Reversible stimulation of sodium transport in the toad bladder by stretch.
Short-circuit current and transepithelial potential difference were measured in toad hemibladders mounted as sacs on glass cannulae. When sac volume was changed by adding or removing fluid, short circuit current responded by increasing or decreasing during the ensuing half-hour. The time course of the response and its magnitude indicated that it was not artefactual. Furthermore, net sodium flux responded similarly. Sac volume, and thus bladder surface area, could be varied from 0.03 to 0.4 cm(2)/mg wet weight. The mean response to either decreases or increases was 10 muA/cm(2). Everted hemibladders, however, responded less. Neither hydrostatic pressure, nor increased chloride conductance, nor increased access of oxygen or glucose to the mucosa was responsible for the response. Tissue conductance did vary markedly with volume, and may have played a role, but sodium conductance did not vary with volume in a consistent manner. The results indicate the existence of an intrinsic mechanism in this tissue which alters sodium transport in response to stretch.
D000818:Animals; D001001:Anura; D001692:Biological Transport; D002712:Chlorides / Q000502:physiology; D004548:Elasticity; D004558:Electric Stimulation; D004594:Electrophysiology; D004848:Epithelium / Q000502:physiology; D005947:Glucose / Q000502:physiology; D008564:Membrane Potentials; D010100:Oxygen / Q000502:physiology; D012964:Sodium / Q000502:physiology*; D012975:Sodium Isotopes; D001743:Urinary Bladder / Q000502:physiology*
D002712:Chlorides; D012975:Sodium Isotopes; D012964:Sodium; D005947:Glucose; D010100:Oxygen
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