Vascular Resistance and Na+–K+ Gradients in the Perfused Rat-Tail Artery

1973 ◽  
Vol 51 (6) ◽  
pp. 410-417 ◽  
Author(s):  
S. M. Friedman ◽  
M. Nakashima ◽  
V. Palatý ◽  
B. K. Walters
Keyword(s):  
Vascular Resistance ◽  
Arterial Wall ◽  
Physiological Salt Solution ◽  
Delayed Response ◽  
Rat Tail Artery ◽  
Free Solution ◽  
Experimental Conditions ◽  
Tail Artery ◽  
External Potassium ◽  
Rat Tail

The changes in the resistance of the perfused ventral rat-tail artery resulting from exposure of the tissue to ouabain-containing and/or K+-free physiological salt solution were studied. In each case, there was an increase in the vascular resistance which was not sustained. The response of the arterial wall to the above stimuli was abolished in the absence of external Ca2+. In contrast to the delayed response of the wall to either ouabain-containing or K+-free solution, an almost instantaneous rise in the resistance was observed if the two stimuli were combined, though the rate of loss of the tissue K+ was not accelerated significantly under these experimental conditions. The tension developed in K+-free solution was relieved almost instantaneously upon readmittance of external potassium.

Release of endogenous noradrenaline from the rat tail artery induced by veratridine

1982 ◽  
Vol 60 (6) ◽  
pp. 805-810 ◽  
Author(s):  
Vladimír Palatý
Keyword(s):  
Sodium Pump ◽  
Rat Tail Artery ◽  
Free Solution ◽  
Release Of Noradrenaline ◽  
Tail Artery ◽  
Low Concentrations ◽  
Endogenous Noradrenaline ◽  
Increased Activity ◽  
Rat Tail ◽  
Isolated Rat

The overflow of endogenous noradrenaline from the isolated rat tail artery was measured using a radioenzymatic method. Veratridine increased the overflow markedly even in the absence of external Ca2+. Modifications of the effect of 5 μM veratridine by tetrodotoxin, pargyline, cocaine, lidocaine, and phenoxybenzamine indicated that interaction of the alkaloid with the sodium channel induces primarily nonexocytotic release of noradrenaline. Ouabain inhibited the effect of 5 μM veratridine on the overflow into Ca2+ -free solution, but it greatly potentiated the effect if external Ca2+ was present. Potentiation of the effect of veratridine in Ca2+-free solution by cyanide was ouabain sensitive. These observations are consistent with the hypothesis that, at low concentrations of veratridine such as 5 μM, the initial cause of enhanced release of noradrenaline may be a consequence of increased activity of the sodium pump, namely increased consumption of ATP by the pump.

Hydrallazine: Mode of Action at the Neuroarterial Junction

1980 ◽  
Vol 59 (s6) ◽  
pp. 445s-447s ◽  
Author(s):  
C. Chevillard ◽  
B. Saiag ◽  
M. Worcel
Keyword(s):  
Wistar Rats ◽  
Direct Action ◽  
Nerve Terminals ◽  
Rat Tail Artery ◽  
Experimental Conditions ◽  
Tail Artery ◽  
Marked Inhibition ◽  
6 Hydroxydopamine ◽  
Rat Tail

1. Hydrallazine relaxes the rat tail artery by a direct action on vascular smooth muscle cells, which appears to be modulated by the action of sympathetic nerve terminals. 2. There is a gradient of response to hydrallazine in arteries from normotensive Wistar rats, the proximal segments being poorly responsive. This gradient disappears after denervation with 6-hydroxydopamine in vitro. 3. Exogenously added purines inhibit noncompetitively the vasodilator response to hydrallazine in denervated segments from normotensive Wistar rats. Their order of potency is 2-Cl-adenosine > adenosine > ATP > inosine. 4. The effect of hydrallazine in innervated, poorly responsive segments is greatly potentiated by theophylline (50 μmol/l) and propranolol (5 μmol/l). These results, together with the effect of denervation, suggest that there are endogenous purines leaking from the nerve terminals under our experimental conditions. 5. Hydrallazine produces a marked inhibition of stimulus-induced contraction and 3H release after [3H]noradrenaline loading. The mechanism of this prejunctional action appears to be different from the mechanism of the postjunctional effect.

