Enzymes that Inactivate Vasoactive Peptides

Erdös, Ervin G.

doi:10.1007/978-3-642-65177-9_36

Cited by 3 publications

(3 citation statements)

References 167 publications

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“…Because the latter function is inhibited in vitro by angiotensin I (Alabaster and Bakhle, 1973), when renin levels are high, the elevation of angiotensin I may decrease the rate of bradykinin destruction. Although this is a tempting hypothesis proposed by Wong et al (1975) and recently reiterated and supported by Mersey et al (1977), it ignores the contribution made by other kininases (Erdos, 1971). Also, this theory does not accommodate well the fact that the level of plasma renin activity and plasma bradykinin are not always related, as during ACTH when levels of angiotensin I were undoubtedly high, and as during indomethacin (Vinci et al, 1978) which decreased renin but not bradykinin in normals.…”

Section: Discussionmentioning

confidence: 94%

“…Although there are several enzymes that destroy bradykinin (Erdos, 1971), peptidyl dipeptide hydrolase (commonly known as angiotensin-converting enzyme or kininase II) not only hydrolyzes bradykinin but also hydrolyzes angiotensin I to angiotensin II (Igic et al, 1972). This pivotal enzyme generates the potent pressor peptide, angiotensin II, and inactivates the potent depressor peptide, bradykinin.…”

Section: Discussionmentioning

confidence: 99%

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Human urinary and plasma kinins: relationship to sodium-retaining steroids and plasma renin activity.

Vinci¹,

Zusman²,

Izzo³

et al. 1979

Circulation Research

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Sodium-retaining steroids increase urinary kallikrein but their effects on urinary kinins and plasma bradykinin are not known. Thirty-six normal subjects were studied during several different manipulations of dietary sodium and potassium or the administration of fludrocortisone or adrenocorticotropic hormone (ACTH). Urinary kallikrein and aldosterone excretion changed pari passu over a 30-fold range for kallikrein and an 80-fold range for aldosterone. Urinary kinin excretion was invariant. Plasma, bradykinin, on the other hand, responded to the same stimuli as plasma renin activity and not primarily to the level of sodium-retaining steroid. These studies show that: (1) urinary kallikrein is dependent on the level of aldosterone over a wide range of excretion values; (2) urinary kallikrein determines neither the level of urinary kinins nor the level of plasma kinins; (3) urinary kinins are independent of the level of sodium-retaining steroid; and (4) there is a strong correlation between plasma bradykinin and renin activity but not between plasma bradykinin and sodium-retaining steroid activty. We suggest that: (1) urinary kallikrein is an index of sodium-retaining steroid activity and may participate in the antinatriuretic and kaliuretic effects of these hormones; (2) plasma bradykinin is highly correlated with plasma renin activity because both responded to changes in extracellular fluid volume and not because angiotensin-converting enzyme controls both systems in an interrelated fashion; and (3) plasma bradykinin may act physiologically to antagonize angiotensin II and may contribute to maintenance of normal blood pressure in hyperreninemic states. Ore Res 44: [228][229][230][231][232][233][234][235][236][237]1979

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Human urinary and plasma kinins: relationship to sodium-retaining steroids and plasma renin activity.

Vinci¹,

Zusman²,

Izzo³

et al. 1979

Circulation Research

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show abstract

“…1, Table I). Al (42) which are more important in the destruietioni of' plasma bradykinin (43). In(leed, in 10 hypertenesive patienits with tune(quiivocal biochemical evidenee of converting enzymiie inhibition with SQ20881, plasmiia bradykinini wasi not change(d (44).…”

Section: Discussionmentioning

confidence: 99%

The Kallikrein-Kinin System in Bartter's Syndrome and Its Response to Prostaglandin Synthetase Inhibition

Vinci¹,

Gill²,

Bowden³

et al. 1978

J. Clin. Invest.

120

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A B S T R A C T The kallikrein-kinin system was characterized in seven patients with Bartter's syndrome on constant metabolic regimens before, during, and after treatment with prostaglandin synthetase inhibitors. Patients with Bartter's syndrome had high values for plasma bradykinin, plasma renin activity (PRA), urinary kallikrein, urinary immunoreactive prostaglandin E excretion, and urinary aldosterone; urinary kinins were subnormal and plasma prekallikrein was normal. Treatment with indomethacin or ibuprofen which decreased urinary immunoreactive prostaglandin E excretion by 67%, decreased mean PRA (patients recumbent) from 17.3+5.3 (S.E.M.) ng/ml per h to 3.3±1.1 ng/ml per h, mean plasma bradykinini (patients recumbent) from 15.4±4.4 ng/ml to 3.9±0.9 ng/ml, mean urinary kallikrein excretion from 24.8±3.2 tosyl-arginine-methyl ester units (TU)/ day to 12.4±2.0 TU/day, but increased mean urinary kinin excretion from 3.8±1.3 ,ug/day to 8.5±2.5 ,ug/day. Plasma prekallikrein remained unchanged at 1.4 TU/ml. Thus, with prostaglandin synthetase inhibition, values for uriniary kallikrein and kinin and plasma bradykinin returned to normal pari passu with changes in PRA, in aldosterone, and in prostaglandin E. The

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The Pathophysiology of Shock

George¹,

Tinker²

1983

Care of the Critically Ill Patient

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Enzymes that Inactivate Vasoactive Peptides

Cited by 3 publications

References 167 publications

Human urinary and plasma kinins: relationship to sodium-retaining steroids and plasma renin activity.

Human urinary and plasma kinins: relationship to sodium-retaining steroids and plasma renin activity.

The Kallikrein-Kinin System in Bartter's Syndrome and Its Response to Prostaglandin Synthetase Inhibition

The Pathophysiology of Shock

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