A COMPARISON OF VASOPRESSIN AND NORADRENALINE ON OXYGEN-UPTAKE BY PERFUSED RAT HINDLIMB, KIDNEY, INTESTINE AND MESENTERIC ARCADE SUGGESTS THAT IT IS IN PART DUE TO CONTRACTILE WORK BY BLOOD-VESSELS

1. The rat hindlimb, kidney and intestine were each perfused in a nonrecirculating mode at 25°C using an artificial perfusate (initial pressure 85 ± 5 mmHg) and the effects of vasopressin and noradrenaline on oxygen uptake and perfusion pressure determined. 2. Both vasopressin (K0.5 = 0.1 nM) and noradrenaline (K0.5 = 2 nM) increased oxygen uptake as well as perfusion pressure by the perfused hindlimb; changes in oxygen uptake were closely matched by changes in pressure. The maximum increase in oxygen uptake was approx. 9 μmol/hr per g wet wt of hindlimb. 3. The perfused kidney also responded to vasopressin and noradrenaline with parallel increases in oxygen uptake and perfusion pressure for each agent. The largest increase in oxygen uptake was approx. 30 μmol/hr per g wet wt but this was not maximal. 4. Vasopressin increased oxygen uptake and pressure by the perfused intestine over the range 0.01-2 nM, but the changes in pressure only became significant at doses >0.1 nM. 5. Noradrenaline inhibited oxygen uptake and increased perfusion pressure in a dose-dependent manner at pharmacological concentrations (> 30 nM) when shunting of perfusate may have contributed to unperfused regions. 6. A network of mesenteric blood vessels estimated to contain approx. 6% vascular tissue by weight, with the remainder white fat cells, lymphatics and connective tissue, was also perfused. 7. Vasopressin (K0.5 = 0.3 nM) and noradrenaline (K0.5 = 30 nM) each increased oxygen uptake and perfusion pressure in a dose-dependent manner. 8. Calculations, based on the vascular tissue content and the overall oxygen uptake in the mesenteric artery preparation suggest that perfused blood vessels consume oxygen at very high rates (115 μmol/hr per g wet wt at 25°C) and that this consumption is further increased by 75% when the smooth muscle constricts. 9. It is concluded that agonist-mediated constriction of blood vessels is energetically expensive and that the consumption of oxygen for this process has significant implications for whole body thermogenesis. © 1990.