EFFECTS OF IONS ON VASCULAR SMOOTH MUSCLE 



hypertension that may persist after excision of an 

 ischemic kidney all show an increase in aorta Na and 

 K.. This increase seemed to them to represent a true 

 gain in Na, and K,. There is a suggestion that these 

 studies may be pertinent to the problem of hyper- 

 tension in man, for Tobian & Binion ( 1 95 ) found an 

 increase of both Na and water in the renal arteries of 

 human hypertensives. Na was increased more than 

 water, but the technique used cannot distinguish 

 intracellular from extracellular locations. Not too 

 much weight should be given this type of stud\ , 

 however, for as all workers in the field know, electro- 

 lytes may exchange rapidly across vessel walls both 

 immediately preceding and certainly after death. 



In general, experiments in many laboratories 

 support the thesis that Na and K in tissues are altered 

 in hypertension, but the emphasis shifts now to the 

 one, now to the other. Thus, Eichelberger (53) long 

 ago measured an increase in Na and fall in K in the 

 skeletal muscle of dogs made hypertensive by renal 

 constriction. Assuming an extracellular position for 

 chloride there appeared to be a true rise in Na, and 

 fall in K,. Laramore & Grollman (132) found a 

 general rise in tissue Na and water and a fall in K 

 in the later stages of renal hypertension in the rat. 

 Later, however, Grollman (96) found the same 

 quantities unchanged in hypertension produced as a 

 late sequela of choline deficiency. More recently 

 Kolctsky et al. (i2g) analyzed the mesenteric arteries 

 of rats with acute renal hypertension and also found 

 a gain in Na, K, chloride, and water. These authors, 

 however, cautiously refrained from attempting to 

 partition the electrolytes on the basis of chloride 

 space. 



In agreement with Tobian and associates, Freed 

 et al. (70) found an elevation in aorta K in renal 

 hypertensive rats but a less well-defined increase in 

 Na. The reduction of the hypertension by dietary K 

 deprivation was followed by a proportionate decrease 

 in aorta K, and the return to hypertensive levels on 

 refeeding K was accompanied by a return rise in 

 aorta K. On examining the data, however, it is 

 evident that the increase in aorta K occurs in rats 

 with renal constriction whether or not the pressure 

 goes up. This same inconsistency was noted by 

 Tobian & Binion (196). 



Laszt (133) does not find an increase in aorta Na 

 at all consistent with the presence of hypertension in 

 rats, but claims the rise of K to be so. 



Houck (119) pointed out that dogs maintained in 

 good balance for 5 to 1 1 1 days following bilateral 

 nephrectomy show a gain in tissue Na and fall in K 



despite relatively normal extracellular values. This 

 apparently indicates an association of their sustained 

 hypertension with an elevation of Na, and fall in K.,. 

 Greene & Sapirstein (95) found an increase in total 

 body Na in rats made hypertensive by subtotal 

 nephrectomy. Haight & Weller (103) studied rats 

 made hypertensive by chronic high salt feeding; 

 they found hypernatremia and an increase in skeletal 

 and heart muscle Na and K. especially pronounced in 

 the hypertensive rats but no conspicuous differences 

 in aorta electrolytes. 



Other sustained abnormal blood pressures. The regularly 

 observed fall in blood pressure in Addison's disease or 

 following adrenalectomy requires no comment. 

 Among other phenomena, it is associated with a 

 reduction of tissue Na from both intracellular and 

 extracellular compartments (30, 52). 



Freed et al. (69) examined the relation of plasma 

 to aorta Na and K in rats made hypotensive by K 

 deprivation. Both Na and K declined in plasma as 

 well as in the aorta, although the authors stress only 

 the change in K. Tobian (191) found that rats on a 

 low Na diet lose a sizeable amount of aorta Na, while 

 serum Na may actually rise a little. Although blood 

 pressure was not measured it was assumed to tend 

 toward lower values. 



Trauma may lead to a "posttraumatic sodium- 

 potassium shift" during which plasma Na falls and 

 K rises. This is associated with hypotension (186). 



MEASUREMENT OF Na AND K IN ACUTE HYPERTENSION 



or hypotension. Although investigation of the 

 association between acute changes in blood pressure 

 and electrolyte exchanges is comparatively recent, 

 the findings are more clear-cut than any we have so 

 far considered. The independent findings from 

 different laboratories all fit together nicely even 

 though interpretations vary. Since this approach 

 bears directly on the relation of ions to vascular 

 smooth muscle tension, the facts obtained must form 

 the basis of all theoretical discussion. Accordingly, 

 we shall present these facts in some detail. 



Perhaps the earliest report of a relation between 

 ionic concentration in the serum and a pressor agent 

 was that of D'Silva (50) in 1934. He reported that, 

 in the cat, following the intravenous injection of 50 

 /ig of epinephrine or 10 units of Pitressin intra- 

 venously serum K. rose sharply as much as 3 meq per 

 liter within 1 min. Since these massive doses of the 

 order of 10 fig per kg epinephrine and 2 units of 

 Pitressin per kg also caused a rise in blood sugar, this 

 author related the K rise to the glycogenolytic effect 



