title: Excessive vasoconstriction after stress by the aging kidney: inadequate prostaglandin modulation of increased endothelin activity.
abstract: 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 1, 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 E2 (PGE2), and 6-keto-prostaglandin F1alpha (6-keto PGF1alpha)(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.
authors.affiliation: Istituto di Clinica Medica Generale e Cardiologia, Dipartimento di Fisiopatologia Clinica, Università di Firenze, Italy.
authors.forename: S
authors.initials: S
authors.lastname: Castellani
authors.forename: A
authors.initials: A
authors.lastname: Ungar
authors.forename: C
authors.initials: C
authors.lastname: Cantini
authors.forename: G
authors.initials: G
authors.lastname: La Cava
authors.forename: C
authors.initials: C
authors.lastname: Di Serio
authors.forename: A
authors.initials: A
authors.lastname: Altobelli
authors.forename: B
authors.initials: B
authors.lastname: Vallotti
authors.forename: M
authors.initials: M
authors.lastname: Pellegri
authors.forename: A
authors.initials: A
authors.lastname: Brocchi
authors.forename: A
authors.initials: A
authors.lastname: Camaiti
authors.forename: M
authors.initials: M
authors.lastname: Coppo
authors.forename: U
authors.initials: U
authors.lastname: Meldolesi
authors.forename: G
authors.initials: G
authors.lastname: Messeri
authors.forename: G
authors.initials: G
authors.lastname: Masotti
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000652:urine; D000222:Adaptation, Physiological; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000502:physiology*; D002395:Catecholamines / Q000097:blood; D006152:Cyclic GMP / Q000652:urine; D015232:Dinoprostone / Q000652:urine*; D019332:Endothelin-1 / Q000652:urine*; D005260:Female; D005919:Glomerular Filtration Rate / Q000502:physiology; D006157:Guanosine Monophosphate / Q000652:urine; D006439:Hemodynamics; D006801:Humans; D007668:Kidney / Q000502:physiology*; D012016:Reference Values; D017596:Renal Plasma Flow, Effective / Q000502:physiology; D012083:Renin / Q000097:blood; D013312:Stress, Physiological / Q000503:physiopathology*; D014661:Vasoconstriction / Q000502:physiology*
chemical_list: D002395:Catecholamines; D019332:Endothelin-1; D015121:6-Ketoprostaglandin F1 alpha; D006157:Guanosine Monophosphate; D012083:Renin; D006152:Cyclic GMP; D015232:Dinoprostone