AJP - Renal Physiology, Vol 248, Issue 1 93-F99, Copyright © 1985 by American Physiological Society
Effect of phosphate depletion on blood pressure and vascular reactivity to norepinephrine and angiotensin II in the rat
Y. Saglikes, S. G. Massry, K. Iseki, N. Brautbar, R. Barndt, L. L. Brunton, I. L. Buxton, N. Vlachakis and V. M. Campese
Phosphate depletion (PD) adversely affects myocardial function but its
influence on blood pressure is not well elucidated. In this study we
evaluated whether PD influences blood pressure and/or affects its hormonal
regulation or the peripheral vascular response to pressor agonists. Mean
arterial pressure (MAP) in PD rats was lower than in normal animals,
whereas heart rate was not significantly different between the two groups.
Cardiac index (CI) in PD rats was lower and systemic vascular resistance
(SVR) was higher than in controls. Plasma norepinephrine (NE) in the
resting state and during the stress of immobilization was significantly
greater in PD rats than in controls. Base-line plasma renin activity was
also significantly higher in PD rats and increased similarly in the two
groups of rats after administration of isoproterenol. Bolus injections of
NE or angiotensin II produced a smaller rise in MAP in PD rats than in
controls. Reduced responsiveness to NE was also demonstrated in isolated
hind-limb preparation from PD rats. When NE was infused to achieve a rise
in MAP of 30 mmHg, the dose required in PD was higher than in controls.
Treatment with indomethacin did not affect the response in MAP to NE. The
content and affinity of both alpha- and beta-receptors in PD hearts were
not different from those of control hearts. The contents of PiATP, and AMP
in the mesenteric vessels of PD rats were significantly lower than in
control animals. These data show that PD leads to reductions in MAP,
arteriolar response to pressor agents, and CI with appropriate compensatory
rise in NE but with inadequate compensatory increase in SVR.(ABSTRACT
TRUNCATED AT 250 WORDS)
