Ein neues Kreislaufhormon und seine Wirkung

Frey, E. K.; Kraut, Heinrich

doi:10.1007/bf01955578

Cited by 145 publications

(14 citation statements)

References 4 publications

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“…Dale and Richards (8) have noted that the vasodepressor effect of histamine is maintained after animals have been eviscerated. Frey and Kraut (9) have concluded that the vasodepressor effect of certain organic substances depends on vasodilatation in the skin and muscles. Weiss, Robb and Ellis (10) and Wollheim (11) indicated that the subpapillary venous plexuses of the skin under certain conditions represent important blood reservoirs.…”

Section: Discussionmentioning

confidence: 99%

The Rôle of the Venous System in Circulatory Collapse Induced by Sodium Nitrite 1

Wilkins¹,

Haynes²,

Weiss³

1937

J. Clin. Invest.

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An experimental study of the vasomotor collapse induced by sodium nitrite in normal subjects in the upright position has revealed that the state of collapse is accompanied by a fall in venous pressure and an inadequate return of venous blood to the heart from the lower half of the body (1).As long as the subject remains in the prone position, a small dose of sodium nitrite will produce no symptoms and only slight, if any, measurable circulatory changes in terms of blood pressure. heart rate, arterial blood flow or venous pressure. When the subject is raised from the horizontal to the upright position after the same dose of nitrite, however, he soon develops signs and symptoms of collapse. After nitrite has been given, the peripheral circulation is unable to adjust itself to the strain of the orthostatic position.Our purpose in the present work was further to clarify the mechanism of the nitrite collapse. On rising to the upright position, the greatest relative change in the circulation is on the venous side of the vascular system in the lower half of the body. Here the venous pressure is normally raised from an average prone value of 5 cm. of water to about 100 cm. of water in the feet and 50 cm. in the abdomen. This consideration, as well as the fact that previous studies revealed no appreciable dilatation of the arterioles or change in the cardiac output after nitrite (2), turned our attention to the venous side of the circulation as possibly one of the most important sites of action of sodium nitrite. We therefore undertook to test the effect of nitrite on the distensibility of the peripheral vascular beds under increases in venous pressure.WVe were particularly interested to know whether the effect of nitrite on the venous systemi is generalized or limited to certain vascular areas, such as the splanchnics.In the present study, the hands of normal sub- ' This investigation was aided in part by a grant from the Josiah Macy, Jr., Foundation. jects were placed under known increases in venous pressure, anid the corresponding increases in hand volume were measured both before and after the administration of nitrite. The subject remained in the prone position and in this way other factors, such as changes in arterial blood pressure, pulse or blood flow, were eliminated. Capps, working in this laboratory, developed this method as a means of measuring the tone or " resistance to stretch " of the capillaries. venules and veins of the hands in both normal and diseased states (3). WVe have used this procedure, with minor modifications, with satisfactory results. METHODThe subject rested in a comfortable horizontal position for at least 45 minutes after all apparatus had been adjusted before any observations were begun, and remained in this position throughout an experiment. Arterial blood pressure was determined in the arm by the usual auscultatory method, using a mercury manometer. The heart rate was counted by arterial palpation or from the plethysmographic tracings. The rate of blood flow was determined by Freeman'...

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Section: Discussionmentioning

confidence: 99%

The Rôle of the Venous System in Circulatory Collapse Induced by Sodium Nitrite 1

Wilkins¹,

Haynes²,

Weiss³

1937

J. Clin. Invest.

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“…Tissue kallikrein was discovered in human urine and shown to elicit a hypotensive action (Abelous and Bardier, 1909;Frey and Kraut, 1928;Kraut et al, 1928). Oral administration of tissue kallikrein purified from porcine pancreas resulted in blood pressure reduction in hypertensive patients (Overlack et al, 1980(Overlack et al, , 1981.…”

Section: Beneficial Effects Of Tissue Kallikrein In Hypertension and mentioning

confidence: 97%

Tissue kallikrein in cardiovascular, cerebrovascular and renal diseases and skin wound healing

Chao

Shen

Gao

et al. 2010

Biological Chemistry

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Tissue kallikrein (KLK1) processes low-molecular weight kininogen to produce vasoactive kinins, which exert biological functions via kinin receptor signaling. Using various delivery approaches, we have demonstrated that tissue kallikrein through kinin B2 receptor signaling exhibits a wide spectrum of beneficial effects by reducing cardiac and renal injuries, restenosis and ischemic stroke, and by promoting angiogenesis and skin wound healing, independent of blood pressure reduction. Protection by tissue kallikrein in oxidative organ damage is attributed to the inhibition of apoptosis, inflammation, hypertrophy and fibrosis. Tissue kallikrein also enhances neovascularization in ischemic heart and limb. Moreover, tissue kallikrein/kinin infusion not only prevents but also reverses kidney injury, inflammation and fibrosis in salt-induced hypertensive rats. Furthermore, there is a wide time window for kallikrein administration in protection against ischemic brain infarction, as delayed kallikrein infusion for 24 h after cerebral ischemia in rats is effective in reducing neurological deficits, infarct size, apoptosis and inflammation. Importantly, in the clinical setting, human tissue kallikrein has been proven to be effective in the treatment of patients with acute brain infarction when injected within 48 h after stroke onset. Finally, kallikrein promotes skin wound healing and keratinocyte migration by direct activation of protease-activated receptor 1.

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“…Kinin-like activity was first demonstrated by the presence of a hypertensive substance in human urine (Frey and Kraut, 1928). Rocha e Silva et al (1949) found that trypsinization of mammalian blood serum released a substance that -= <1 ng; + = 1-100 ng; ++ = 100-1000 ng; +++ >1000 ng, per venom resevoir, per milliliter or per milligram, which is roughly equivalent.…”

Section: Wasp Kininsmentioning

confidence: 99%

Wasp Kinins and Kinin Analogues

Piek¹

2000

Animal Toxins

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Ein neues Kreislaufhormon und seine Wirkung

Cited by 145 publications

References 4 publications

The Rôle of the Venous System in Circulatory Collapse Induced by Sodium Nitrite 1

The Rôle of the Venous System in Circulatory Collapse Induced by Sodium Nitrite 1

Tissue kallikrein in cardiovascular, cerebrovascular and renal diseases and skin wound healing

Wasp Kinins and Kinin Analogues

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