Scandinavian journal of urology and nephrology · 2007
Intracellular calcium in hypertrophic smooth muscle from rat urinary bladder.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Arner Anders, Sjuve Scott Rolf, Haase Hannelore, Morano Ingo, Uvelius Bengt
Аннотация
OBJECTIVE: To explore whether infravesical outlet obstruction is associated with alterations in calcium activation of detrusor smooth muscle.
MATERIAL AND METHODS: Outlet obstruction was created by partial ligature of the urethra in female rats. Western blotting was performed using an antibody against the cytoplasmatic region of the alpha1c subunit of the L-type Ca2+ channel. Intracellular calcium was measured using Fura-2 in detrusors that had been obstructed for 10 days and activated by high K+ concentrations at different extracellular Ca2+ concentrations. The rate of force development after rapid opening of L-type Ca2+ channels was measured in contractions initiated by flash photolysis of nifedipine in Ca2(+)-containing depolarizing solution.
RESULTS: Bladder weight increased from 62 +/- 3 to 254 +/- 43 mg after 10 days of obstruction. Expression of the alpha1c subunit increased after 3 days and continued to increase until it was about fourfold greater after 10 days; however, it had not increased further at 6 weeks. This change was reversible after removal of obstruction. Activation with K+ produced a stable force at different extracellular Ca2+ concentrations, with no difference in response between controls and rats that had been obstructed for 10 days. Intracellular Ca2+ concentrations were lower in the obstructed group, showing that the calcium sensitivity of the contraction force had increased. The delay between the opening of L-type channels and the onset of contraction was longer in obstructed detrusors.
CONCLUSIONS: Growth of detrusor muscle following obstruction is accompanied by attenuated calcium transients following activation, despite upregulation of L-type Ca2+ channels. The Ca2+ sensitivity of contraction was increased in obstructed detrusors. We suggest that the decreased surface: volume ratio in hypertrophic smooth muscle cells is partly involved in the lowered Ca2+ transients. The increases in L-type calcium channels and in calcium sensitivity may be compensatory mechanisms.
MATERIAL AND METHODS: Outlet obstruction was created by partial ligature of the urethra in female rats. Western blotting was performed using an antibody against the cytoplasmatic region of the alpha1c subunit of the L-type Ca2+ channel. Intracellular calcium was measured using Fura-2 in detrusors that had been obstructed for 10 days and activated by high K+ concentrations at different extracellular Ca2+ concentrations. The rate of force development after rapid opening of L-type Ca2+ channels was measured in contractions initiated by flash photolysis of nifedipine in Ca2(+)-containing depolarizing solution.
RESULTS: Bladder weight increased from 62 +/- 3 to 254 +/- 43 mg after 10 days of obstruction. Expression of the alpha1c subunit increased after 3 days and continued to increase until it was about fourfold greater after 10 days; however, it had not increased further at 6 weeks. This change was reversible after removal of obstruction. Activation with K+ produced a stable force at different extracellular Ca2+ concentrations, with no difference in response between controls and rats that had been obstructed for 10 days. Intracellular Ca2+ concentrations were lower in the obstructed group, showing that the calcium sensitivity of the contraction force had increased. The delay between the opening of L-type channels and the onset of contraction was longer in obstructed detrusors.
CONCLUSIONS: Growth of detrusor muscle following obstruction is accompanied by attenuated calcium transients following activation, despite upregulation of L-type Ca2+ channels. The Ca2+ sensitivity of contraction was increased in obstructed detrusors. We suggest that the decreased surface: volume ratio in hypertrophic smooth muscle cells is partly involved in the lowered Ca2+ transients. The increases in L-type calcium channels and in calcium sensitivity may be compensatory mechanisms.