N. Freestone et al., EARLY POSTNATAL CHANGES IN SARCOPLASMIC-RETICULUM CALCIUM-TRANSPORT FUNCTION IN SPONTANEOUSLY HYPERTENSIVE RATS, Molecular and cellular biochemistry, 164, 1996, pp. 57-66
This comparative study investigates the relationship between sarcoplas
mic reticulum (SR) calcium(Ca2+)-ATPase transport activity and phospho
lamban (PLB) phosphorylation in whole cardiac homogenates of spontaneo
usly hypertensive rats (SHR) and their parent, normotensive Wistar Kyo
to (WKY) strain during early postnatal development at days 1, 3, 6, 12
and at day 40 to ascertain any difference in SR Ca2+ handling before
the onset of hypertension. At day 1, the rate of homogenate oxalate-su
pported Ca2+ uptake was significantly higher in SHR than in WKY (0.25
+/- 0.02 vs 0.12 +/- 0.01 nmoles Ca2+/mg wet ventricular weight/min, r
espectively; p < 0.001). This interstrain difference disappeared with
further developmental increase in SR Ca2+ transport. Western Blot anal
ysis and a semiquantitative ELISA did not reveal any difference in the
amount of immunoreactive PLB (per mg of total tissue protein) between
strains at any of the ages studied. In addition, levels of phosphoryl
ated PLB formed in vitro in the presence of radiolabelled ATP and cata
lytic (C) subunit of protein kinase A did not differ between SHR and W
KY at days 1, 3, 6 and 12. At day 40, C subunit-catalyzed formation of
P-32-PLB was reduced by 66% (p < 0.001) in SHR when compared to age-m
atched WKY. In the early postnatal period between day 1 and 12 SR Ca2-transport values were linearly related to the respective P-32-PLB lev
els of both SHR and WKY rats. The results indicate that cardiac SR of
SHR can sequester Ca2+ at a much higher rate immediately after birth c
ompared to WKY rats. The disappearance of this interstrain difference
with further development suggests that some endogenous neuroendocrine
or nutritional factor(s) from the hypertensive mother may exert an inf
luence upon the developing heart in utero resulting in a transiently a
dvanced maturation of the SR Ca2+ transport function in SHR pups at th
e time of birth.