scholarly journals THE VASOCONSTRICTOR ACTION OF PLASMA FROM HYPERTENSIVE PATIENTS AND DOGS

1940 ◽  
Vol 72 (3) ◽  
pp. 301-310 ◽  
Author(s):  
Irvine H. Page

1. Plasma from the renal vein, femoral artery or vein of normal dogs and plasma from the femoral artery, femoral and antecubital veins of man cause little or no vasoconstriction when added in small amounts to blood from a bilaterally nephrectomized dog used as perfusing medium in an isolated rabbit's ear. 2. Plasma from the femoral vessels and antecubital vein of patients with essential hypertension, malignant hypertension, and chronic nephritic hypertension causes marked vasoconstriction under the same circumstances. The plasma of dogs made hypertensive either by constriction of the parenchyma by the scar of silk perinephritis or by constriction of the renal artery by a clamp also causes pronounced vasoconstriction. 3. Plasma from the renal vein of normal dogs produces little or no vasoconstriction, but that of hypertensive dogs elicits vasoconstriction but usually not so marked as that elicited by plasma collected from peripheral vessels. A sample of renal venous plasma from one hypertensive patient caused severe vasoconstriction, not quite so intense as that produced by the peripheral vein plasma. 4. Since renin is liberated into the renal vein in large amounts in hypertensive dogs and reacts with renin-activator to produce angiotonin and since the conditions of the experiment are such as to enhance greatly the sensitivity of the ear preparation to angiotonin, it is believed that the vasoconstriction is the result of the presence of angiotonin in the peripheral blood. 5. Since vasoconstriction occurs under the same experimental conditions with plasma from both hypertensive patients and dogs, this is considered cogent evidence in favor of the view that the chemical mediator of both is similar and is possibly angiotonin. 6. A method is presented which is believed will distinguish between plasma from patients with normal blood pressure and that from those with hypertension, and between plasma from normal dogs and that from dogs with experimental renal hypertension.

1963 ◽  
Vol 26 (1) ◽  
pp. 107-111 ◽  
Author(s):  
S. TALANTI ◽  
A. EISALO

SUMMARY The effect of experimental renal hypertension on the hypothalamo-hypophysial neurosecretory system was studied histologically. The amount of neurosecretory material decreased, especially in the neurohypophysis. A marked reduction in the nuclear volume of the neurosecretory ganglion cells occurred, while that of the cells of the other hypothalamic nuclei investigated remained unchanged. The results suggest that the activity of the neurosecretory system is diminished in the experimental conditions used.


1970 ◽  
Vol 27 (5) ◽  
pp. 799-810 ◽  
Author(s):  
CARLOS M. FERRARIO ◽  
IRVINE H. PAGE ◽  
JAMES W. McCUBBIN

1957 ◽  
Vol 5 (4) ◽  
pp. 426-434 ◽  
Author(s):  
G. E. WAKERLIN ◽  
W. G. MOSS ◽  
J. P. KIELY ◽  
Mrs. Gloria Fein ◽  
Mr. Frank Kejikawa

1939 ◽  
Vol 40 (4) ◽  
pp. 708-709 ◽  
Author(s):  
J. S. Mansfield ◽  
D. M. Weeks ◽  
A. Steiner ◽  
J. Victor

1978 ◽  
Vol 88 (4) ◽  
pp. 729-736 ◽  
Author(s):  
R. M. Schimpff ◽  
D. Lebrec ◽  
M. Donnadieu ◽  
A. M. Repellin

ABSTRACT Serum somatomedin (SM) activity, measured as sulphation factor on chick embryo cartilage, and growth hormone (GH) levels were measured in peripheral, hepatic and renal veins of 23 patients with alcoholic cirrhosis. SM activity (mean ± sem) was 0.65 ± 0.05 U/ml in peripheral vein, 0.59 ± 0.04 U/ml in hepatic vein, and 0.74 ± 0.07 U/ml in renal vein. Mean GH levels were respectively 2.8, 2.5 and 3.1 ng/ml. Compared to peripheral vein, SM increase in renal vein was 19% (P < 0.05). Serum SM activity was significantly lower in 13 patients with alcoholic hepatitis associated with cirrhosis than in other 10 patients (P < 0.02 in hepatic blood and P < 0.05 in peripheral blood). The decrease of SM activity seems related to cytolysis and hepato-cellular insufficiency. At last, in patients with alcoholic hepatitis, SM activity was lower in the hepatic vein than in the peripheral vein (P < 0.05). The cause of this difference remains under discussion, no SM inhibitors being found in the serum samples used in this study.


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