The vasoconstrictor response of Angiotensin II on AT1 receptors in rabbit afferent arterioles is counteracted by vasodilatory prostaglandins and nitric oxide.
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Demonstrates counter-regulation of Ang II vasoconstriction by prostaglandins and NO in rabbit afferent arterioles; leaves open applicability to human renal hemodynamics.
We examined the effects of angiotensin II (Ang II) on isolated rabbit afferent arterioles to assess the direct effect of Ang II at the resistance vessel level in the kidney. We microdissected the superficial afferent arteriole from the kidney of New Zealand White rabbits. The afferent arteriole was cannulated with a micropipette system, and the intraluminal pressure was set at 80 mmHg. Ang II did not change the lumen diameter of the afferent arterioles. After the afferent arterioles were pretreated with aspirin DL-lysine or indomethacin, Ang II (10(-7) M) caused transient vasoconstriction in the afferent arterioles. Ang II (10(-7) M) caused persistent constriction in the afferent arterioles pretreated with NG-nitro-L-arginine (10(-4) M). Physiological doses of Ang II decreased the lumen diameter of the isolated afferent arterioles pretreated with NG-nitro-L-arginine and aspirin DL-lysine. Dup753 (10(-6) M), an AT1-receptor antagonist, abolished the vasoconstrictor effects of Ang II. These findings suggest that the isolated rabbit afferent arteriole has AT1 receptors, and the vasoconstrictor response of Ang II is counteracted by vasodilatory prostaglandins and nitric oxide.
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Yoshida et al. (1994) studied this question.
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