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Articles in PresS, published online ahead of print December 4, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.00233.2001
Submitted on July 26, 2001
Accepted on November 27, 2001
1 Smooth Muscle Research Group, University of Calgary, Calgary, Alberta, Canada
* To whom correspondence should be addressed. E-mail: rloutzen{at}acs.ucalgary.ca.
Proteinase-activated receptors (PARs) are a novel class of G protein-coupled receptors that respond to signals through endogenous proteinases. PAR activation involves the enzymatic cleavage of the extracellular N-terminal domain and unmasking of a new N-terminus which serves as an anchored ligand to activate the receptor. At least four PAR subtypes have been identified to date. In the present study we examined the effects of activating PAR-2 on the afferent arteriole using the in vitro perfused hydronephrotic rat kidney. The synthetic peptide SLIGRL-NH2, which corresponds to the exposed ligand sequence and selectively activates PAR-2, did not alter basal afferent arteriolar diameter but caused a concentration-dependent vasodilation (3-30 µM) of arterioles pre-constricted by angiotensin II (0.1 nM). A modified peptide sequence (LSIGRL-NH2, inactive at PAR-2) had no effect. This vasodilation was characterized by an initial transient component followed by a smaller sustained response. A similar pattern of vasodilation was seen when SLIGRL-NH2 was administered to the isolated perfused normal rat kidney. The sustained component of the PAR-2 induced afferent arteriolar vasodilation was eliminated by nitric oxide (NO) synthase inhibition (100 µM L-NAME). In contrast, the transient vasodilation persisted under these conditions. This transient response was not observed when afferent arterioles were pre-constricted with elevated KCl, suggesting the involvement of an endothelium-derived hyperpolarizing factor. Finally, RT-PCR revealed the pressence of PAR-2 mRNA in isolated afferent arterioles. These findings indicate that PAR-2 is expressed in the afferent arteriole and that its activation elicits afferent arteriolar vasodilation by both NO-dependent and NO-independent mechanisms.
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