Involvement of the kallikrein-kinin system in the antihypertensive effect of the angiotensin converting enzyme inhibitors.

1. Studies were performed in normal subjects and in rats to assess the effect of angiotensin converting enzyme (ACE) inhibition on the kallikrein-kinin system. As ACE is identical to kininase II, one of the enzymes physiologically involved in bradykinin degradation, bradykinin may be expected to accumulate during ACE inhibition. 2. A competitive antagonist of bradykinin was used to explore in unanaesthetized rats the contribution of circulating bradykinin to blood pressure control under ACE inhibition. 3. No evidence was found for a role of this vasodilating peptide in the blood pressure lowering effect of acute ACE inhibition. 4. The plasma activity of carboxypeptidase N (= kininase I), another pathway of bradykinin degradation, remained intact during a 1 week course of treatment with an ACE inhibitor in normal subjects. This therefore indicates that bradykinin formed during ACE inhibition can still be metabolized.

[1]  B. Waeber,et al.  Influence of Endogenous Bradykinin on Acute Blood Pressure Response to Vasopressors in Normotensive Rats Assessed with a Bradykinin Antagonist , 1988, Journal of cardiovascular pharmacology.

[2]  J. Stewart,et al.  INFLUENCE OF BRADYKININ ON BLOOD PRESSURE REGULATION OF SPONTANEOUSLY HYPERTENSIVE RATS MAINTAINED ON DIFFERENT SODIUM INTAKES , 1987, Clinical and experimental pharmacology & physiology.

[3]  M. Rawlins,et al.  Effects of intradermal bradykinin after inhibition of angiotensin converting enzyme. , 1987, British medical journal.

[4]  J. Mcgiff,et al.  The antihypertensive effect of captopril in essential hypertension: relationship to prostaglandins and the kallikrein-kinin system. , 1987, Journal of hypertension.

[5]  J. Stewart,et al.  Lack of a role of circulating bradykinin in the blood pressure response to acute angiotensin converting enzyme inhibition in rats. , 1987, Agents and actions. Supplements.

[6]  P. Barnes,et al.  The effect of an angiotensin converting enzyme inhibitor, ramipril, on bronchial responses to inhaled histamine and bradykinin in asthmatic subjects. , 1987, British journal of clinical pharmacology.

[7]  C. Dollery,et al.  Effect of enalapril on the skin response to bradykinin in man. , 1987, British journal of clinical pharmacology.

[8]  H. Gavras,et al.  Hypertensive effect of a bradykinin antagonist in normotensive rats. , 1986, Hypertension.

[9]  J. Stewart,et al.  Vasodepressor role of endogenous bradykinin assessed by a bradykinin antagonist. , 1986, Hypertension.

[10]  M. Kohzuki,et al.  Effects of ouabain on blood pressure regulation in rats. , 1986, Journal of hypertension.

[11]  I. A. Sheikh,et al.  Studies of the digestion of bradykinin, lysyl bradykinin, and kinin-degradation products by carboxypeptidases A, B, and N. , 1986, Biochemical pharmacology.

[12]  J. Funder,et al.  The cellular physiology of glandular kallikrein. , 1986, Kidney international.

[13]  J. Stewart,et al.  Competitive antagonists of bradykinin , 1985, Peptides.

[14]  B. Waeber,et al.  Hypotensive effect of human factor XII active fragment in conscious normotensive rats: role of bradykinin. , 1984, Journal of hypertension. Supplement : official journal of the International Society of Hypertension.

[15]  H. Margolius.  The kallikrein-kinin system and the kidney. , 1984, Annual review of physiology.

[16]  B. Karlberg,et al.  Captopril, aldosterone and urinary kallikrein in primary hypertension. , 1983, Clinical and experimental hypertension. Part A, Theory and practice.

[17]  F. Bühler,et al.  Antihypertensive and renal effects of captopril in relation to renin activity and bradykinin‐induced vasodilation , 1982, Clinical pharmacology and therapeutics.

