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1 Smooth Muscle Research Group, Department of Pharmacology and Therapeutics, University of Calgary, Calgary, Alberta, Canada
* To whom correspondence should be addressed. E-mail: rloutzen{at}ucalgary.ca.
The determinants of bradykinin (BK) induced afferent arteriolar vasodilation were investigated in the in vitro perfused hydronephrotic rat kidney. BK elicited a concentration-dependent vasodilation of afferent arterioles which had been pre-constricted with angiotensin II (0.1 nmol/l), but this dilation was transient in character. Pre-treatment with the nitric oxide synthase (NOS) inhibitor L-NAME (100 µmol/l) and the cyclooxygenase (COX) inhibitor ibuprofen (10 µmol/l) did not prevent this dilation when tone was established by angiotensin II, but fully blocked the response when tone was established by elevated extracellular KCl, suggesting a role of both NO and EDHF. We had previously shown that the EDHF-like response of the afferent arteriole evoked by acetylcholine was fully abolished by a combination of 10 nmol/l charybdotoxin (ChTX) and 1µmol/l apamin (AP) (36). However, in the current study ChTX+AP treatment only reduced the EDHF-like component of the BK response from 98±5 to 53±6% dilation. Tetraethylammonium (1 mmol/l, TEA), which had no effect on the EDHF-induced vasodilation associated with acetylcholine, reduced the EDHF-like response to BK to 88±3% dilation. However, the combination of TEA+ChTX+AP abolished the response (0.3±1 % dilation). Similarly, 17-octadecynoic acid (17-ODYA) did not prevent the dilation when administered alone (77±9% dilation), but fully abolished the EDHF-like response when added in combination with ChTX+AP (-0.5±4 % dilation). These findings suggest that BK acts via multiple EDHFs; one which is similar to that evoked by acetylcholine, in that it is blocked by ChTX+AP, and a second which is blocked by either TEA or 17-ODYA. Our finding that a component of the BK response is sensitive to TEA and 17-ODYA is consistent with previous suggestions that the EDHF released by BK is an epoxyeicosatrienoic acid (EET).
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