EFFECTS OF IONS ON VASCULAR SMOOTH MUSCLE I 1 55 



""" man 



8.M9 NOREPI 

 14 kg cf 



fig. 8. Changes in blood (Na + ) and (K + J monitored with the Na electrode (Na/K = 250/1) 

 and K electrode (K/Na = 5/1) in the dog during A, systemic blood pressure rise induced with 

 norepinephrine and B, limb pressure rise induced with norepinephrine. [.4, from Friedman et at. 

 (81).] 



found that dog carotid artery rings stimulated electri- 

 cally gained Na and lost K. Epinephrine, however, in 

 an amount sufficient to produce the same contractile 

 response did not produce these changes. 



We may conclude that, in general, an acute in- 

 crease in tension of vascular smooth muscle is asso- 

 ciated with a gain in Na, and a gain in water. There 

 is a strong suggestion that in some instances, at 

 least, the gain in water may overshadow the gain in 

 Na and may also anticipate it. A loss in K from cells 

 to environment is almost always observed. Similar 

 ionic exchanges have been observed both in taenia 

 coli and uterus during activity (16, 124). 



These experiments give no information regarding 

 the time relations connecting these phenomena nor do 

 they suggest which event is cause and which is effect. 



Evidence from Studies of the Relation of Electrical 

 Activity to Tension in Vascular or Analogous Tissues 



Bacq & Monnier (7) studied the relation of electri- 

 cal activity to tension in a variety of smooth muscles 

 obtained from the cat. They claimed that the laws 

 common to all excitable tissues apply to smooth 

 muscle as well. In their view the response to every 

 excitation, in this case contraction or increase in tone, 

 no matter how produced, is accompanied by a de- 

 crease in polarization. They considered the change in 

 polarization to be the cause of the change in tonus. 

 In accordance with theories current at that time de- 



polarization was attributed to the exit of K + from 

 cells. 



Although Bozler (17) carried out the first basic 

 studies of electrical activity in smooth muscle using 

 modern techniques it remained for Bulbring and her 

 associates to carry out the difficult task of denning the 

 ionic basis of that activity. In 1954 data were pre- 

 sented for guinea pig taenia coli suggesting that 

 tension is inversely, and spike frequency directly, re- 

 lated to the membrane potential (19). 



We can summarize these first experiments in a 

 simplified form. A resting membrane potential of 60 

 ± 9 mv fell to 43 ± 10 and spike frequency increased 

 when the tissue was stretched (increased tension). 

 Histamine induced a fall in potential from 58 to 40 mv 

 while tension and spike frequency increased. Epi- 

 nephrine induced an increase in potential and a de- 

 crease in tension and spike frequency. Acetylcholine 

 caused a fall in potential and increase in spike fre- 

 quency and tension. Shortly thereafter Bulbring (20) 

 reported that the increase in rate of spike discharge 

 was proportional to the increase in tension. Then, 

 in 1 955 (2 1 ), fluctuations in membrane potential were 

 observed to be related to the spontaneous rhythm of 

 the taenia coli strip and periods of depolarization as- 

 sociated with increased tension and increased rate of 

 spike discharge alternated with periods of repolariza- 

 tion, reduced spike frequency, and lower tension. 



From this basis Born & Bulbring (16) then pro- 

 ceeded to the still more difficult technical problem of 



