Pharmacology and inotropic potential of forskolin in the human heart.
Key result
Forskolin activated human myocardial adenylate cyclase with maximal effects 4.82 and 6.13 times greater than isoproterenol in normal and failing left ventricles, respectively.
Authors
Discussion
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Implication
Does not support clinical use; leaves open direct cyclase activation as a hypothesis-generating target in HF.
PICO
P
Population
Heart failure (n=16)
I
Intervention / Comparator
Forskolin vs Isoproterenol (0.1 mM)
O
Primary Outcome
Maximal adenylate cyclase stimulation
Limitations
- As a nonspecific activator of adenylate cyclase, forskolin may prove to be too toxic to be used clinically.
- Positive chronotropic effects observed in open-chest, anesthetized dogs may prove to be limiting.
Cite This Study
Bristow et al. (1984) studied Heart failure (n=16). Forskolin vs. Isoproterenol was evaluated on Maximal adenylate cyclase stimulation. Forskolin activated human myocardial adenylate cyclase with maximal effects 4.82 and 6.13 times greater than isoproterenol in normal and failing left ventricles, respectively.