S. Castellani et al., EXCESSIVE VASOCONSTRICTION AFTER STRESS BY THE AGING KIDNEY - INADEQUATE PROSTAGLANDIN MODULATION OF INCREASED ENDOTHELIN ACTIVITY, The Journal of laboratory and clinical medicine, 132(3), 1998, pp. 186-194
Citations number
51
Categorie Soggetti
Medicine, General & Internal","Medicine, Research & Experimental","Medical Laboratory Technology
The adaptive capacity of the aging kidney to stimulation of the sympat
hetic nervous system, as induced by a 30-minute mental stress (MS), wa
s assessed in 8 elderly healthy women (68 to 82 years of age) and comp
ared with that of 8 younger women (24 to 40 years of age). The study e
ncompassed 4 consecutive 30-minute periods (baseline, mental stress, r
ecovery 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 iothalam
ate clearance) was proportionally less reduced than in the younger gro
up; the filtration fraction (FF) was higher. The elderly group excrete
d 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, l
imited to the stimulation period. In the elderly group, mental stress
caused a prolonged decrease in ERPF that reached its maximum 60 minute
s after mental stress (-33%, P < .05), while GFR remained constant dur
ing the whole experiment, so that FF increased. In the younger subject
s, 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 gr
oup, but the elderly group differed from the younger in that vasodilat
ing prostaglandins increased only during mental stress. In conclusion,
the aging kidney reacts to adrenergic stimulation with more-pronounce
d and -prolonged vasoconstriction that is probably caused by a defect
in prostaglandin modulation of endothelin activity Autoregulation of G
FR is maintained at the expense of increased intraglomerular pressure.