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The purposes of our study were (1) to investigate whether a 3-min short-term hyperventilation leads to posthyperventilatory hypoxemia and (2) to assess the role of transcutaneous blood gas measurements for monitoring oxygen and carbon dioxide changes during and after the test. In 10 male volunteers arterial and transcutaneous blood gases were measured simultaneously before, during and after a 3-min voluntary hyperventilation maneuver. Baseline arterial PO₂ increased from 13.7 ± 0.4 kPa (103 ± 3 mm Hg) to 18.6 ± 0.3 kPa (139 ± 2.3 mm Hg; p < 0.005 compared to baseline) during hyperventilation. After the provocation test posthyperventilatory hypoxemia occurred with a minimal mean value of 7.8 ± 1.3 kPa (58.5 ± 9.8 mm Hg; p < 0.05 compared to baseline). Whereas close agreement between arterial and transcutaneous measurements was obtained for carbon dioxide values before hyperventilation, transcutaneous O₂ consistently underestimated arterial O₂. A short-term over-breathing of 3 min causes a significant posthyperventilatory hypoxemia. We hypothesize that posthyperventilatory hypoxemia is caused by hypopnea as a result of depleted CO₂ body stores. Noninvasive transcutaneous blood gas measurements are not reliable for monitoring blood gas changes during and after hyperventilation, most probably because of the slow response time of the electrodes and the reflex vasoconstriction of the skin vessels.

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In the present study 43 patients with unilateral parenchymatous kidney disease and hypertension were investigated. 20 patients were nephrectomized, 23 treated with antihypertensive drugs. Both therapeutic approaches showed an excellent and sustained blood pressure-(BP)-lowering effect. BP fell from 185 ± 27/116 ± 13 to 138 ± 20/86 ± 10 mm Hg in the operated and from 194 ± 32/116 ± 13 to 149 ± 22/95 ± 12 mm Hg in the medically treated patients after 2 and 6 weeks, respectively (p < 0.001). BP was 142 ± 16/89 ± 11 and 136+ 16/90 ± 10 mm Hg at the long-term follow-up in the 2 subgroups. In the operated group 70% (n = 14) were cured, 20% (n = 4) were improved and 10% (n = 2) unimproved. In the medically treated group 65% (n = 15) were normotensive, 26% (n = 6) improved and 9% (n = 2) treatment resistant. No significant correlation between postoperative BP reduction and lateralization of renin secretion (PRA-ratio > 1.5) was found. Although cured patients showed a higher mean PRA-ratio, 4 patients with a PRA-ratio < 1.5 were cured (n = 2) or improved (n = 2) postoperatively. Our results document an excellent and sustained antihypertensive effect of both nephrectomy and medical treatment in patients with unilateral parenchymatous kidney disease and hypertension. They further limit the predictive value of renal venous renin determination in the preoperative workup.