Functional effects of C-type natriuretic peptide and nitric oxide are attenuated in hypertrophic myocytes from pressure-overloaded mouse hearts

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Population

Ventricular myocytes from aortic stenosis-induced hypertrophic mice and age-matched control mice

Comparison

S-nitroso-N-acetyl-penicillamine (SNAP, an NO… vs Ventricular myocytes from age-matched control mice

Design

Preclinical

Authors

Discussion

Attenuated NO/CNP effects in hypertrophy should not alter clinical practice; leaves open PKG modulation as a research target in cardiac disease.

Population

Ventricular myocytes from aortic stenosis-induced hypertrophic mice and age-matched control mice

Intervention

S-nitroso-N-acetyl-penicillamine (SNAP, an NO donor, 10(-6) and 10(-5) M) or C-type natriuretic peptide (CNP, 10(-8) and 10(-7) M)

Comparator

Ventricular myocytes from age-matched control mice

Outcome

Contractile function (percentage shortening, maximal rates of shortening and relaxation)surrogate

The negative inotropic effects of NO and CNP are attenuated in hypertrophic cardiac myocytes due to diminished cGMP-dependent kinase (PKG) signaling.

Su et al. (2004) studied this question.

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Attenuated NO/CNP effects in hypertrophy should not alter clinical practice; leaves open PKG modulation as a research target in cardiac disease.