Isolated Rat Portal Vein Research Articles

Cell volume as a factor influencing electrical and mechanical activity of vascular smooth muscle.

ABSTRACTThe effects of variations in the extracellular osmolarity on the electrical and mechanical activity of the isolated rat portal vein were studied. Addition of sucrose or xylose (20–100 mmoles/l) to the “normal” solution caused inhibition of contractile activity which could be ascribed to changes in the electrical discharge pattern. Increasing osmolarity with urea produced transient inhibition, return to control activity, and, on return to normal solution, a transient excitation. Reducing osmolarity by 30–60 mOsm/l by decreasing the [Na+] and [Cl] of the medium caused sustained excitation with continuous spike discharge and tetanic contraction. Comparable decreases in the ionic concentrations but with osmotic substitution by sucrose or xylose had little influence on muscle activity. Substituting Na+ and Cl with urea on an equiosmolar basis caused excitation resembling that in hypoosmotic solution. If the smooth muscle cells are looked upon as osmotic cells with membranes that are freely permeable to H2O and urea but less permeable to sugar and ions, the results indicate a consistent correlation between cell volume and state of activity; shrinkage associated with inhibition, swelling with excitation. Changes in the transuiembrane concentration gradients for K+, Na+ and Cl‐, caused by the cellular volume changes, are not sufficient to explain the electrical responses. Changes in ionic membrane permeability are assumed to occur.

Cell Volume as a Factor Influencing Electrical and Mechanical Activity of Vascular Smooth Muscle

The effects of variations in the extracellular osmolarity on the electrical and mechanical activity of the isolated rat portal vein were studied. Addition of sucrose or xylose (20–100 mmoles/l) to the “normal” solution caused inhibition of contractile activity which could be ascribed to changes in the electrical discharge pattern. Increasing osmolarity with urea produced transient inhibition, return to control activity, and, on return to normal solution, a transient excitation. Reducing osmolarity by 30–60 mOsm/l by decreasing the [Na+] and [Cl] of the medium caused sustained excitation with continuous spike discharge and tetanic contraction. Comparable decreases in the ionic concentrations but with osmotic substitution by sucrose or xylose had little influence on muscle activity. Substituting Na+ and Cl with urea on an equiosmolar basis caused excitation resembling that in hypoosmotic solution. If the smooth muscle cells are looked upon as osmotic cells with membranes that are freely permeable to H2O and urea but less permeable to sugar and ions, the results indicate a consistent correlation between cell volume and state of activity; shrinkage associated with inhibition, swelling with excitation. Changes in the transuiembrane concentration gradients for K+, Na+ and Cl-, caused by the cellular volume changes, are not sufficient to explain the electrical responses. Changes in ionic membrane permeability are assumed to occur.

Influence of the ionic environment on spontaneous electrical and mechanical activity of the rat portal vein.

The effects of variations in external K + and Ca 2+ concentrations on electrical and mechanical activity of the isolated rat portal vein were studied using a sucrose-gap technique. Spontaneous activity in normal Krebs solution consists of bursts of action potentials accompanied by phasic contractions. Moderate reduction in [K+] o results in slight hyperpolarization with decreased discharge frequency. Greater reduction or total removal of extracellular K causes a temporary increase in burst frequency. Graded increases in [K+] o from 6 up to 128 mM cause depolarization with an increase in discharge frequency and in contraction amplitude until [K+] o reaches a level of 6 to 7 times normal when spike potentials are abolished and a contracture develops. The relationship between membrance potential and log [K + ] o indicates a relatively low permeability to K + . Increasing [Ca 2+ ] o causes slight hyperpolarization, decreased burst frequency, increased burst duration and increased contraction amplitude. Reducing [Ca 2+ ] o causes increased frequency of discharge and shortening of bursts, until single spikes appear, each preceded by a prepotential; thus the activity resembles that in cardiac pacemaker cells. In Ca 2+ -free solution, electrical and mechanical activity ceases within 10 to 15 min. Calcium is essential for activation of the contractile mechanism and for maintenance of spontaneous spike discharge.