Altered purine nucleotide degradation during exercise in patients with essential hypertension

Purine degradation occurs during strenuous muscle exercise and plasma levels of hypoxanthine (HX), purine degradation intermediate, increase. Purine nucleotide degradation has not been investigated in patients with essential hypertension (HTN). The present study determined whether purine nucleotide degradation is altered in patients with HTN. Cardiopulmonary exercise test was performed with serial measurements in blood lactate and plasma HX in 24 patients (14 men and 10 women) with essential HTN (World Health Organization [WHO] class I to II; mean age, 57.7 [plusmn] 2.1 years) and 24 age-, sex-matched normal subjects. Exercise was terminated either by severe fatigue or excess blood pressure increase. Peak work rate (WR) (normal v HTN, 151 [plusmn] 10 v 135 [plusmn] 8 W, not significant [NS]) was not different, but peak oxygen uptake (peak Vo2, 26.3 [plusmn] 1.5 v 22.2 [plusmn] 0.9 mL/min/kg, P [lt ] .05) and anaerobic threshold were lower in patients with HTN. Resting levels of blood lactate and plasma HX were similar, but the increment from rest to peak exercise ([Delta ]) for lactate ([Delta ]lactate: 4.4 [plusmn] 0.4 v 3.4 [plusmn] 0.4 mmol/L, P [lt ] .05) and for HX ([Delta ]HX, 15.9 [plusmn] 2.2 v 9.1 [plusmn] 1.1 [mu ]mol/L, P [lt ] .05) were significantly smaller in patients with HTN. When normalized by the peak WR, [Delta ]HX/peak WR (0.105 [plusmn] 0.013 v 0.069 [plusmn] 0.007 [mu ]mol/L/W, P [lt ] .05) was significantly lower in patients with HTN. Patients with HTN exhibited reduced HX response to exercise with impaired exercise capacity. The exercise-induced changes in plasma HX were smaller in patients with HT when normalized with peak WR. These results suggest that the purine nucleotide degradation is reduced in patients with HTN.