The actions of altered osmolarity on guinea-pig detrusor smooth muscle contractility and intracellular calcium

Abstract

The study measured the effects in vitro of changing extracellular osmolarity on the contractility of detrusor smooth muscle strips. The data were interpreted in the context of separate measurements from isolated cells of alterations to the intracellular [Ca2+], [Ca2+]i. Increased osmolarity (300-700 mosmol l-1) reduced phasic contractions but increased resting tension regardless of whether sucrose, LiCl or NaCl were used as osmolytes. [Ca2+]i was decreased slightly only when NaCl increased osmolarity, otherwise it was unchanged. The contractile effects may be explained by tissue shrinkage and reduction of detrusor excitability. Lowered osmolarity (300-64 mosmol l-1) decreased phasic contractions but increased resting tension and [Ca2+]i. The raised resting tension was due solely to low osmolarity and was independent of changes to [Na], [Cl] or ionic strength. The rise of [Ca2+]i was due partly to Ca2+ influx through Na(+)-Ca2+ exchange but a fraction was independent of extracellular Ca, unaffected by Gd3+, and persisted in the presence of caffeine. By contrast, reduction of phasic tension was due mainly to the reduced ionic strength, not osmolarity. The results do not support the presence of functional stretch-activated channels and suggest only a minor role for Na(+)-Ca2+ exchange under these conditions. However, they do suggest an intracellular source of Ca2+, which is independent of the sarcoplasmic reticulum.

Ionic basis for the regulation of spontaneous excitation in detrusor smooth muscle cells of the guinea‐pig urinary bladder

“…The spontaneous action potentials in bladder strips have been mostly studied in preparations where contractions have been diminished by a high extracellular osmolarity (Mostwin, 1986; Fujii et al , 1990 ; Heppner et al , 1997 ). In this condition, Ca 2+ homeostasis is likely to be different from that in physiological conditions (Proctor & Fry, 1999). Thus, only limited information is available about the regulatory mechanisms for spontaneous excitation in intact bladder smooth muscle so far ( Hashitani et al , 2001 ).…”