Impaired renal adaptation to stress in the elderly with isolated systolic hypertension

Citation
S. Castellani et al., Impaired renal adaptation to stress in the elderly with isolated systolic hypertension, HYPERTENSIO, 34(5), 1999, pp. 1106-1111
Citations number
31
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
HYPERTENSION
ISSN journal
0194911X → ACNP
Volume
34
Issue
5
Year of publication
1999
Pages
1106 - 1111
Database
ISI
SICI code
0194-911X(199911)34:5<1106:IRATSI>2.0.ZU;2-U
Abstract
The aim of this study was to evaluate the renal response in the elderly wit h isolated systolic hypertension (ISH) when an adrenergic activation, as in duced by mental stress, is applied. Renal hemodynamics and kidney neurohumo ral response to mental stress were studied in 8 elderly patients with ISH ( aged 63 to 82 years) along with 8 elderly normotensive subjects. The study encompassed four 30-minute experimental periods (baseline, mental stress, a nd recovery I and II). In these patients, the mental stress-induced blood p ressure rise was associated with a significant increase in both effective r enal plasma flow (I-131-labeled hippurate clearance) and glomerular filtrat ion rate (I-125-labeled iothalamate clearance) (+42% and +29%, respectively ; P<0.01 for both), without variations in filtration fraction, while elderl y normotensives reacted to adrenergic stimulation with renal vasoconstricti on but with the glomerular filtration rate constant. Variations in renal va soactive substances, which paralleled hemodynamics of the kidney, differed in the 2 groups. In normotensives, excretion (radioimmunoassay) of endothel in-1, prostaglandin E-2, and cGMP increased during the stimulus (+50%, +54% , and +59%, respectively; P<0.05). In ISH patients the release of these aut acoids did not vary in any of the experimental periods. In conclusion, in p atients with ISH the renal adaptive capacity to sympathetic activation is i mpaired, and the data may suggest that the glomerulus passively suffers the blood pressure increase, probably because of the insufficiency of the neur ohumoral response, particularly in regard to the increase of endothelin-1. This hemodynamic pattern may predispose TSH patients to a higher risk of re nal injury.