Calcium-dependent fluxes of potassium-42 and chloride-36 during norepinephrine activation of rat aorta.

Abstract

This study was designed to determine whether alpha-receptor-stimulated monovalent ionic fluxes in rat aorta required calcium, and, if so, whether both extracellular calcium and cellularly stored calcium are active. Calcium removal in the presence of 10 mM magnesium (to maintain membrane stability) inhibited the norepinephrine-stimulated increase in potassium-42 and chloride-36 efflux. However, the norepinephrine-stimulated increase in sodium-24 influx was relatively resistant to calcium depletion. Protocols were designed to measure the time course for the changes in potassium-42 efflux and contraction when calcium was removed or replaced in the presence of norepinephrine. The dose-dependent effect of a calcium antagonist (diltiazem) was also measured. A close correlation (r = 0.94) was found between inhibition of contraction and potassium-42 effluxes which followed the regression: % potassium-42 response = 1.0 X (% contraction) + 1.8%). The slope of 1.0 and intercept near zero suggests the hypothesis that norepinephrine-stimulated potassium-42 efflux and contraction are codependent on cellular calcium concentration. This co-dependence held for short phasic responses (approximately 1 minute), as well as longer tonic responses (greater than or equal to 5 minutes). It appears that calcium-dependent potassium-42 effluxes can be supported by both the influx of extracellular calcium and release of cellular stores. It is concluded that calcium-dependent potassium channels (and possibly chloride channels) are operative in rat aorta and are an important component of the graded membrane response to norepinephrine. The sodium channels, however, do not appear to share this same calcium dependency.

Calcium currents are altered in the vascular muscle cell membrane of spontaneously hypertensive rats.

“…The final concentration of cytoplasmic calcium available to bind the contractile proteins will be determined simultaneously by not only the pattern of calcium influx, but also intracellular calcium binding, release, reuptake, and active extrusion by the sarcolemma (for review, see Kwan 1 )-The influx of calcium also will activate other ion channels, such as the calcium-activated K + channels, 26 -29 whose function also could be altered in the hypertensive state. 30 The major role for L calcium channels in initiating and maintaining vascular tone is likely but still speculative.…”

The action of noradrenaline on single smooth muscle cells freshly dispersed from the guinea‐pig pulmonary artery

“…In whole tissue preparations bathed in low chloride solution noradrenaline evokes hyperpolarization (Large, unpublished), which suggests that areceptor stimulation does lead to an increase in potassium conductance in the pulmonary artery. It is interesting that in the rabbit pulmonary artery noradrenaline increases the efflux of 42K, 'Cl and 22Na (Casteels et al, 1977;Smith & Jones, 1985).…”

Altered biochemical and functional responses in aorta from hypertensive rats.

“…The relations were shifted to the left (indicating supersensitivity) in AHR. Since these processes are calciumdependent in rat aorta, 27 the shift in both responses indicates that a common defect may exist between aadrenergic receptor occupancy and calcium signaling. The effects of NE were also evaluated in the presence of lithium, because the protocol for measuring IP and IP 2 employed lithium, an ion that is known to alter Na + -K + transport.…”