The effects of adenosine triphosphate (ATP) on the renal vasculature o
f isolated kidneys from control, hyper- and hypothyroid rats were char
acterized. ATP responsiveness was evaluated in basal tone and in raise
d tone (phenylephrine 10(-6) M) preparations. These responses were com
pared with those obtained with barium chloride or sodium nitroprusside
(SNP), used respectively as nonreceptor agonists for vasoconstriction
or vasodilation. In preparations at basal tone, ATP produced dose-rel
ated vasoconstriction, which was increased in hyperthyroid kidneys, an
d was severely attenuated in kidneys from hypothyroid rats. In raised
tone preparations from control rats ATP produced a dual response: vaso
constriction at low doses, which declined with increasing doses to giv
e way to vasodilator responses; biphasic responses were found in some
kidneys. Hyperthroid kidneys showed increased presser responses and a
vasodilator response similar to those seen in kidneys from control rat
s. However, in hypothyroid kidneys the vasodilator response was abolis
hed. The responses to barium chloride and to SNP were significantly in
creased and decreased in hyper- and hypothyroid kidneys, respectively;
vasoconstrictor responses to SNP were also found in hypothyroid kidne
ys. Hence the abnormal responses to ATP observed in both thyroid dysfu
nctions may be partially explained by unspecific alterations in the co
ntractile machinery of the renal vasculature in these kidneys. However
, ATP responsiveness (vasoconstriction at low tone and vasodilation at
raised tone) was more severely affected in hypothyroid kidneys, sugge
sting that purinergic (P-2X and P-2Y) receptor activity may be decreas
ed in these organs.