Metabolism and force in hypertrophic smooth muscle from rat urinary bladder

Summary, in English

Ten days of urinary outlet obstruction in the rat induced a threefold increase in bladder weight. Active force of control and hypertrophic bladder muscle strips was measured at varying PO2 levels after high-K+, carbachol, or electrical field stimulation. Highest force output was obtained with carbachol. Force per muscle area was lower in the hypertrophic muscles. The basal rates of oxygen consumption and lactate formation were similar in the two groups. The metabolic tension cost (ATP turnover/active force) was similar in the two groups for activation with high K+ and carbachol. In anoxia the active force decreased, but this was less pronounced in the hypertrophied muscle. Hypertrophied muscle could, in contrast to the controls, maintain a sustained K+ contracture in anoxia. Basal metabolic rates and tension cost were markedly reduced in anoxia for both groups. The lower force per area with unaltered tension cost, in hypertrophic muscles under all experimental conditions, may reflect unaltered intrinsic properties of the contractile system, although the amount of contractile material has decreased relative to cell volume. The increased resistance to anoxia may reflect a metabolic adaptation to impaired oxygen supply to the hypertrophied tissue.

• Author: Anders Arner; Ulf Malmqvist; Bengt Uvelius
• Department/s: Vascular Physiology; Division of Clinical Chemistry and Pharmacology; Urology
• Publishing year: 1990
• Language: English
• Pages: 923-932
• Publication/Series: American Journal of Physiology: Cell Physiology
• Volume: 258
• Issue: 5 Pt 1
• Links: http://ajpcell.physiology.org/cgi/reprint/258/5/C923
• Document type: Journal article
• Publisher: American Physiological Society
• Topic: Medicinal Chemistry; Pharmacology and Toxicology; Urology and Nephrology; Physiology
• Status: Published
• Research group: Vascular Physiology; Urology
• ISBN/ISSN/Other: ISSN: 1522-1563