Changes in renal autacoids in aged human hypertensives.
The aging process determines several modifications of the kidney, that, however, do not provoke any dysfunction in normal conditions. But in the elderly--in the presence of stressful situations and particularly when adrenergic activation is present--the kidney is more vulnerable than in the young, and renal failure may arise. Variations typical of the aging kidney are accelerated when hypertension overlaps the physiological renal process, because both senescence and hypertension weight on the same structures, i.e. glomeruli. We studied renal hemodynamic adaptation capacity both in the healthy elderly and in patients affected by isolated systolic hypertension, in an acute experiment which requires the application of a mental stress-induced adrenergic activation. In hypertensive patients we have already demonstrated a total lack of renal adaptation capacity. In fact, while the elderly normotensives react with a prolonged and pronounced vasoconstriction, in those with isolated systolic hypertension, adrenergic activation induces a passive renal vasodilation and glomerular hyperfiltration. The anomalous adaptation capacity of renal hemodynamics is probably due to an impairment in the paracrine response of renal vasculature. Indeed in the hypertensive elderly, unlike in the normotensive one, no variations of autacoid production occur during the adrenergic activation. Following on from this, pattients affected by isolated systolic hypertension passively suffer the many hypertensive peaks which characterize their every day life. The altered renal autoregulation of the elderly with isolated systolic hypertension may explain the accelerated glomerulosclerosis and the greater incidence of renal damage and end-stage renal disease which characterize this condition. These aspects underline the primary role of the antihypertensive treatment of isolated systolic hypertension, not only for the prevention of cardiovascular mortality but also of renal damage and/or end-stage renal disease.
Ungar
A
A
Dipartimento di Area Critica Medico Chirurgica, Università degli Studi di Firenze e Azienda Ospedaliera Careggi, Italy. aungar@unifit.it
Cristofari
C
C
Torrini
M
M
Di Serio
C
C
Cantini
C
C
Vallotti
B
B
La Cava
G
G
Castellani
S
S
Masotti
G
G
D000375:Aging / Q000502:physiology*; D000818:Animals; D012898:Autacoids / Q000378:metabolism*; D006152:Cyclic GMP / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D019332:Endothelin-1 / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism* / Q000502:physiology / Q000503:physiopathology; D051437:Renal Insufficiency / Q000503:physiopathology; D013312:Stress, Physiological
D012898:Autacoids; D019332:Endothelin-1; D006152:Cyclic GMP; D015232:Dinoprostone