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1 Physiology Laboratory,
Bradykinin (BK)-induced changes in intracellular calcium level
([Ca2+]i)
were studied on fura 2-loaded afferent (AA) and efferent glomerular arterioles (EA) microdissected from juxtamedullary renal cortex. A
distinction was made between thin and muscular EA. In AA and both types
of EA, BK increased
[Ca2+]i
through activation of B2 receptors
located only on the endothelium. The responses were not affected by
nifedipine (10
6 M) and were
smaller in a Ca2+-free medium,
providing evidence that BK opens voltage-independent Ca2+ channels and mobilizes
intracellular Ca2+. Thin EA
differed from AA and muscular EA by a lower sensitivity to BK
(EC50 = 6.95 ± 3.81 vs. 0.21 ± 0.08 and 0.18 ± 0.13 nM, respectively;
P < 0.05), a higher maximal response
(89 ± 5 vs. 57 ± 5 and 44 ± 7 nM;
P < 0.001), and a spontaneous return
to basal Ca2+ level, even in the
presence of BK. Genistein
(104 M) and herbimycin A
(25 × 106
M), specific inhibitors of tyrosine kinases, inhibited the
[Ca2+]i
responses exclusively in AA. Genistein reduced the peak and plateau
phases of responses by 69 ± 9 and 82 ± 6%, respectively, in a
medium with Ca2+ and the peak by
48 ± 9% in a Ca2+-free
medium. Similar reductions were observed with herbimycin A. These results show that dissimilar signal transduction pathways are
involved in BK effects on juxtamedullary arterioles and that a tyrosine
kinase activity could participate in the regulation of BK effect on AA
but not on EA.
calcium; tyrosine kinase
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