Intercellular vascular smooth muscle
calcium results in vasoconstriction and is therefore a potentially adverse mechanism of increased afterload in chronic
congestive heart failure. Therefore, an evaluation was made of supine and tilt hemodynamic data, sympathetic reflexes, and the hormonal response to
calcium channel antagonism after administration of
nifedipine in nine patients with severe chronic
congestive heart failure. After
a 10 mg oral dose, the peak hemodynamic response occurred at 30 minutes and was characterized primarily by afterload reduction, improvement of systemic flow, and reduction of
pulmonary hypertension. Despite reduction of supine blood pressure, there was no
orthostatic hypotension during head-up tilt at the same time of peak response. Reflex responses to sympathetic stimulation (cold pressor test) were improved but still attenuated when compared with normal responses. Plasma
renin activity increased significantly, but a dissociation of the
aldosterone response was observed. Plasma
catecholamine levels were not significantly altered. In summary,
calcium antagonism resulted in significant afterload reduction and hemodynamic improvement in chronic
congestive heart failure. This was associated with improved reflex responsiveness and, potentially, altered other
vasoconstrictor hormones independently of the hemodynamic response.
Calcium antagonism may provide a means to further understand
vasoconstrictor mechanisms in
heart failure and enhance
therapy in appropriate patient subsets.