(Circulation. 1997;95:2303-2311.)
© 1997 American Heart Association, Inc.
Articles |
Effects of the Nitric Oxide Donor Sodium Nitroprusside on Intracellular pH and Contraction in Hypertrophied Myocytes
From the Charles A. Dana Research Institute, the Harvard-Thorndike Laboratory, and the Department of Medicine (Cardiovascular Division), Beth Israel Deaconess Medical Center, and Harvard Medical School, Boston, Mass, and the Department of Medicine (K.W.S.), University of Utah School of Medicine, Salt Lake City.
Correspondence to Beverly H. Lorell, MD, Cardiovascular Division, Beth Israel Deaconess Medical Center, 330 Brookline Ave, Boston, MA 02215.
Background We compared the effects of the nitric oxide donor sodium nitroprusside (SNP) on intracellular pH (pHi), intracellular calcium concentration ([Ca2+]i) transients, and cell contraction in hypertrophied adult ventricular myocytes from aortic-banded rats and age-matched controls.
Methods and Results pHi was measured in individual myocytes with SNARF-1, and [Ca2+]i transients were measured with indo 1 simultaneously with cell motion. Experiments were performed at 37°C in myocytes paced at 0.5 Hz in HEPES-buffered solution (extracellular pH=7.40). At baseline, calibrated pHi, diastolic and systolic [Ca2+]i values, and the amplitude of cell contraction were similar in hypertrophied and control myocytes. Exposure of the control myocytes to 10-6 mol/L SNP caused a decrease in the amplitude of cell contraction (72±7% of baseline, P<.05) that was associated with a decrease in pHi (-0.10±0.03 U, P<.05) with no change in peak systolic [Ca2+]i. In contrast, in the hypertrophied myocytes exposure to SNP did not decrease the amplitude of cell contraction or cause intracellular acidification (-0.01±0.01 U, NS). The cGMP analogue 8-bromo-cGMP depressed cell shortening and pHi in the control myocytes but failed to modify cell contraction or pHi in the hypertrophied cells. To examine the effects of SNP on Na+-H+ exchange during recovery from intracellular acidosis, cells were exposed to a pulse and washout of NH4Cl. SNP significantly depressed the rate of recovery from intracellular acidosis in the control cells compared with the rate in hypertrophied cells.
Conclusions SNP and 8-bromo-cGMP cause a negative inotropic effect and depress the rate of recovery from intracellular acidification that is mediated by Na+-H+ exchange in normal adult rat myocytes. In contrast, SNP and 8-bromo-cGMP do not modify cell contraction or pHi in hypertrophied myocytes.
Key Words: calcium • cells • contractility • hypertrophy • nitric oxide
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