Depolarization-stimulated 42K+ efflux in rat aorta is calcium- and cellular volume-dependent.

Abstract

The purpose of this study was to investigate the factors controlling membrane permeability to potassium of smooth muscle cells from rat aorta stimulated by depolarization. The increase in 42 K + efflux (change in the rate constant) induced by depolarization (application of high concentrations of potassium chloride) was inhibited significantly by the calcium antagonists diltiazem and nisoldipine. Parallel inhibitory effects on contraction were observed. Diltiazem also inhibited potassium-stimulated + efflux also diminished as the potassium chloride concentration was elevated. The component of efflux that was resistant to calcium antagonists probably resulted from a decrease in the electrochemical gradient for potassium. Cellular water did not change during potassium addition. Substitution of 80 and 150 mM KCI for sodium chloride produced cellular swelling and enhanced potassium-stimulated 42 K + efflux compared with potassium chloride addition. The addition of sucrose to prevent cellular swelling reduced efflux response to potassium substitution toward that of potassium addition. A hvpoosmolar physiologic solution produced an increase in the 42 K + efflux and a contracture that were both prevented by the addition of sucrose. We concluded that the depolarization-mediated 42 K + efflux has three components: one is calcium dependent; a second is dependent on cellular volume; and a third is resistant to inhibition by calcium antagonists. (Circulation Research

Calcium antagonists inhibit elevated potassium efflux from aorta of aldosterone-salt hypertensive rats.

“…VSM 25 -29 was shown to increase potassium efflux as well. 30 Both calcium entry and potassium efflux from control VSM were inhibited by concentrations of diltiazem (IC 50 =0.6 yM) and nisoldipine (IC 50 =2 n M)26,27,3o equivalent to those that inhibited the basal potassium efflux in AHR aorta (diltiazem IC 50 =0.2 /JM, nisoldipine IC 50 =1.8 nM). Likewise, the nisoldipine IC 50 was similar to the binding constant for single POC in VSM.…”

“…For example, the diltiazem and nisoldipine IC 50 for inhibition of basal potassium efflux in AHR was similar to that for KCl-stimulated potassium efflux from CS rats, whereas the IC 50 for inhibition of basal tension in AHR was 10-37-fold less than that for inhibition of KClstimulated contraction in control rat aortas ( Figure 7). 30 The reason for the increased sensitivity of basal tension in AHR to calcium antagonists is not readily apparent. Actions on sites other than POC require much higher concentrations.…”

Sarcoplasmic reticulum buffering of myoplasmic calcium in bovine coronary artery smooth muscle.

“…Also, mild depolarization without the effects of extracellular Na+ removal involved adding 25 mM-KCl to increase the total extracellular KCl to 30 mm and adjusting the pH with 5 mM-KOH, rather than NaOH, thus yielding 35 mM-final extracellular [K+] (solution termed + 35 K). The added osmolarity from the KCl was without adverse effects (Magliola & Jones, 1987 [Ca2+] in mock intracellular solutions for the two microfluorometry systems. The data are very similar to other reports (Poenie, Alderton, Steinhardt & Tsien, 1986;Thayer et al 1988) using very Ca2+ BUFFERING IN SMOOTH MUSCLE different optics.…”

Sodium nitroprusside alters Ca2+ flux components and Ca2(+)‐dependent fluxes of K+ and Cl‐ in rat aorta.

“…Noradrenaline (NA)-and KCl depolarization (high potassium)-stimulated 42K+ and 36Cl-effluxes from rat aorta have been shown to depend on [Ca2+]c for their activation (Smith & Jones, 1985;Magliola & Jones, 1987). The Ca2+ dependence was exploited in this study by using the flux responses to NA and high potassium to monitor changes in [Ca2+]c.…”

“…Tissue radioactivity (c.p.m.) was converted to influx values (/4mol (1 cell H2O)W min-') based on the specific activity of the standards and a ratio of 0-791 cell H20 (kg dry weight)-' for rat aorta (Magliola & Jones, 1987).…”