Vol.5, No 1, 1998 pp. 6 - 11
UDC: 612.17
VASOACTIVE NATRIURETIC PEPTIDES AND KIDNEY
Ljiljana Surić-Lambić1,
S.
Plješa1 V. Stojanov2,
D.
Avramović2
1 Department of Nephrology, University
Teaching Hospital Zemun, Belgrade
2 Institute of Cardiovascular diseases,
Clinical Centre of Serbia, Belgrade, Yugoslavia
Summary. The natriuretic peptide family (ANP, BNP, CNP) is responsible
for the body fluid homeostasis and blood pressure control. ANP and BNP
act on guanylate cyclase-A and CNP on guanylate cyclase-B receptors.The
main renal actions of ANP are: 1. direct and indirect effects on the kidney
to alter renal hemodynamics, and to increase fluid and electrolyte excretion;
2. functional antagonism of the renin-angiotensin-aldosterone system (R-A-A)
by inhibiting synthesis and/or relase of renin and aldosterone, and by
antagonising all known effects of angiotensin. ANP increases single nephron
GFR in proportion of total GFR due mainly to an increase in glomerular
capillary hydrostatic pressure that results from efferent arteriolar constriction
and afferent arteriolar dilation. ANP indirectly acts on tubular sites
that are targets of R-A-A system, including proximal tubular sites (angiotensin)
and distal nephron sites (aldosteron). Regulation of CNP secretion is different
from that of ANP and BNP, which are cardiac hormones. The increase of the
plasma CNP in chronic renal failure (CNF) can be due to the diminished
clearance of CNP in the kidney or due to increase in CNP production that
occurs in the renal parenchymal cells. In chronic renal failure (CRF) exists
a downregulation of ANP clearance receptors due to exaggerated ANP-stimulated
cGMP response in CRF glomeruli. In hemodialysis patients, changes in plasma
ANP are greater than in BNP and more responsive to changes in left atrial
volume due to ultrafiltration.
Key words: Natriuretic peptides, renal disease, haemodialysis
VASOAKTIVNI NATRIURETIČKI PEPTIDI I BUBREG
Porodica natriuretskih peptida odgovorna je za homeostazu telesne tečnosti
i kontrolu krvnog pritiska. ANP i BNP deluju preko gvanilat-ciklaza A a
CNP preko gvanilat-ciklaza B receptora. Glavna dejstva ANP su: 1 .neposredni
i posredni uticaj na hemodinamske promene u bubregu, čime je povećano izlučivanje
tečnosti i elektrolita; 2.suprotstavljanje funkciji renin-angiotenzin-aldosteron
(RAA) sistema putem inhibicije stvaranja i/ili oslobađanja renina i aldosterona,
i neutralisanjem svih poznatih efekata angiotenzina. ANP povećava glomerulsku
filtraciju (GF) u svakom pojedinačnom nefronu zavisno od ukupne GF uglavnom
na račun povećanja hidrostatskog pritiska u kapilarima glomerula regulisanim
konstrikcijom eferentne i dilatacijom aferentne arteriole. ANP posredno
deluje na mestima uticaja RAA sistema u tubulima uključujući proksimalni
(angiotenzin) i distalni (aldosteron) tubul. Mehanizam nastanka CNP je
različit od mehanizma nastanka hormona srca-ANP i BNP. U hroničnoj bubrežnoj
insuficijenciji (HBI), smanjeno uklanjanje CNP u bubregu ili povećano stvaranje
CNP od strane bubrežnih parenhimskih ćelija, dovodi do povećanja nivoa
CNP u plazmi. Uz to, u HBI smanjuje se broj receptora za ANP zbog povećanja
nivoa cGMP u glomerulima nastalog kao posledica povišenih vrednosti ANP
u plazmi.U bolesnika na hemodijalizi (HD), promene nivoa ANP u plazmi veće
su nego nivoa BNP i reaktivnije na promene volumena leve pretkomore u toku
HD.
Ključne reči: Natriuretički peptidi, bubrežne bolesti, hemodijaliza
