rise of [Na⁺]_i (Gray et al. 2001) and a decline of pH_i (Wallis et al. 1997). The possibility that alteration of Na⁺-H⁺ exchange activity is involved in these changes was investigated by measuring the rate of pH recovery after intracellular acidosis.

LVH was induced in guinea-pigs by placing a plastic clip (2 mm diameter) around the ascending aorta under anaesthesia (0.22 ml kg^-1 sodium pentobarbitone, followed by 49 %-49 %- 2 %, N₂O-O₂-halothane mixture inhalation). Sham-operated and unoperated animals served as controls. After 40-100 days the heart was removed after humane killing and heart-to-body-weight ratio (HBR) recorded and myocytes isolated (Hall & Fry, 1992). pH_i was measured in myocytes from the left ventricle (septum and free wall) by incubation with BCECF-AM (2Ô,7Ô-bis(carboxyethyl)-5-carboxyfluorescein; 5 mM, 30 min) using epifluorescence microscopy. Myocytes were superfused with Hepes-buffered Tyrode solution at 37°C. Intracellular H⁺ buffering capacity (β_i) was estimated by addition and removal of 10 mM NH₄Cl in the presence of 1 mM amiloride as the ratio of Δ[NH₄⁺]/ΔpH_i on NH₄Cl removal. The rate of pH recovery, ΔpH_i/dt, on NH₄Cl removal in the absence of amiloride was measured and acid efflux rate calculated as the product of β_i (ΔpH_i/dt) between 30 and 150 s after the peak acidosis. Results are means ± S.D. and statistical significance assessed using Student’s t tests.

Mean pH_i was lower in myocytes from aortic constricted (AC) hearts (6.95 ± 0.08 pH units, n = 37) compared with myocytes from unoperated (7.22 ± 0.12, n = 89) or sham-operated hearts (7.20 ± 0.12, n = 37) (P < 0.001). There was a significant negative relationship between pH_i and HBR (r = -0.715, P < 0.001). β_i was significantly increased in myocytes from AC hearts (104.2 ± 25.5 mequiv l^-1 pH unit^-1, n = 19 vs. 30.5 ± 15.1, n = 75, P < 0.001) and was related to increasing HBR (r = 0.625, P < 0.001). β_i increased as steady-state pH_i fell (r = -0.80, P < 0.001). ΔpH_i/dt was slower in myocytes from AC hearts (t = 231 ± 82, n = 26, vs. 165 ± 88 s, n = 88, P < 0.001) but the net acid efflux was not significantly different in the two groups (4.2 ± 1.9, n = 21 vs. 3.7 ± 1.9 mequiv l^-1 min^-1, n = 68, P > 0.05).

LVH is accompanied by a decline in pH_i and an increase in sarcoplasmic H⁺ buffering capacity, which is pH_i dependent. The recovery from intracellular acidosis is slowed in LVH but the H⁺ extrusion rate is unchanged, suggesting that Na⁺-H⁺ exchange activity is not altered in this model of hypertrophy.

We thank the British Heart Foundation for financial assistance.

All procedures accord with current UK legislation.