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Effect of vanadate in acute metabolic acidosis
Author(s) -
EIAMONG Somchai,
CHANKASEM Kannika,
CHOMDEJ Bungorn,
SANGMAL Mariem,
KURTZMAN Neil A.,
SITPRIJA Visith
Publication year - 1996
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1111/j.1440-1797.1996.tb00108.x
Subject(s) - medicine , vanadate , endocrinology , metabolic acidosis , excretion , acidosis , bicarbonate , potassium , renal function , chemistry , biochemistry , organic chemistry
Summary: The effect of vanadate on urinary excretion of acid and electrolyte in dogs with hydrochloric acid (HCI)‐induced acute metabolic acidosis was studied. Vanadate caused no changes in systemic and renal haemodynamics, blood parameters and net acid excretion (NAE) in the control group. In the acute metabolic acidosis group, metabolic acidosis per se also had no effect on haemodymic parameters. Fractional excretion of bicarbonate was decreased, while NAE was markedly increased. Following vanadate treatment, acute acid‐loaded animals showed an increase in mean arterial pressure (MAP), but a decreased glomerular filtration rate and effective renal plasma flow. These animals had reduced NAE compared to that seen with HCI alone. Thus, vanadate impaired the renal adaptive responses to acute metabolic acidosis. the decreased NAE induced by vanadate might be caused by its known inhibitory effect on hydrogen‐potassium‐adenosine triphosphatase (H‐K‐ATPase) and sodium‐potassium‐adenosine triphosphatase (Na‐K‐ATPase), and by renal vasoconstriction.