ANP RECEPTORS IN NEURONS AND ASTROCYTES FROM SPONTANEOUSLY HYPERTENSIVE RAT-BRAIN

Citation
W. Tang et al., ANP RECEPTORS IN NEURONS AND ASTROCYTES FROM SPONTANEOUSLY HYPERTENSIVE RAT-BRAIN, The American journal of physiology, 265(1), 1993, pp. 30000106-30000112
Citations number
33
Categorie Soggetti
Physiology
ISSN journal
00029513
Volume
265
Issue
1
Year of publication
1993
Part
1
Pages
30000106 - 30000112
Database
ISI
SICI code
0002-9513(1993)265:1<30000106:ARINAA>2.0.ZU;2-3
Abstract
In this study we compared the levels and responsiveness of atrial natr iuretic peptide (ANP) receptors in neuronal and astrocyte glial cultur es from spontaneously hypertensive (SH) and normotensive (Wistar-Kyoto ; WKY) rat brain. Both neuronal and astrocyte glial cultures from the hypothalamus and brain stem of 1-day-old SH and WKY rats display speci fic high-affinity binding sites for I-125-labeled ANP. The presence of a large population of ANP-C receptors in each type of culture is indi cated by the strong competition of I-125-ANP binding by the ring-delet ed analogue of ANP [C-ANF (4-23)]. In neuronal cultures from both stra ins, C-type natriuretic peptide (CNP-22) was the most effective natriu retic peptide in stimulating guanosine 3',5'-cyclic monophosphate (cGM P) levels, suggesting the presence of ANP-B receptors in these cells. By contrast, ANP was the most effective stimulator of cGMP levels in S H and WKY rat astrocyte glial cultures, suggesting the presence of ANP -A receptors. Here, we have determined that there is a decrease in the maximum binding capacity for I-125-ANP-specific binding in both SH ra t neuronal and astrocyte glial cultures compared with their respective control cells. The stimulatory effects of CNP-22 on cGMP levels in SH rat neurons and of ANP on cGMP levels in SH rat astrocytes were signi ficantly reduced compared with their respective WKY rat cultures. Our data suggest that the lower number of ANP receptors in SH rat neuronal and astrocyte glial cultures includes a reduction in the guanylate cy clase-coupled ANP receptors.