ATTENUATION BY ALPHA,BETA-METHYLENADENOSINE-5'-TRIPHOSPHATE OF PERIARTERIAL NERVE STIMULATION-INDUCED RENAL VASOCONSTRICTION IS NOT DUE TO DESENSITIZATION OF PURINERGIC RECEPTORS
E. Sehic et al., ATTENUATION BY ALPHA,BETA-METHYLENADENOSINE-5'-TRIPHOSPHATE OF PERIARTERIAL NERVE STIMULATION-INDUCED RENAL VASOCONSTRICTION IS NOT DUE TO DESENSITIZATION OF PURINERGIC RECEPTORS, The Journal of pharmacology and experimental therapeutics, 271(2), 1994, pp. 983-992
We investigated in the isolated rat kidney the modulation of vasoconst
rictor responses to ATP (0.05-0.5 mu mol), renal nerve stimulation (RN
S) (0.5-10.0 Hz), norepinephrine (NE) (0.15-0.9 nmol), angiotensin II
(2 pmol) and arginine vasopressin (3 pmol) by alpha,beta-methylenadeno
sine-5'-triphosphate (alpha beta mATP) infused at 6 mu M (Procedure I)
or for short intervals (5 min) at a low concentration (60 nM) gradual
ly increased to 6 mu M to reduce the dramatic initial vasoconstriction
(Procedure II). Infusion of alpha beta mATP (Procedure I) produced a
marked, transient rise in perfusion pressure of 146 to 198 mm Hg that
returned to basal level within 10 min and thereafter inhibited the vas
oconstrictor response to ATP, RNS (0.5-6.0 Hz), NE, angiotensin II and
arginine vasopressin. Infusion of alpha beta mATP by Procedure II pro
duced a smaller maximal transient increase in perfusion pressure (<100
mm Hg) and reduced the vasoconstrictor responses to RNS at 0.5 to 2.0
Hz and to the lower dose of NE (0.15 nmol) only. ATP infusion reduced
the vasoconstrictor response to both RNS and NE. In animals pretreate
d with reserpine, the effect of RNS to produce vasoconstriction was in
hibited. These data suggest that ATP does not contribute to the renal
vasoconstrictor response elicited by RNS, and that attenuation of rena
l vasoconstrictor responses by alpha beta mATP is not due to desensiti
zation of purinergic receptors.