PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 6998710-0 1980 Prostacyclin mediates the potentiated hypotensive effect of bradykinin following captopril treatment. Captopril 81-90 kininogen 1 Homo sapiens 60-70 6998710-1 1980 The effect of angiotensin-converting enzyme inhibition by captopril on the release of a prostacyclin-like substance by bradykinin, angiotensin I and angiotensin II was studied by means of the blood-bathed bioassay technique of Vane. Captopril 58-67 kininogen 1 Homo sapiens 119-129 6998710-2 1980 Administration of captopril abolished the release of prostacyclin-like substance induced by angiotensin I, potentiated the release provoked by bradykinin and did not alter that due to angiotensin II. Captopril 18-27 kininogen 1 Homo sapiens 143-153 6998710-3 1980 Potentiation of the bradykinin-induced renal vasodilatation with captopril could be completely reversed by indomethacin, which also abolished the kinin-induced release of prostacyclin-like substance. Captopril 65-74 kininogen 1 Homo sapiens 20-30 231702-0 1979 Potentiation of the algogenic action of bradykinin by an inhibitor of angiotensin I converting enzyme, captopril (SQ 14,225). Captopril 103-112 kininogen 1 Homo sapiens 40-50 232084-1 1979 Captopril inhibits angiotensin II formation and bradykinin degradation in vivo. Captopril 0-9 kininogen 1 Homo sapiens 48-58 32220499-6 2020 This antidepressant effect seemed to be independent of the renin-angiotensin system, but dependent on the bradykinin (BK) system, since the decreased BK detected in the stressed mice could be reversed by captopril. Captopril 204-213 kininogen 1 Homo sapiens 106-116 24390175-4 2014 Bradykinin caused concentration-dependent and endothelium-dependent relaxations that were not affected by DIZE but were potentiated to a similar extent by angiotensin-(1-7) and captopril, given alone or in combination. Captopril 177-186 kininogen 1 Homo sapiens 0-10 32144755-2 2020 This clinical transformation started just over 50 years ago, with the unexpected identification of a bradykinin potentiating peptide from snake venom, as a potent inhibitor of angiotensin converting enzyme which led to the development of the first synthetic inhibitor, captopril, followed by the angiotensin receptor blockers. Captopril 269-278 kininogen 1 Homo sapiens 101-111 28939029-2 2017 Captopril dilates blood vessels, reducing blood pressure clinically and bradykinin, as the downstream signaling moiety of captopril, is capable of dilating blood vessels and effectively increasing vessel permeability. Captopril 0-9 kininogen 1 Homo sapiens 72-82 28939029-2 2017 Captopril dilates blood vessels, reducing blood pressure clinically and bradykinin, as the downstream signaling moiety of captopril, is capable of dilating blood vessels and effectively increasing vessel permeability. Captopril 122-131 kininogen 1 Homo sapiens 72-82 28939029-7 2017 Immunofluorescence-staining of tumor slices demonstrated that captopril significantly increased bradykinin expression, possibly explaining tumor perfusion improvements and endothelial gap enlargement. Captopril 62-71 kininogen 1 Homo sapiens 96-106 28554847-6 2017 We also investigated whether intra-dPAG injection of captopril, an inhibitor of the angiotensin-converting enzyme (ACE) that also degrades BK, causes a panicolytic-like effect. Captopril 53-62 kininogen 1 Homo sapiens 139-141 28554847-9 2017 Finally, intra-dPAG injection of captopril also impaired escape in a dose-dependent way, and this panicolytic-like effect was blocked by pretreatment with HOE-140, suggesting mediation by endogenous BK. Captopril 33-42 kininogen 1 Homo sapiens 199-201 24390175-5 2014 Bradykinin responses potentiated by angiotensin-(1-7) and captopril were not affected by the BK1 antagonist SSR240612 and remained augmented in the presence of either N-nitro-L-arginine methyl ester hydrochloride plus indomethacin or TRAM-34 plus UCL-1684. Captopril 58-67 kininogen 1 Homo sapiens 0-10 24390175-7 2014 These results suggest that in coronary arteries, angiotensin-(1-7) and captopril both improves NO bioavailability and enhances endothelium-dependent hyperpolarization to bradykinin solely by ACE1 inhibition. Captopril 71-80 kininogen 1 Homo sapiens 170-180 24138103-6 2014 Thiorphan, captopril, and omapatrilat all enhanced the vasodilator response to bradykinin (all P < 0.01). Captopril 11-20 kininogen 1 Homo sapiens 79-89 23603844-7 2013 Moreover, we found that in the coronary arterioles of obese patients, BK-induced dilation was augmented by in vitro captopril administration. Captopril 116-125 kininogen 1 Homo sapiens 70-72 21835190-0 2012 Bradykinin-potentiating peptides: beyond captopril. Captopril 41-50 kininogen 