Alterations of Sodium Transport in Vascular Smooth Muscle in Hypertension

Author(s):  
Francis J. Haddy ◽  
Mortilal B. Pamnani ◽  
David L. Clough
Hypertension ◽  
1995 ◽  
Vol 25 (1) ◽  
pp. 117-123 ◽  
Author(s):  
Michael Christ ◽  
Kathrin Douwes ◽  
Christoph Eisen ◽  
Günther Bechtner ◽  
Karl Theisen ◽  
...  

1982 ◽  
Vol 243 (4) ◽  
pp. H551-H559
Author(s):  
J. G. De Mey ◽  
P. M. Vanhoutte

The effect of altering active sodium transport was compared in the denervated canine femoral artery and saphenous vein, which respond differently to a variety of humoral and physical stimuli. Potassium removal and ouabain caused contractions that were larger in the vein than in the artery. Activation of sodium transport, by exposing sodium-loaded preparations to potassium, caused transient ouabain-sensitive relaxations in both blood vessels; depending on the contractile agonist used, this relaxant effect was comparable (BaCl2) in both preparations or was larger (norepinephrine) in the artery than in the vein. In both the artery and the vein, potassium-induced relaxations were larger during contractions evoked by BaCl2 than those caused by norepinephrine. In the vein, contractions caused by acetylcholine were inhibited by potassium to the same extent as those caused by BaCl2. These results 1) are compatible with a contribution of sodium transport mechanism to the control of cell membrane permeability for extracellular calcium in vascular smooth muscle; 2) suggest that active sodium-calcium exchanges are functionally more important in venous than in arterial smooth muscle; and 3) illustrate that the heterogeneous behavior of vascular smooth muscle of different anatomic origins reflects differences in excitation-contraction coupling.


1989 ◽  
Vol 413 (5) ◽  
pp. 493-497 ◽  
Author(s):  
Michael Tuck ◽  
Patrick Hannaert ◽  
Elisabeth Jeanclos ◽  
Fran�oise Russo-Marie ◽  
Ricardo Garay

1995 ◽  
Vol 18 (7) ◽  
pp. 581-581
Author(s):  
M. Christ ◽  
K. Douwes ◽  
C. Eisen ◽  
G. Bechtner ◽  
K. Theisen ◽  
...  

Author(s):  
Martin Hagopian ◽  
Michael D. Gershon ◽  
Eladio A. Nunez

The ability of cardiac tissues to take up norepinephrine from an external medium is well known. Two mechanisms, called Uptake and Uptake respectively by Iversen have been differentiated. Uptake is a high affinity system associated with adrenergic neuronal elements. Uptake is a low affinity system, with a higher maximum rate than that of Uptake. Uptake has been associated with extraneuronal tissues such as cardiac muscle, fibroblasts or vascular smooth muscle. At low perfusion concentrations of norepinephrine most of the amine taken up by Uptake is metabolized. In order to study the localization of sites of norepinephrine storage following its uptake in the active bat heart, tritiated norepinephrine (2.5 mCi; 0.064 mg) was given intravenously to 2 bats. Monoamine oxidase had been inhibited with pheniprazine (10 mg/kg) one hour previously to decrease metabolism of norepinephrine.


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