Evidence for prejunctionally located ?2-adrenoceptors in the cat spleen

1986 ◽  
Vol 333 (4) ◽  
pp. 362-367 ◽  
Author(s):  
C. Dahl�f ◽  
A. Hedberg ◽  
V. Nerme
Keyword(s):  
Cat Spleen

What do antagonists tell us about α-adrenoceptors?

1985 ◽  
Vol 68 (s10) ◽  
pp. 15s-19s ◽  
Author(s):  
G. M. Drew
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Isolated Heart ◽  
Coupling Mechanism ◽  
Sympathetic Nerve Stimulation ◽  
Stimulus Response ◽  
Adrenoceptor Agonist ◽  
Tissue Responses ◽  
Cat Spleen ◽  
Relative Potencies

The early proposals that pre- and post-junctional α-adrenoceptors might be different stemmed largely from two separate observations. Firstly, the orders of potency of a series of agonists at inhibiting the response to sympathetic nerve stimulation and in increasing inotropic activity in the rabbit isolated heart were different [1, 2]. Secondly, phenoxybenzamine was more potent in inhibiting vasoconstrictor responses to sympathetic nerve stimulation than in increasing transmitter overflow from the cat spleen [3]. These experiments illustrate the most fundamental, pharmacological ways of distinguishing between receptors: namely, by comparing the relative potencies of agonists and/or antagonists in producing, or preventing, pharmacological effects. There are, however, difficulties in using agonists to classify receptors because their ability to generate a response depends not only upon their intrinsic properties of affinity for, and efficacy at, the receptors but also upon the capacity of the tissue to translate the stimulus into a response. Thus agonists with a relatively low intrinsic efficacy may produce a small response, or no response at all, in a tissue in which the efficiency of the stimulus-response coupling mechanism is low. The importance of this phenomenon in influencing tissue responses to agonists with low efficacy has been demonstrated for the α-adrenoceptor agonist prenalterol [4] and for the α-adrenoceptor agonist oxymetazoline [5].

pH environmental of red cells in the spleen

1976 ◽  
Vol 231 (6) ◽  
pp. 1672-1678 ◽  
Author(s):  
MJ Levesque ◽  
AC Groom
Keyword(s):  
Splenic Tissue ◽  
Red Cells ◽  
Red Cell ◽  
Cat Spleen ◽  
Flow Through ◽  
Red Pulp ◽  
Reduced Flow

Intrasplenic pH in vivo was deduced from measurements on blood drained from cat spleen during contraction with the inflow occluded. The pH of blood in the red pulp is normally 7.20, but stasis or reduced flow through the pulp causes pH to fall toward 6.8. The splenic pulp contains blood of high hematocrit. To evaluate the role of buffering by the red cells themselves, intrasplenic p/ in red cell-free spleens was, therefore, estimated atering and leaving the spleen during red cell washout. At inflow pH less than 6.8 the outflow pH was raised, at inflow pH = 6.8 there was no change, b,t at inflow pH greater than 6.8 the outflow pH was lowered. These results indicate that the pH environment of red cells in the spleen results indicate that the pH environment of red cells in the spleen results from the interplay of two separate factors: i) pH-determining elements of the splenic tissue that buffer at 6.8, and ii) buffering provided by red cells passing through the pulp.

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
Keyword(s):  
Smooth Muscle ◽  
Ambient Temperature ◽  
Cold Storage ◽  
Sodium Pump ◽  
Intracellular Sodium ◽  
Free Medium ◽  
Bathing Medium ◽  
Cat Spleen ◽  
Sodium And Potassium ◽  
Low Ambient Temperature

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.

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