Malignant Hypertension: A Syndrome Associated with Low Plasma Kininogen and Kinin Potentiating Factor

SUMMARY Plasma levels of kininogen, kallikrein, and prekalllkrein were determined in patients with malignant hypertension (MH) and compared to nonnotensive controls (NC) and patients with mild to moderate essential hypertension (EH). Also, a recently described kinin potentiating factor (KPF) was estimated by dividing the value of kininogen determined by trypsln (Kgn-Try) by that of kininogen determined by human urinary kallikrein (Kgn-HuUK). No significant alterations were detected among plasma values of prekallikrein and kallikrein of MH as compared to NC. However, Kgn-HuUK values were significantly lower in MH (1.9±OJ MgLBK/ml) as compared to EH and NC (2.7±0.1 MgLBK/ml and 3.0±0.2 MgLBK/ml respectively, p < 0.05). Furthermore, KPF values were also low (p < 0.05) in MH (1.6±03) when compared with similar values obtained in EH and NC (3.0±0.2 and 2.8±0.1, respectively). Adequate control of blood pressure levels for 90 days in MH group caused no significant alterations in plasma levels of kininogen and KPF. It is suggested that diminished kininogen levels as well as a decrease in a kinin potentiation KPF that is generated in plasma by trypsln may be involved in the patbogenesis of human malignant hypertension. (Hypertension 3 (suppl II): II-46-II-49, 1981)

[1]  R. Geiger,et al.  Isolation of an enzymatically active glandular kallikrein from human plasma by immunoaffinity chromatography. , 1980, Hoppe-Seyler's Zeitschrift fur physiologische Chemie.

[2]  M. Villa,et al.  Brasil factor. A new prekallikrein activator in human plasma. , 1979, Biochemical pharmacology.

[3]  J. Iwao,et al.  Potentiating mechanism of bradykinin action on smooth muscle by sulfhydryl compounds. , 1979, European journal of pharmacology.

[4]  M. Maxwell,et al.  The kallikrein-kinin system in blood pressure homeostasis. , 1979, Clinical science.

[5]  D. Haack,et al.  Vasopressor role of ADH in the pathogenesis of malignant DOC hypertension. , 1977, The American journal of physiology.

[6]  J. Giese The Renin—Angiotensin System and the Pathogenesis of Vascular Disease in Malignant Hypertension , 1976 .

[7]  R. Colman,et al.  Response of the kallikrein-kinin and renin-angiotensin systems to saline infusion and upright posture. , 1975, The Journal of clinical investigation.

[8]  H. Margolius,et al.  Urinary Kallikrein Excretion in Hypertensive Man: Relationships to Sodium intake and Sodium‐Retaining Steroids , 1974, Circulation research.

[9]  N. Fleischer,et al.  Radioimmunoassay of angiotensin I, for estimation of plasma renin activity. , 1974, Clinical chemistry.

[10]  M. Böhmer,et al.  Eine mikromethode 7air kreatininbestimmung , 1971 .

[11]  S. Ferreira,et al.  Isolation of bradykinin-potentiating peptides from Bothrops jararaca venom. , 1970, Biochemistry.

[12]  M. Robinson,et al.  Ultrastructural injury of arterial endothelium. II. Effects of vasoactive amines. , 1969, Archives of pathology.

[13]  U. Hamberg,et al.  Tryptic and plasmic peptide fragments increasing the effect of bradykinin on isolated smooth muscle. , 1969, Scandinavian journal of clinical and laboratory investigation. Supplementum.

[14]  P. Murtaugh,et al.  The biological properties of peptides derived from fibrinogen. , 1968, Biochemical pharmacology.

[15]  M. Rocha e Silva,et al.  Bradykinin, a hypotensive and smooth muscle stimulating factor released from plasma globulin by snake venoms and by trypsin. , 1949, The American journal of physiology.