216 E. G. HOSKINS 



is depressed pari passu with the vasoconstrictor effect. This renders 

 important, *as bearing on renal physiology, a definite determination 

 whether the vasodilatation reported by Bardier and Frenkel and by Ogawa 

 is a significant feature of the response to epinephrin injection. If such 

 dilatation is characteristic, then epinephrin diuresis (such as has been 

 described by Kleiner and Meltzer) may be ascribed to local vasomotor ef- 

 fects in the kidneys. The fact that vasodilatation was observed only as 

 a secondary effect with larger doses when the epinephrin would supposedly 

 be largely destroyed, or as a primary effect only when very small concen- 

 trations were employed, points toward this as a physiological mechanism, 

 since it is probable that the body normally has to deal with only very 

 high dilutions. This might be correlated with the fact observed by 

 Kleiner and Meltzer that in order to produce diuresis epinephrin must 

 be administered so as to be slowly absorbed, whereas in cases in which 

 it reaches the kidneys promptly it acts as a renal depressant (Cow, 

 1914). 



In view of the important theoretical question involved, the relation 

 of ephinephrin to renal circulation was further studied by Hart- 

 man and McPhedran and by Hoskins and Gunning(&) in 1917. Hartman 

 and McPhedran made four oncometer experiments, two on cats and two 

 on dogs. In every instance epinephrin caused vasoconstriction. With 

 small doses this was the only effect. In two cases in which large doses were 

 used, the contraction was followed by a secondary dilatation. This dilata- 

 tion persisted a considerable period after blood-pressure had regained its 

 normal level. 



Hoskins and Gunning made determinations of volume changes or of 

 venous outflow in sixteen dogs. In their experiments the outstanding 

 feature of the reaction was a sharp contraction of volume (Fig. 9). 

 In most instances this was preceded by a brief preliminary expansion, 

 inconsequential in degree and interpreted as purely passive. The contrac- 

 tion outlasted for a half to two minutes the arterial pressure reaction. 

 In one case only was a different type of reaction observed. In this, after 

 the passive preliminary dilatation, as the blood-pressure rose the organ 

 contracted; then, as arterial pressure began to fall, the kidney dilated 

 and returned to its initial volume a minute after the normal blood- 

 pressure was restored. This result was obtained when 0.5 c.c. of 1 : 100,000 

 solution was administered. When the dose was doubled the ordinary 

 renal contraction picture appeared and outlasted the change of blood- 

 pressure. In no case was a pure dilatation observed. It was found that 

 the kidneys could be held for at least ten minutes in a uniform state of 

 contraction. The threshold dosage for changes in kidney volume and 

 for changes in blood-pressure were approximately the same. The re- 

 actions in the kidney were qualitatively similar, irrespective of whether 

 pressor or depressor dosages were employed. The observations on venous 



