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PMID: 19871025 Published · ppublish English Journal Article

THE VASOCONSTRICTOR ACTION OF PLASMA FROM HYPERTENSIVE PATIENTS AND DOGS.

The Journal of experimental medicine ·Vol. 72 ·No. 3 ·1940-08-31 ·Pages 301-10

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Abstract

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.

Authors & Affiliations
1 authors, click to expand affiliations / ORCID
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Lilly Laboratory for Clinical Research, Indianapolis City Hospital, Indianapolis.
References (7)
7 references, click to expand
  1. A CRYSTALLINE PRESSOR SUBSTANCE (ANGIOTONIN) RESULTING FROM THE REACTION BETWEEN RENIN AND RENIN-ACTIVATOR.
    J Exp Med. 1940 Jan 1;71(1):29-42 PMID: 19870942
  2. ANGIOTONIN-ACTIVATOR, RENIN- AND ANGIOTONIN-INHIBITOR, AND THE MECHANISM OF ANGIOTONIN TACHYPHYLAXIS IN NORMAL, HYPERTENSIVE, AND NEPHRECTOMIZED ANIMALS.
    J Exp Med. 1940 Mar 31;71(4):495-519 PMID: 19870977
  3. The blood-pressure raising secretion of the ischaemic kidney.
    J Physiol. 1938 Dec 14;94(3):281-93 PMID: 16995044
  4. A METHOD FOR PRODUCING PERSISTENT HYPERTENSION BY CELLOPHANE.
    Science. 1939 Mar 24;89(2308):273-4 PMID: 17758517
  5. THE EFFECTS OF PRESSOR DRUGS AND OF SALINE KIDNEY EXTRACTS ON BLOOD PRESSURE AND SKIN TEMPERATURE.
    J Clin Invest. 1938 Mar;17(2):189-206 PMID: 16694564
  6. STUDIES ON EXPERIMENTAL HYPERTENSION : I. THE PRODUCTION OF PERSISTENT ELEVATION OF SYSTOLIC BLOOD PRESSURE BY MEANS OF RENAL ISCHEMIA.
    J Exp Med. 1934 Feb 28;59(3):347-79 PMID: 19870251
  7. ON THE NATURE OF THE PRESSOR ACTION OF RENIN.
    J Exp Med. 1939 Oct 31;70(5):521-42 PMID: 19870928
Article Info
Journal
The Journal of experimental medicine
Abbr.
J Exp Med
ISSN
0022-1007
Published
1940-08-31
Pages
301-10
Language
English
Region
United States
NLM ID
2985109R
PMCID
PMC2135062
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