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LOCAL CONTROL OF CIRCULATION
1Department of Medicine, Saitama Medical College, Iruma, Saitama 3500495; and 2Department of Medicine, School of Medicine, Keio University, Shinjuku, Tokyo 160-8582, Japan
Submitted 25 November 2002 ; accepted in final form 13 February 2003
To investigate the role of ryanodine receptors in glomerular arterioles, experiments were performed using an isolated perfused hydronephrotic kidney model. In the first series of studies, BAYK-8644 (300 nM), a calcium agonist, constricted afferent (19.6 ± 0.6 to 17.6 ± 0.5 µm, n = 6, P < 0.01) but not efferent arterioles. Furthermore, BAYK-8644 elicited afferent arteriolar oscillatory movements. Subsequent administration of nifedipine (1 µM) inhibited both afferent arteriolar oscillation and constriction by BAYK-8644 (to 19.4 ± 0.5 µm). In the second group, although BAYK-8644 constricted afferent arterioles treated with 1 µM of thapsigargin (19.7 ± 0.6 to 16.8 ± 0.6 µm, n = 5, P < 0.05), it failed to induce rhythmic contraction. Removal of extracellular calcium with EGTA (2 mM) reversed BAYK-8644-induced afferent arteriolar constriction (to 20.0 ± 0.5 µm). In the third series of investigations, ryanodine (10 µM) but not 2-aminoethoxyphenyl borate (100 µM) abolished afferent arteriolar vasomotion by BAYK-8644. In the fourth series of experiments, in the presence of caffeine (1 mM), the stronger activation of voltage-dependent calcium channels by higher potassium media resulted in greater afferent arteriolar constriction and faster oscillation. Our results indicate that L-type calcium channels are rich in preglomerular but not postglomerular microvessels. Furthermore, the present findings suggest that either prolonged calcium influx through voltage-dependent calcium channels (BAYK-8644) or sensitized ryanodine receptors (caffeine) is required to trigger periodic calcium release through ryanodine receptors in afferent arterioles.
glomerular circulation; voltage-dependent calcium channel; caffeine; BAYK-8644; tubuloglomerular feedback
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