Abstract
The candidates for circulatory mediators are evaluated in venous effluent from mucles. In chemical analyses experiments the muscle preparation has been perfused by a pump with arterial blood at a constant flow rate. During isotonic contractions produced by brief tetanic stimulation every 2 seconds or by twitch stimulation at 2 per second, venous potassium, inorganic phosphate, osmolarity and pCO2 increase, and pH and pO2 decrease. Among these factors, however, vascular resistance correlates to only venous potassium concentration (P<0.05) and pO2 (P<0.001). There is also a close inverse relationship between venous potassium and pO2 (P<0.001). At the beginning of reactive hyperemia after 2-min ischemia, only venous pO2 reduces maximally and recovers in parallel with the course of the hyperemia. Venous potassium slightly decreases during reactive hyperemia. In bioassay experiments the muscle and the kidney preparation have been supplied with donor's arterial blood through two separate pumps at constant flow rates. A part of venous effluent from muscles has been admixed to renal arterial blood by a third pump. Exercise and reactive hyperemias induce renal vasoconstriction in 5 out of 7 cases, which indicates release of adenosine and/or AMP. In conclusion, released potassium, local hypoxia, and adenosine and/or AMP contribute to exercise hyperemia. For reactive hyperemia the latter two factors seem to be responsible. After ischemic contraction adenosine and/or AMP may play a major role.
