1. The effects of altering extracellular pH on the electrically evoked contractions of ferret and human bladder (detrusor) smooth muscle have been investigated. pH was varied by changing superfusate PCO2 or NaHCO3 concentration. Acidosis increased force when superfusate PCO2 was raised but decreased force when the NaHCO3 concentration was reduced. 2. Intracellular pH (pHi) in isolated ferret detrusor cells was measured separately by epifluorescence microscopy. Extracellular pH changes caused by altering superfusate PCO2 were accompanied by similar changes of pHi, whereas variation of the NaHCO3 concentration had smaller effects on pHi. 3. It was proposed that intracellular acidosis increased contraction but extracellular acidosis depressed contraction. 4. Other interventions, such as addition and removal of NH4Cl, Cl- replacement, and NaHCO3 replacement with HEPES, changed pHi and had predictable effects on force. It was possible to describe unique relationships between tension and either intracellular or extracellular pH regardless of the means whereby pH changes were brought about. 5. Resting tension was reduced whether brought about by either intracellular or extracellular acidosis. K+ contractures were similarly affected by acidosis. Ferret preparations showed low levels of spontaneous activity, which was reduced by acidosis and enhanced by alkalosis.

1. The haemodynamic and hormonal changes following glucose ingestion (1 g/kg) were determined before and after pretreatment with either placebo or the somatostatin analogue, octreotide (SMS 201-995, 50 micrograms subcutaneously), in seven patients with chronic autonomic failure. 2. In the placebo phase, after glucose, there was a marked and prolonged fall in blood pressure with no change in cardiac index and peripheral blood flow. Plasma insulin and neurotensin levels increased, whereas glucagon, vasoactive intestinal polypeptide, noradrenaline and adrenaline levels were unchanged. 3. Octreotide transiently raised blood pressure and prevented glucose-induced hypotension. There were no changes in cardiac index or peripheral blood flow. Plasma insulin and neurotensin levels did not rise. Plasma glucose levels increased more slowly but reached a similar level to the placebo phase. 4. We conclude that in autonomic failure patients, glucose-induced hypotension was not accompanied by changes in cardiac index or peripheral blood flow, indicating a lack of compensation to probable splanchnic vasodilatation. The hypotension was prevented by the peptide release inhibitor, octreotide, with no change in cardiac index or in peripheral blood flow, suggesting an effect on the splanchnic vasculature, probably through inhibiting release of vasodilatatory pancreatic and gut peptides.

No abstract