Spieker C, Pan N, Schlüter H, Zidek W
Med. Univ.-Poliklinik, Münster, Germany.
Clin Exp Hypertens. 1993 Jan;15(1):143-52. doi: 10.3109/10641969309041616.
In 15 patients with essential hypertension, 16 patients with renal hypertension and in 12 healthy subjects Ca2+ ATPase activity was determined in red blood cells both in the basal state and after maximal stimulation with calmodulin. Normal subjects showed a basal and maximal activity of 7.1 +/- 3.6 and 16.0 +/- 2.3 pmol phosphate/min.10(6) RBC, respectively. Renal hypertensives had a similar basal Ca2+ ATPase activity (5.4 +/- 4.1 pmol phosphate/min.10(6) RBC) and a lowered maximal Ca2+ ATPase activity (9.8 +/- 5.4 pmol phosphate/min.10(6) RBC, p < 0.05). In essential hypertensives basal and maximal Ca2+ ATPase activity was 9.0 +/- 5.3 and 35.4 +/- 14.4 pmol phosphate/min.10(6) RBC, respectively, the latter being significantly increased (p < 0.01). This finding, which is in contrast to earlier results indicating a lowered Ca2+ ATPase activity in essential hypertension, may be explained as a consequence of an increased Ca2+ influx in essential hypertension. A lowered Ca2+ ATPase activity does not seem to be involved in the pathogenesis of essential hypertension.
在15例原发性高血压患者、16例肾性高血压患者及12名健康受试者中，测定了红细胞在基础状态及用钙调蛋白最大刺激后的Ca2+ATP酶活性。正常受试者的基础活性和最大活性分别为7.1±3.6和16.0±2.3 pmol磷酸盐/分钟·10⁶个红细胞。肾性高血压患者的基础Ca2+ATP酶活性相似（5.4±4.1 pmol磷酸盐/分钟·10⁶个红细胞），而最大Ca2+ATP酶活性降低（9.8±5.4 pmol磷酸盐/分钟·10⁶个红细胞，p<0.05）。原发性高血压患者的基础Ca2+ATP酶活性和最大Ca2+ATP酶活性分别为9.0±5.3和35.4±14.4 pmol磷酸盐/分钟·10⁶个红细胞，后者显著升高（p<0.01）。这一发现与早期表明原发性高血压中Ca2+ATP酶活性降低的结果相反，可能是由于原发性高血压中Ca2+内流增加所致。Ca2+ATP酶活性降低似乎不参与原发性高血压的发病机制。
