The effects of a high caiciwn diet (2.5 96) on blood pressure, electrolyte
balance, cytosolic free calcium concentration. (intracellular calcium) were
studied in one-kidney deoxy corticosterone sodium chloride hypertensive
rats (Doc-NaC1).
Calcium supplementation for 8 weeks markedly attenuated the development
of Doc-NaCl hypertension, and prevented the Doc-NaCl-induced
sodium-volume retention as judged by reduced plasma Na+in high calcium-
fed Doc-NaC1 rats. However, calcium supplementation did not affect
the Doc-NaCl induced r ise in platrlet intracellular calcium.
Calcium supplementation clearly attenuated the development of hypertension
and sodium retention induced by the Doc-NaCl treatment. However,
the associated rise in platelet intracellular calcium was not prevented,
suggesting that in this form of experimental hypertension, increased dietary
calcium does not lower blood pressure by reducing intracellular calcium.
The Doc-NaCl treatment increased sensitivity to depolarization. voltage-
dependent Ca2+ entry, and cell membrane permeability to ions, and
attenuated arterial relaxation and vascular Nat K+ - ATPose function.
The results further suggest reduced ability of the cell membrane to transport
Ca2+ (possibly via Ca2+ - ATPase) in Doc hypertension. The high calcium
diet opposed these alterations. The present results thus provide evidence
that the antihypertensive effect of a high calcium diet in
mineralocorticoid-salt hypertension is mediated by its beneficial effects on
systemic sodium balance and arterial smooth muscle function. |
