- Email: [email protected]
Species differences in catecholamine resistance
64 A Haldenstrtim, A SPECIES DIFFERENCES IN CATECHOLAMINE RESISTANCE. Departments of Medicine I and CliniHjalmarson, 0 Poupa and L Thornell. University of Gateborg, Goteborg cal Physiology, Sahlgren's Hospital, and Department of Anatomy, University of Umea, Umeh, Sweden. living at high altitude) and In this study, guinea pigs (GP; normally rats (living at low altitude) were injected with isoprenaline (IP). Hearts from untreated animals of the two species were perfused with noradrenaline (NA) in bicarbonate buffer. Results: IP-treated GP showed less signs of histological necrosis than rats. GP myocardium also showed a better capillarization with myofibers GP hearts perfused with NA reof a smaller diameter t$an that of rats. leased less ASAT (0.23 - 0.05 ukat/l) to the perfusion buffer than rats (1.0 + 0.23 ukat/l) (p < 0.05). ATP levels were initially higher in GP (35 2 1.53 umol/g d w) than in rats (26 f 2.19 umol/g d WI (p < 0.05) but were reduced to the same extent compared to rats. Glycogen levels were initially higher in GP (38.9 t 3.7 umol/g d w) than rats (23.5 5 1.8) (p < 0.051, but were far more reduced during MA perfusion (rats 10 k 0.8; GP 1.89 l 0.45; p < 0.05). Comments: Myocardial glycogen levels and utilization as well as better capillarization are probably one important explanation to the better reThis could also be one reason for sistance of GP to anoxia and catechols. the lower incidence of AMI of people living at high altitude as Mortimer (1977) has shown that people living at high altitude run a lower risk to get AMI.
REGULATION OF SODIUM PUMP DENSITY DURING PROLONGED DIETARY POTASSIUM DEPLETION. J. P. T. Ward and I. R. Cameron, Dept. of Medicine, St. Thomas's Hospital, London, S. E. 1. During prolonged dietary potassium depletion in NZW rabbits the heart does not lose potassium although skeletal muscle intracellular potassium may fall by 25%. If the animals are then returned to a normal diet there is a significant increase of potassium in cardiac tissue after a week, whereas skeletal muscle returns to normal. After three weeks all tissues are back to control values (Hall and Cameron, J. Physiol. 251, 7Op, 1975). This 'overshoot' in the heart suggests a protective mechanism that comes into play during depletion, but persists for at least one week of repletion. In an attempt to elucidate this mechan'sm we found that uptake of b2K into cardiac tissue was maintained at low Kf ],,in depleted animals, and that the maximally stimulated rate of uptake c as increased (Ward and Cameron, Clin. Sci. 55, 5p, 1978). These findings would be compatible with an increase in activity or number of sodium pump sites in the heart, and so we have attempted to yuantitate pump density by specific binding of 3H-ouabain to cardiac membranes. There was a significant increase in the number of binding sites for 3H-ouabain in membranes prepared from depleted animals, and this increase was still present, though reduced, after one week's repletion. (Control 21.1 -+ 0.5; depleted 31.0 2 0.9; repleted 27.9 2 1.2 pmoles mg protein-l 2 SEM, ~(0.01 in both cases). This suggests that potassium depletion stimulates synthesis of Na+-K' ATPase.
REGULATION OF SODIUM PUMP DENSITY DURING PROLONGED DIETARY POTASSIUM DEPLETION. J. P. T. Ward and I. R. Cameron, Dept. of Medicine, St. Thomas's Hospital, London, S. E. 1. During prolonged dietary potassium depletion in NZW rabbits the heart does not lose potassium although skeletal muscle intracellular potassium may fall by 25%. If the animals are then returned to a normal diet there is a significant increase of potassium in cardiac tissue after a week, whereas skeletal muscle returns to normal. After three weeks all tissues are back to control values (Hall and Cameron, J. Physiol. 251, 7Op, 1975). This 'overshoot' in the heart suggests a protective mechanism that comes into play during depletion, but persists for at least one week of repletion. In an attempt to elucidate this mechan'sm we found that uptake of b2K into cardiac tissue was maintained at low Kf ],,in depleted animals, and that the maximally stimulated rate of uptake c as increased (Ward and Cameron, Clin. Sci. 55, 5p, 1978). These findings would be compatible with an increase in activity or number of sodium pump sites in the heart, and so we have attempted to yuantitate pump density by specific binding of 3H-ouabain to cardiac membranes. There was a significant increase in the number of binding sites for 3H-ouabain in membranes prepared from depleted animals, and this increase was still present, though reduced, after one week's repletion. (Control 21.1 -+ 0.5; depleted 31.0 2 0.9; repleted 27.9 2 1.2 pmoles mg protein-l 2 SEM, ~(0.01 in both cases). This suggests that potassium depletion stimulates synthesis of Na+-K' ATPase.