The biological properties of peptides derived from fibrinogen

Gladner, Jules A.; Murtaugh, Patricia A.; Houck, J. C.

doi:10.1016/0006-2952(68)90311-0

Cited by 12 publications

(4 citation statements)

References 18 publications

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“…Bradykinin-potentiating activity has been detected in snake venom other than that of B. jararaca Suzuki et al, 1967) in a mixture of peptides derived from trypsintreated plasma (Aarsen, 1968;Hamberg et al, 1968), in the peptidic fraction of a porcine liver extract (Tewksbury and Stahman, 1965), in some fibrinopeptides (Gladner et al, 1968), and in the carboxyl-terminal pentapeptide of bradykinin (Garbe, 1967). Of these, the amino acid sequence is known only for the fibrinopeptides and the bradykinin fragment.…”

Section: Discussionmentioning

confidence: 99%

Isolation of bradykinin-potentiating peptides from Bothrops jararaca venom

Ferreira,

Bartelt,

Greene

1970

Biochemistry

547

263

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Section: Discussionmentioning

confidence: 99%

Isolation of bradykinin-potentiating peptides from Bothrops jararaca venom

Ferreira,

Bartelt,

Greene

1970

Biochemistry

547

263

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“…On the one hand, initiation of clotting by thrombin involves the splitting off of two small bioactive peptides from fibrinogen monomer (31) and subsequent limited proteolysis of fibrinogen or fibrin by plasmin yields other biologically potent fragments (31). The phalmacologic properties of these fibrinogen/fibrin derivatives are as yet poorly characterized, particularly in man, but include potentiation of bradykinin-induced smooth muscle contraction (32), increased vascular permeability (33,34), and chemotaxis of granulocytes (35,36). Finally, insertion of a loose meshwork of long chain, insoluble fibrin polymer into the connective tissue matrix could lead to an expansion of the extravascular space with accumulation of water and plasma proteins.…”

Section: Discussionmentioning

confidence: 99%

Role of the Clotting System in Cell-Mediated Hypersensitivity

Colvin

Johnson

Mihm

et al. 1973

The Journal of Experimental Medicine

182

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Indirect evidence has implicated the coagulation system in the pathogenesis of cell-mediated hypersensitivity. Thus, anticoagulants have been shown to inhibit the expression of a variety of delayed-type reactions in vivo in animals including classic tuberculin skin hypersensitivity (1-5) and allergic contact dermatitis (2), the ocular reaction to tuberculin (6), and the antigen-induced maerophage disappearance reaction (1, 7). Moreover, a variety of agents that interfere with different steps in the clotting sequence has each been effective in suppressing delayed reactivity (1, 2, 4, 5). In studies with one such agent, heparin, suppression occurred under conditions that did not measurably inhibit the complement system (1, 2), the competence of sensitized lymphocytes to transfer cell-mediated hypersensitivity passively (2), or the anamnestic antibody response (2). Despite these data there has been reluctance to accept a role for the coagulation system in the expression of delayed hypersensitivity, and, in fact, no direct evidence has been presented for activation of clotting in the evolution of these reactions.Our interest in this problem stems from the recent observation that substantial amounts of a fibrin-like material accumulate in the dermis in lesions of allergic contact dermatitis (8). We have pursued this observation with fluorescent antibody methods and here demonstrate that fibrin deposition is a prominent and consistent feature of both allergic contact dermatitis and classic delayed hypersensitivity skin reactions in man.

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“…' In the present work we evaluated the levels of some plasma precursors of kallikrein-kinin system in malignant hypertension, compared to "benign" hypertension and normal subjects, by studying plasma levels of kininogen, kallikrein, and prekallikrein. Also, a newly described kinin potentiating factor* was estimated in these subjects since it is known that several potentiating substances of both exogenous' 110 or endogenous origin 11 ' " may influence the activity of the kallikrein-kinin system.…”

mentioning

confidence: 99%

Malignant hypertension: a syndrome associated with low plasma kininogen and kinin potentiating factor.

Almeida¹,

Stella²,

Voos³

et al. 1981

Hypertension

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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. which several humoral alterations ofvasopressor systems like renin-angiotensin system, 1 catecholamines,* and more recently vasopressin 8 have been implicated in the pathogenesis of the vascular lesion. The kallikrein-kinin system has been implicated in several hypertensive states, since kinins are vasodilators 4 and also influence water and electrolyte excretion.8 -• A defective kallikrein-kinin system has been recently suggested in malignant, but not benign, hypertension in the rat.'In the present work we evaluated the levels of some plasma precursors of kallikrein-kinin system in malignant hypertension, compared to "benign" hypertension and normal subjects, by studying plasma levels of kininogen, kallikrein, and prekallikrein. Also, a newly described kinin potentiating factor* was estimated in these subjects since it is known that several potentiating substances of both exogenous' 110 or endogenous origin 11 ' " may influence the activity of the kallikrein-kinin system.

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The biological properties of peptides derived from fibrinogen

Cited by 12 publications

References 18 publications

Isolation of bradykinin-potentiating peptides from Bothrops jararaca venom

Isolation of bradykinin-potentiating peptides from Bothrops jararaca venom

Role of the Clotting System in Cell-Mediated Hypersensitivity

Malignant hypertension: a syndrome associated with low plasma kininogen and kinin potentiating factor.

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