Potassium and the recovery of splenic capsular smooth muscle after cold storage

1976 ◽  
Vol 54 (3) ◽  
pp. 322-326
Author(s):  
D. Bose ◽  
I. R. Innes

Cat spleen capsular smooth muscle, depleted of potassium and enriched with sodium by cold storage in a potassium free medium, relaxed and underwent transient reduction in responsiveness to noradrenaline when potassium was introduced into the bathing medium. Both these effects could be blocked by ouabain, lithium substitution for sodium or low ambient temperature, suggesting possible involvement of the sodium pump. In the continued presence of potassium, relaxation was maintained but sensitivity to noradrenaline increased, possibly due to restoration of normal intracellular sodium and potassium concentrations.

1972 ◽  
Vol 50 (4) ◽  
pp. 378-380 ◽  
Author(s):  
Deepak Bose ◽  
Ian R. Innes

Ouabain or replacement of NaCl by LiCl abolishes the relaxation due to addition of KCl to sodium-rich cat carotid artery strips kept in a K+-free medium. Neither treatment antagonizes the relaxation due to β-adrenoceptor stimulation by l-isoprenaline. Unlike KCl-induced relaxation, the relaxation induced by l-isoprenaline is not due to stimulation of an electrogenic sodium pump.


1975 ◽  
Vol 53 (4) ◽  
pp. 586-591 ◽  
Author(s):  
D. Bose ◽  
I. R. Innes

Isometric contraction of cat spleen capsule due to noradrenaline had a fast and a slow phase. These phases were due to a tightly and a loosely bound (or extracellular) pool of calcium, respectively. Depolarization due to high potassium caused mainly a reduction of the slow phase. In sodium-loaded spleen strips recovering from potassium deprivation, the sodium pump is electrogenic and the muscle cells are probably hyperpolarized. In this situation also the slow phase of noradrenaline response is reduced. It is concluded that both depolarization and hyper-polarization affect the utilization of loosely bound calcium and that tightly bound calcium may be released during 'pharmacomechanical coupling' in splenic smooth muscle.


1987 ◽  
Vol 65 (2) ◽  
pp. 159-164 ◽  
Author(s):  
B. A. Mallick ◽  
D. Bose ◽  
T. Chau ◽  
B. Y. Ong

Cerebral blood flow autoregulation is impaired in newborn animals when a brief period of hypoxia is followed by normoxia. Because myogenic mechanisms are widely thought to be responsible for autoregulation, this study examined the effect of hypoxia and reoxygenation on the isometric mechanical function of isolated cerebral (basilar) arterial smooth muscle made to contract rhythmically and thus simulate the behaviour of arterioles. Although at rest a small amount of active tension was present in these preparations, this tension was further increased and the muscle was rendered spontaneously rhythmic by treatment with 4-aminopyridine. Reduction of bath [Formula: see text] from 120 to 25 mmHg (1 mmHg = 133.32 Pa) caused an increase in tension followed by a return towards normal tension. At this time rhythmic oscillations gradually decreased in amplitude. Restoration of normal oxygen tension caused a rapid reduction and an undershoot in tension followed by recovery to normal level. Two possible mechanisms for this undershoot, which may be due to a decrease in myogenic responsiveness and therefore of autoregulatory function, were tested. 8-Phenyltheophylline, an antagonist of adenosine receptors, caused a decrease in the inhibitory mechanical effects of adenosine (10−6–10− M). However, in the presence of 8-phenyltheophylline, there was no change in the undershoot in tension caused by reoxygenation, thus ruling out involvement of adenosine released from the vessel in smooth muscle inhibition due to hypoxia. In a separate series of experiments, the role of an electrogenic sodium pump in causing the undershoot was tested. Treatment with 5-hydroxytryptamine in a K+ -free bathing medium caused an increase in basilar artery tension. When normal potassium concentration was restored the muscle relaxed with a transient undershoot below the basal tension level. In muscle preparations pretreated with ouabain (3 × 10−6 M), the K+-induced undershoot was abolished and replaced by a transient contraction. The same concentration of ouabain decreased by 92% the tension undershoot caused by reoxygenation. These experiments rule out participation of adenosine released from the blood vessel in the loss of myogenic tone during reoxygenation. The data also indicate that reactivation of the sodium pump may be responsible to some extent for the undershoot in tone during reoxygenation of isolated canine basilar artery.


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