Response of isolated renal arterioles to acetylcholine, dopamine, and bradykinin

Abstract

The effect of acetylcholine (ACh), dopamine (DA), and bradykinin (BK) on vascular tone was examined in interlobular arteries and superficial afferent and efferent arterioles isolated from rabbit kidney. A single microvessel was dissected and cannulated, and lumen diameter was measured at a fixed intraluminal pressure. ACh caused a dose-dependent relaxation of norepinephrine-induced tone in all three vessel types. Significant relaxation (10-20%) was observed with 10(-8) M ACh and higher concentrations caused complete relaxation. In afferent and efferent arterioles DA caused a dose-dependent relaxation that was indistinguishable from the one caused by ACh. However, DA was much less effective on interlobular arteries. Significant relaxation was not observed until 10(-5) M DA, and 10(-4) M caused only a 30-40% relaxation. In afferent arterioles atropine blocked the effect of ACh, and metoclopramide selectively inhibited DA-induced relaxation. BK (10(-9) to 10(-5) M) caused a dose-dependent relaxation of norepinephrine-induced tone only in efferent arterioles. BK, either in the bath or lumen, had no effect on the preglomerular microvessels. ACh and DA also caused relaxation of afferent arterioles with spontaneous tone while all three vasodilators relaxed efferent arterioles with spontaneous tone. The results demonstrate segmental heterogeneity for these vasodilators in the rabbit renal microvasculature, with ACh causing relaxation in all three vessel types, DA acting primarily on the glomerular arterioles, and BK affecting only the efferent arteriole.

Endothelium-derived relaxing factor modulates endothelin action in afferent arterioles.

“…This may indicate that the renal microvasculature downstream from the main renal artery produces little EDRF in response to acetylcholine. In contrast, results from both the present study and that by Edwards 18 have demonstrated that acetylcholine dilates isolated afferent arterioles preconstricted by either endothelin or norepinephrine, strongly suggesting that renal microvasculature can produce EDRF.…”

Vasodilator and constrictor actions of platelet-activating factor in the isolated microperfused afferent arteriole of the rabbit kidney. Role of endothelium-derived relaxing factor/nitric oxide and cyclooxygenase products.

“…Consequently, these studies provide evidence that prostaglandins may play no role in the renal vasodilator actions of PAF. We (23,32) and others (33) have demonstrated that acetylcholine dilates isolated afferent arterioles preconstricted with endothelin or norepinephrine, suggesting that the renal microvasculature can produce EDNO. Furthermore, this locally produced EDNO may be an important modulator of the vascular response to angiotensin II and endothelin (23,32).…”

Intrarenal Vascular Sites of Action of Adenosine and Glucagon

“…A similar pressure-flow relation would have been expected as it would be induced by ACh that dilates both afferent and efferent arterioles (14,16,17). Renal vasodi lation induced by ACh might be a maximum, since other vasodilators such as bradykinin and prostaglandin E2 could not ailate the renal blood vessels to a greater extent than the dilation that would occur with ACh (23)(24)(25).…”

“…In contrast, if a vasodilator increases RBF at reduced RPP, its site of action is presumably the efferent arteriole. Based on the above argument, pressure-RBF and pressure-GFR relations were obtained during infusion of adenosine and glucagon, or acetylcholine (ACh) which dilates both the afferent and the efferent arterioles (14,16,17). In addition, the effects of adenosine in combination with glucagon and the effects of ACh on pressure RBF and pressure-GFR relations were com pared.…”