Some effects of the ionophore X-537A on the isolated rat tail artery

1978 ◽  
Vol 56 (3) ◽  
pp. 474-482 ◽  
Author(s):  
Vladimír Palatý ◽  
Mary E. Todd
Keyword(s):  
Smooth Muscle ◽  
Contractile Response ◽  
Rat Tail Artery ◽  
Concentration Gradients ◽  
Irreversible Loss ◽  
Tail Artery ◽  
Endogenous Catecholamines ◽  
Rat Tail ◽  
Isolated Rat ◽  
Stimulation Of

The effects of micromolar concentrations of the ionophore X-537A (RO 2-2985) were studied using isolated preparations of the rat tail artery. The ionophore causes complete release of catecholamines from adrenergic nerves, which is the sole cause of the transient contractile response. The amines are released by a nonexocytotic process which seems to be related to the ability of X-537A to act as an efficient transmembrane carrier of Na+, K+, and H+ The ionophore also causes an almost complete and irreversible loss of the cocaine-sensitive component of metaraminol uptake by the tissue. X-537A dissipates the transmembrane concentration gradients of Na and K in the smooth muscle component of the preparation. This effect is unrelated to the release of endogenous catecholamines, and it can also be observed after the Na pump has been inhibited with ouabain. It is fully reversible, though not readily, and it can be induced repeatedly. In catecholamine-depleted strips, X-537A dissipates the transmembrane Na+ and K+ gradients without causing any change in tension. Stimulation of the rate of O2 consumption by X-537A in catecholamine-depleted tissue is reversible, and it is unaffected by ouabain and (or) removal of external Ca2+.

The transient contractile response of the isolated rat tail artery to inhibition of the sodium pump

1980 ◽  
Vol 58 (4) ◽  
pp. 336-339 ◽  
Author(s):  
Vladimír Palatý
Keyword(s):  
Smooth Muscle ◽  
Sodium Pump ◽  
Contractile Response ◽  
Physiological Salt Solution ◽  
Rat Tail Artery ◽  
Active Tension ◽  
Tail Artery ◽  
Endogenous Catecholamines ◽  
Rat Tail ◽  
Isolated Rat

The isolated rat tail artery responds to incubation in 1 mM ouabain containing, K-free physiological salt solution by transient contraction which is due to release of endogenous catecholamines. The eventual decline in active tension cannot be attributed solely to the decreasing rate of release of endogenous catecholamines, for the latter remains quite high even after the preparation has relaxed completely. It seems, therefore, that the relaxation is due also to the substantial decrease in the responsiveness of smooth muscle cells to (−)-norepinephrine that accompanies dissipation of the transmembrane gradients of Na+ and K+.

Protein kinase C reduces the KCa current of rat tail artery smooth muscle cells

1999 ◽  
Vol 276 (3) ◽  
pp. C648-C658 ◽  
Author(s):  
Rudolf Schubert ◽  
Thomas Noack ◽  
Vladimir N. Serebryakov
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Rat Tail Artery ◽  
Tail Artery ◽  
Kinase C ◽  
Rat Tail ◽  
Isolated Rat

The hypothesis that protein kinase C (PKC) is able to regulate the whole cell Ca-activated K (KCa) current independently of PKC effects on local Ca release events was tested using the patch-clamp technique and freshly isolated rat tail artery smooth muscle cells dialyzed with a strongly buffered low-Ca solution. The active diacylglycerol analog 1,2-dioctanoyl- sn-glycerol (DOG) at 10 μM attenuated the current-voltage ( I- V) relationship of the KCa current significantly and reduced the KCacurrent at +70 mV by 70 ± 4% ( n = 14). In contrast, 10 μM DOG after pretreatment of the cells with 1 μM calphostin C or 1 μM PKC inhibitor peptide, selective PKC inhibitors, and 10 μM 1,3-dioctanoyl- sn-glycerol, an inactive diacylglycerol analog, did not significantly alter the KCa current. Furthermore, the catalytic subunit of PKC (PKCC) at 0.1 U/ml attenuated the I- Vrelationship of the KCa current significantly, reduced the KCacurrent at +70 mV by 44 ± 3% ( n = 17), and inhibited the activity of single KCa channels at 0 mV by 79 ± 9% ( n = 6). In contrast, 0.1 U/ml heat-inactivated PKCC did not significantly alter the KCacurrent or the activity of single KCa channels. Thus these results suggest that PKC is able to considerably attenuate the KCa current of freshly isolated rat tail artery smooth muscle cells independently of effects of PKC on local Ca release events, most likely by a direct effect on the KCa channel.

Two types of calcium channels in isolated smooth muscle cells from rat tail artery

1989 ◽  
Vol 256 (5) ◽  
pp. H1361-H1368 ◽  
Author(s):  
R. Wang ◽  
E. Karpinski ◽  
P. K. Pang
Keyword(s):  
Smooth Muscle ◽  
Steady State ◽  
Calcium Channels ◽  
Rat Tail Artery ◽  
Inward Current ◽  
Tail Artery ◽  
Channel Current ◽  
Steady State Inactivation ◽  
Channel Currents ◽  
Rat Tail

Whole cell patch-clamp recordings were carried out on smooth muscle cells from rat tail artery in short-term culture to verify the existence of and to characterize the calcium channels that are present. Two types of voltage-dependent calcium channels were identified in 55 of 63 cells studied. The T-type calcium channel was activated at -50 mV, and the peak inward current occurred at -10 mV, whereas the L-type channel was activated at -20 mV, and the peak inward current occurred at +10 or +20 mV. The T-type channel current inactivated quickly in contrast to the much slower inactivation of the L-channel current. The voltage dependence of steady-state inactivation of the two channels was similar to that reported for other vascular smooth muscle preparations. An internal solution containing Cs2-aspartate maintained the calcium-channel currents for at least 20 min with only a 5-10% decline. BAY K 8644 had no effect on T-channel currents, but the L-channel current was increased by at least a factor of two. In addition, BAY K 8644 shifted the activation threshold, the peak inward current, and the steady-state inactivation-activation curves of L-type channel currents in the direction of hyperpolarization.

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