alpha-adrenergic receptor

TCAs act by blocking presynaptic reuptake of norepinephrine or serotonin; they theoretically increase the effects of direct- or indirect-acting agonists at these synapses.[4] TCAs may also block alpha-adrenergic receptors, which causes hypotension resulting from reduction of myocardial contractility and systemic vascular resistance.[4],[5] TCAs inhibit Na/K-ATPase and act like quinidine-like antiarrhythmics by stabilizing excitable membranes and delaying His bundle conduction.

TABLE 1: Alpha-adrenergic receptor gene expression in the kidney cortex of Zucker lean (ZL), untreated Zucker diabetic fatty (ZD), and fenofibrate-treated diabetic fatty (F-ZD) rats.

It showed that blocking the beta-receptor alone promotes cardiac remodelling via growth of cardiac fibroblasts induced by alpha-adrenergic receptor signaling.

Nevertheless the measurement of alpha-adrenergic receptor subtypes via PCR is a well-established method to investigate the adrenergic receptor system in hypertensive patients.

(5) At that time, it was shown that aerobic exercisers had greater alpha-adrenergic receptor density and significantly lower beta-adrenergic receptor density than weight trainers.