Can a single vasodilator be responsible for both coronary autoregulation and metabolic vasodilation?
To test the hypothesis that both coronary autoregulation and metabolic vasodilation can be mediated by the same substance, we have analysed measured autoregulation curves with the aid of a simple mass balance model. In an open-chest dog preparation, increasing the heart rate by pacing results in a nearly parallel shift of the autoregulation curve to a higher flow (Q) level. We assume a unique relationship between vascular conductance and interstitial concentration of a vasodilating substance [A]. Applying a compartmental mass balance, it is possible to predict with a minimum of assumptions the increase of flow between two points with increased production but having the same vasodilator concentration. The simple result of this analysis is: delta Q = delta production/[A]. If the vasodilator concentration varies by more than a factor 2 between low and high conductance points, the autoregulation curve cannot shift in a parallel fashion as a result of an increased production rate, but rather will become less and less steep. We conclude that a single vasodilator cannot be responsible for both autoregulation and metabolic vasodilation unless complex assumptions are made, for which there is as yet no experimental support.
D000241:Adenosine / Q000378:metabolism / Q000494:pharmacology*; D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects*; D004285:Dogs; D006706:Homeostasis / Q000187:drug effects*; D008955:Models, Cardiovascular; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology*
D014665:Vasodilator Agents; D000241:Adenosine