Release of 3,4-dihydroxyphenylglycol from the rat tail artery induced by veratridine

1984 ◽  
Vol 62 (1) ◽  
pp. 151-152 ◽  
Author(s):  
Vladimír Palatý
Keyword(s):  
Amperometric Detection ◽  
Neuronal Uptake ◽  
Rat Tail Artery ◽  
Free Solution ◽  
Release Of Noradrenaline ◽  
Tail Artery ◽  
Storage Vesicles ◽  
Rat Tail ◽  
Isolated Rat ◽  
External K

The overflow of endogenous 3,4-dihydroxyphenylethylene glycol and noradrenaline from the isolated rat tail artery was measured by high pressure liquid chromatography with amperometric detection. Veratridine, but not elevated external K, caused a significant increase in the overflow of the glycol under conditions when formation of the latter from released noradrenaline was prevented by blockade of neuronal uptake1 with desipramine. The results support the hypothesis that, in addition to evoking exocytotic release of noradrenaline into Ca-containing solution, the alkaloid also increases leakage of noradrenaline from storage vesicles. The latter process seems responsible for veratridine-induced release of noradrenaline into Ca2+-free solution.

Sodium binding in the arterial wall

1969 ◽  
Vol 47 (9) ◽  
pp. 763-770 ◽  
Author(s):  
Vladimír Palatý ◽  
Brigid Gustafson ◽  
Sydney M. Friedman
Keyword(s):  
Arterial Wall ◽  
Plasma Concentrations ◽  
Carboxyl Groups ◽  
Rat Tail Artery ◽  
Sodium Ions ◽  
Tail Artery ◽  
Sodium Binding ◽  
Average Size ◽  
Rat Tail ◽  
Sulfo Groups

There are two fractions of sodium in the arterial wall which can be selectively and reversibly exchanged for other ions. These fractions are believed to be bound to the acid mucopolysaccharide – protein component of the paracellular matrix. The first fraction seems to be loosely bound by weakly acidic groups, probably the carboxyl groups of the hexuronic acid moieties. It can be exchanged for hydrogen even in neutral solutions by reducing the concentration of sodium ions in the medium. In the rat tail artery, the average size of this fraction did not exceed 0.5 meq/100 g of dry fat-free tissue. The second fraction behaves as if it is more tightly bound, apparently by strongly acidic groups like the sulfo groups of the mucopolysaccharides. It amounts to 2.21 ± 0.20 meq/100 g of dry fat-free tissue if a simplified system of sodium and calcium chloride solutions is used. In the presence of normal plasma concentrations of potassium and magnesium, the sum of both sodium fractions is increased substantially and is equal to approximately 5 meq/100 g of dry fat-free tissue. This bound sodium is increased in arteries of immature animals and animals with established DOCA hypertension, both of which have a higher content of the acid mucopolysaccharides.

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+.

Fine tuning by protein kinases of CaV1.2 channel current in rat tail artery myocytes

2020 ◽  
Vol 182 ◽  
pp. 114263
Author(s):  
F. Fusi ◽  
P. Mugnai ◽  
A. Trezza ◽  
O. Spiga ◽  
G. Sgaragli
Keyword(s):  
Protein Kinases ◽  
Fine Tuning ◽  
Rat Tail Artery ◽  
Tail Artery ◽  
Channel Current ◽  
Cav1.2 Channel Current ◽  
Rat Tail

Neural control of reinnervated rat tail artery is restored despite incomplete perivascular plexus

2007 ◽  
Vol 135 (1-2) ◽  
pp. 130
Author(s):  
James A. Brock ◽  
Diana Tripovic ◽  
Svetlana Pianova ◽  
Elspeth M. McLachlan
Keyword(s):  
Neural Control ◽  
Rat Tail Artery ◽  
Tail Artery ◽  
Perivascular Plexus ◽  
Rat Tail

Ca2+-dependence of endothelin-1 induced contraction of rat tail artery

1991 ◽  
Vol 22 (2) ◽  
pp. 399-402 ◽  
Author(s):  
Xie-Nan Huang ◽  
Issei Takayanagi ◽  
Ryuichi Kurata ◽  
Tetsuhiro Hisayama
Keyword(s):  
Rat Tail Artery ◽  
Tail Artery ◽  
Endothelin 1 ◽  
Rat Tail

Calcium Efflux in Rat Tail Artery during Potassium Induced Relaxation

1980 ◽  
Vol 164 (3) ◽  
pp. 252-256 ◽  
Author(s):  
R. C. Webb ◽  
P. M. Vanhoutte ◽  
D. F. Bohr
Keyword(s):  
Rat Tail Artery ◽  
Calcium Efflux ◽  
Tail Artery ◽  
Rat Tail
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