Excessive vasoconstriction after stress by the aging kidney: Inadequate prostaglandin modulation of increased endothelin activity
Excessive vasoconstriction after stress by the aging kidney: Inadequate prostaglandin modulation of increased endothelin activity
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DOI：
10.1016/s0022-2143(98)90167-6
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发表时间：
1998-09-01
期刊：
影响因子：
--
通讯作者：
Masotti, G
中科院分区：
文献类型：
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作者：
Castellani, S;Ungar, A;Masotti, G
对8名老年健康女性(68~82岁)和8名年轻女性(24~40岁)的肾脏老化对30分钟精神应激(MS)刺激交感神经系统的适应能力进行了评估。这项研究包括4个连续的30分钟阶段(基线、精神压力、恢复I和恢复2)。老年组基础有效肾血浆流量(ERPF)(131I标记的马尿酸清除量)低于青年组，肾小球滤过率(GFR)(125I标记的硫代巴比妥酸清除量)按比例减少，滤过分数(FF)高于青年组。老年组内皮素-1(ET-1)、前列腺素E-2(PGE(2))和6-酮-前列腺素F-1α(6-keto-PGF(1α))(P<；0.05)和6-酮-前列腺素F-1α(6-keto-PGF(1α))分泌较多(P<；0.05)。精神应激导致两个年龄组的血压、心率和血浆儿茶酚胺的增加相似，仅限于刺激期。在老年组，心理应激引起ERPF的持续下降，在心理应激后60min达到最大值(-33%，P<；0.05)，而GFR在整个实验过程中保持不变，使Ff增加。在较年轻的受试者中，肾脏血流动力学的变化仅限于精神应激期。老年组ET-1在精神应激期和第一个恢复期(+50%和+25%，P<；0.05)升高，与青年组相同，但老年组与青年组不同，扩张性前列腺素仅在精神应激期增加。总之，衰老的肾脏对肾上腺素能刺激的反应是更明显和更长时间的血管收缩，这可能是由于前列腺素调节内皮素活性的缺陷引起的，GFR的自动调节是以肾小球内压增加为代价的。
The adaptive capacity of the aging kidney to stimulation of the sympathetic nervous system, as induced by a 30-minute mental stress (MS), was assessed in 8 elderly healthy women (68 to 82 years of age) and compared with that of 8 younger women (24 to 40 years of age). The study encompassed 4 consecutive 30-minute periods (baseline, mental stress, recovery I,and recovery 2). In the elderly subjects, baseline effective renal plasma flow (ERPF)(iodine 131-labeled hippurate clearance) was lower and glomerular filtration rate (GFR)(iodine 125-labeled iothalamate clearance) was proportionally less reduced than in the younger group; the filtration fraction (FF) was higher. The elderly group excreted more endothelin 1 (ET-1) (P < .05), prostaglandin E-2 (PGE(2)), and 6-keto-prostaglandin F-1 alpha (6-keto PGF(1 alpha))(P < .001 for both)(radioimmunoassay). Mental stress induced similar increases in blood pressure, heart rate, and plasma catecholamines in the 2 age groups, limited to the stimulation period. In the elderly group, mental stress caused a prolonged decrease in ERPF that reached its maximum 60 minutes after mental stress (-33%, P < .05), while GFR remained constant during the whole experiment, so that FF increased. In the younger subjects, renal hemodynamic changes were limited to the mental stress period. ET-1 increased during mental stress and the first recovery period in the elderly group (+50% and +25%, P < .05) as it did in the younger group, but the elderly group differed from the younger in that vasodilating prostaglandins increased only during mental stress. In conclusion, the aging kidney reacts to adrenergic stimulation with more-pronounced and -prolonged vasoconstriction that is probably caused by a defect in prostaglandin modulation of endothelin activity Autoregulation of GFR is maintained at the expense of increased intraglomerular pressure.