Hypoxia causes a simultaneous increase in intracellular calcium and relaxation which, we propose, is the consequence of inhibition of oxidative phosphorylation with loss of high energy phosphates, necessary for the homeostasis of Ca2+ and the contractile mechanism of the cavernosal smooth muscle.

Summary. Intracellular C1, K and Na activities (a~l, ak and a~,) and transmucosal membrane potential (Lm) in epithelial cells of Necturus gallbladder were measured at different external Na concentrations ([Na]o), with liquid ion-exchanger and conventional microelectrodes. Bladders were mounted in a divided chamber at 23 ~ between identical HCO3-free Ringer solutions containing 5 mM K. The pH was 7.2. Tris was substituted for Na. Measurements were made under steady-state conditions as determined by the constancy of the transepithelial potential difference. Both, a~l and aN,~ increased in a saturable fashion with [Na]o. Em did not change significantly. Average values (• normal conditions ([Na]o= 100 mM)for acl,i aN,i andE,,were 16.8+0.8 mM (n=9), 9.7 + 0.6 mM (n = 10) and -52.6 _+ 0.6 mV (n = 26), respectively. In Na-free media a~a declined to its equilibrium value, a~: (96_+ 2 mM; n = 7) did not change when [Na]o was varied between 100 and 10mM but decreased to 80 + 3 m~ (n = 4) in Na-free media.Transmembrane electrochemical potential differences, Afij, for C1 and Na were calculated at four different [Na]o levels. A highly significant linear relation between A/~c~ and AfiNa was found, indicating that C1 and Na transport are energetically linked. The results support the view that the energy necessary for intracellular C1 accumulation is derived from the simultaneous dissipation of the chemical potential gradient of Na across the apical membrane and that the coupled entry mechanism is electroneutral.

Intracellular Na+, K+, and Cl- activities (aiNa, aiK, aiCl) and transapical membrane potentials (V0) were measured with liquid ion-exchanger and open-tip microelectrodes in isolated short-circuited frog skins (R. pipiens) incubated at 23 degrees C in normal amphibian Ringer's solution. Under control conditions aiNa = 14 +/- 3 mM, aiK = 132 +/- 10 mM and aiCl = 18 +/- 3 mM (SD). The value of aiCl is 4.4 times the value corresponding to electrochemical equilibrium for this ion. Thus, Cl- is actively accumulated by epithelial cells of the frog skin. Shortly after addition of amiloride (2--5 microM) to the apical bathing medium, aiK, aiNa, and aiCl were essentially unchanged although V0 had hyperpolarized by about 30--40 mV. During long-term exposure to amiloride aiK and aiCl did not change significantly, V0 depolarized by about 16 mV from the maximal value and aiNa decreased to 8 +/- 3 mM. Immediately after exposure to amiloride the transmembrane driving force for Na+ increased from 124 to 154 mV. During further exposure to amiloride, despite changes in both V0 and aiNa, this driving force remained virtually constant. Since Isc during this period was close to zero, it is suggested that the observed driving force for Na+ under these condition approximates the maximal driving force generated by the Na+--K+ ATP-ase pump in the basolateral cell membrane.

No abstract