Adenylate cyclase activity coupled to the stimulatory guanine nucleotide binding protein in patients having electrophysiologic studies and either structurally normal hearts or idiopathic myocardial disease

Abstract

There has been much recent interest in transmembrane signaling involving adrenergic and other receptors both in animals and humans with congestive heart failure (CHF). In patients with idiopathic dilated cardiomyopathy and severe CHF, β-adrenoceptor density and maximal adenylate cyclase activity stimulated by (−)-isoproterenol in the presence of guanosine triphosphate (GTP) are reduced. 1 Other studies in animal models of CHF preceded by myocardial hypertrophy have revealed an increase in β-adrenoceptor density accompanied by reduced receptor affinity for agonist and a decrease in the stimulatory guanine nucleotide binding protein (Gs). 2,3 To date, there are no data reporting functional alterations in Gs in humans.