The mechanism and the mediator(s) responsible for translation of changes in perfusion pressure into alterations in coronary vascular resistance to maintain blood flow constant remains unknown. However, several hypotheses have been proposed. Myogenic factors—the shear forces of perfusion pressure on vascular smooth muscles may mediate constriction. As perfusion pressure increases, the distending pressure on the vessel wall musculature causes reflex spasm, and returns blood flow to the previous steady state level. This phenomenon cannot explain coronary autoregulation in its entirety. buy asthma inhalers
Metabolic controls—this potential mechanism of autoregulation shares the principles of metabolic control of blood flow, namely: maintenance of a set-point concentration of a metabolite (or metabolites) is the goal of the regulatory system. If the concentration of this substance decreases as a result of increased perfusion pressure and blood flow, vascular smooth muscles constrict and coronary blood flow is limited until the previously established concentration of the above metabolite is reached. Adenosine was noted as the prototypic agent under metabolic control of blood flow, however, as previously noted, there seems to be a variety of potential mediators that work in concert.