[18]  C. Johnston,et al.  Effect of angiotensin-converting enzyme inhibition on circulating and local kinin levels. , 1982, The American journal of cardiology.

[19]  T. Ogihara,et al.  Hormonal responses to long‐term converting enzyme inhibition in hypertensive patients , 1981, Clinical pharmacology and therapeutics.

[20]  H. Gavras,et al.  Converting Enzyme Inhibition During Chronic Angiotensin II Infusion in Rats: Evidence Against a Nonangiotensin Mechanism , 1981, Hypertension.

[21]  T. Plummer,et al.  An improved spectrophotometric assay for human plasma carboxypeptidase N1. , 1980, Analytical biochemistry.

[22]  N. Hollenberg,et al.  Differences in Response to the Peptidyldipeptide Hydrolase Inhibitors SQ 20,881 and SQ 14,225 in Normal‐Renin Essential Hypertension , 1980, Hypertension.

[23]  A. White,et al.  Activation of membrane-bound kallikrein and renin in the kidney. , 1980, Proceedings of the National Academy of Sciences of the United States of America.

[24]  N. Hollenberg,et al.  Captopril-induced changes in prostaglandin production: relationship to vascular responses in normal man. , 1980, The Journal of clinical investigation.

[25]  O. Carretero,et al.  The renal kallikrein-kinin system. , 1980, The American journal of physiology.

[26]  H. Gavras,et al.  Converting enzyme inhibition during chronic angiotensin II infusion in rats: evidence against a non-angiotensin mechanism. , 1980, Clinical science.

[27]  M. Schalekamp,et al.  Activation of inactive plasma renin by tissue kallikreins. , 1979, The Journal of clinical endocrinology and metabolism.

[28]  C. Johnston,et al.  LONG-TERM EFFECTS OF CAPTOPRIL (SQ14 225) ON BLOOD-PRESSURE AND HORMONE LEVELS IN ESSENTIAL HYPERTENSION , 1979, The Lancet.

[29]  K. Catt,et al.  The Effect of Converting Enzyme Inhibition with SQ20,881 on Plasma and Urinary Kinins, Prostaglandin E, and Angiotensin II in Hypertensive Man , 1979, Hypertension.

[30]  N. Levinsky.  The renal kallikrein-kinin system. , 1979, Circulation research.

[31]  B. Hökfelt,et al.  The effect of the converting enzyme inhibitor SQ 20.881 on kinins, renin-angiotensin-aldosterone and catecholamines in relation to blood pressure in hypertensive patients. , 2009, Acta medica Scandinavica.

[32]  J. Laragh,et al.  Human urinary kallikrein converts inactive to active renin and is a possible physiological activator of renin , 1978, Nature.

[33]  R. Buckingham,et al.  Hypotension associated with prekallikrein activator (Hageman-factor fragments) in plasma protein fraction. , 1978, The New England journal of medicine.

[34]  W F Ganong,et al.  The renin-angiotensin system. , 1978, Annual review of physiology.

[35]  G. Marshall,et al.  Blood vessel-hormone interactions: angiotensin, bradykinin, and prostaglandins. , 1977, The American journal of physiology.

[36]  R. Alexander,et al.  Urinary Kallikrein Excretion in Normal Man: Relationships to Sodium Intake and Sodium‐Retaining Steroids , 1974, Circulation research.

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

[38]  S. Oparil,et al.  The renin-angiotensin system (first of two parts). , 1974, The New England journal of medicine.

[39]  J. Stewart,et al.  Inhibition of the Conversion of Angiotensin I to II and Potentiation of Bradykinin by Small Peptides Present in Bothrops jararaca Venom , 1972, Circulation research.

[40]  K. Malik,et al.  Release of a Prostaglandin E‐Like Substance from Canine Kidney by Bradykinin: COMPARISON WITH ELEDOISIN , 1972, Circulation research.

[41]  Kaplan Ap,et al.  A pre-albumin activator of prekallikrein. , 1970, Journal of immunology.

[42]  K. Austen,et al.  A pre-albumin activator of prekallikrein. , 1970, Journal of immunology.