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and NO
Division of Nephrology and Hypertension, Georgetown University Medical Center, Washington, District of Columbia
Thromboxane A2 (TxA2) preferentially constricts
the renal afferent arteriole. Nitric oxide (NO) modulates
vasoconstriction and is rapidly degraded by superoxide radical
(O2
). We investigated the roles of NO and
O2 in rabbit isolated, perfused renal afferent
arteriole responses to the TxA2/prostaglandin
H2 (TP) receptor agonist U-46,619. U-46,619 (1010-106 M) dose-dependently reduced
afferent arteriolar luminal diameter (ED50 = 7.5 ± 5.0 nM), which was blocked by the TP receptor antagonist ifetroban (106 M). Tempol (103 M)
pretreatment, which prevented paraquat-induced vasoconstriction in
afferent arterioles, blocked the vasoconstrictor responses to U-46,619.
To test whether U-46,619 stimulates NO and whether tempol prevents
U-46,619-induced vasoconstriction by enhancing the biological activity
of NO, we examined the luminal diameter response to U-46,619 in
arterioles pretreated with
Nw-nitro-L-arginine methyl ester
(L-NAME, 104 M) or L-NAME + tempol. During L-NAME, the sensitivity and maximal responses of the afferent arteriole to U-46,619 were significantly (P < 0.05) enhanced. Moreover, L-NAME
restored a vasoconstrictor response to U-46,619 in vessels pretreated
with tempol. In conclusion, in isolated perfused renal afferent
arterioles TP receptor activation stimulates NO production, which
buffers the vasoconstriction, and stimulates O2
production, which mediates the vasoconstriction, in part, through interaction with NO.
thromboxane A2; nitric oxide; superoxide; afferent arteriole; tempol
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