1 Homo sapiens 0-10 21835190-2 2012 The discovery of bradykinin (1949) and the bradykinin-potentiating peptides (1965) had a pivotal influence in the field, respectively, in understanding cardiovascular pathophysiology and in the development of captopril, the first active-site directed inhibitor of angiotensin-converting enzyme, and used worldwide to treat human hypertension. Captopril 209-218 kininogen 1 Homo sapiens 17-27 21835190-2 2012 The discovery of bradykinin (1949) and the bradykinin-potentiating peptides (1965) had a pivotal influence in the field, respectively, in understanding cardiovascular pathophysiology and in the development of captopril, the first active-site directed inhibitor of angiotensin-converting enzyme, and used worldwide to treat human hypertension. Captopril 209-218 kininogen 1 Homo sapiens 43-53 11330881-9 2001 A bradykinin B2 receptor antagonist abolished the suppressive effect of captopril on PAI-1 antigen. Captopril 72-81 kininogen 1 Homo sapiens 2-12 15325012-7 2004 We concluded that the effects of captopril, an ACE inhibitor, on TAME-esterase induced contractions could thus be due to the degradation of bradykinin by the enzyme kininase being blocked. Captopril 33-42 kininogen 1 Homo sapiens 140-150 21651905-6 2011 Application of captopril 1 muM (angiotensin-converting enzyme inhibitor) or phosphoramidon 10 muM (neutral endopeptidase inhibitor) induced a leftward shift of bradykinin-elicited responses in human umbilical vein with endothelium while no effect was observed in tissues denuded of endothelium under the same treatment. Captopril 15-24 kininogen 1 Homo sapiens 160-170 10191623-10 1999 In allergic patients, captopril enhanced BK-induced vascular permeability, but not glandular secretion. Captopril 22-31 kininogen 1 Homo sapiens 41-43 10741903-8 2000 The enzymes were able to hydrolyze angiotensin I (AI) (P0 and P0N about 25%, P1 and P1N about 70%, P2 100% and P2N 66%) and bradykinin (BK) (P0N 22%, P1N 81%, P2N 62%, P0 and P1 50% and P2 35%), and their activities were inhibited by captopril. Captopril 234-243 kininogen 1 Homo sapiens 124-134 10741903-8 2000 The enzymes were able to hydrolyze angiotensin I (AI) (P0 and P0N about 25%, P1 and P1N about 70%, P2 100% and P2N 66%) and bradykinin (BK) (P0N 22%, P1N 81%, P2N 62%, P0 and P1 50% and P2 35%), and their activities were inhibited by captopril. Captopril 234-243 kininogen 1 Homo sapiens 136-138 10594341-1 1999 The influence of the angiotensin-converting enzyme inhibitor captopril on bradykinin-and angiotensin I-induced responses with special regard to nitric oxide (NO) was studied. Captopril 61-70 kininogen 1 Homo sapiens 74-84 10594341-3 1999 Captopril potentiated bradykinin-induced contraction of preparations with intact endothelium; this potentiation was not seen with the kininase I inhibitor mergepta or a bradykinin B(1)-receptor antagonist. Captopril 0-9 kininogen 1 Homo sapiens 22-32 10594341-5 1999 The captopril-mediated increase of bradykinin-induced contraction was only seen in preparations with intact endothelium, while captopril did not affect arterial strips treated with Nomega-nitro-L-arginine. Captopril 4-13 kininogen 1 Homo sapiens 35-45 10594341-9 1999 In conclusion, captopril increased bradykinin-induced contraction in a NO-dependent manner. Captopril 15-24 kininogen 1 Homo sapiens 35-45 10444513-5 1999 The decrease in perfusion pressure observed with bradykinin was potentiated by captopril and was significantly attenuated in the presence of HOE-140, the B(2)-receptor antagonist, or by pretreatment with an inhibitor of nitric oxide synthase, but not by an inhibitor of cyclooxygenase. Captopril 79-88 kininogen 1 Homo sapiens 49-59 10412558-7 1999 The participation of BK in this response was investigated in subjects given the BK-potentiating drug captopril prior to food intake. Captopril 101-110 kininogen 1 Homo sapiens 80-82 10102747-4 1999 It appears that captopril potentiates chorda tympani-induced salivation through endogenously accumulated bradykinin, which acts on kinin B2 receptors, mediating production of nitric oxide and cyclooxygenase products. Captopril 16-25 kininogen 1 Homo sapiens 105-115 10769288-7 2000 The ACE inhibitor captopril (1 micromol/L) also selectively reduced tdP/dt(min) in shams via a bradykinin/NO-dependent mechanism but had no effect in banded animals. Captopril 18-27 kininogen 1 Homo sapiens 95-105 27093744-8 1999 The mechanism involved in the decrease of IOP and blood pressure with captopril could be due to inhibition in the formation of angiotensin-II and sparing of bradykinin. Captopril 70-79 kininogen 1 Homo sapiens 157-167 9951431-5 1999 Enalaprilat and captopril increased the sensitivity to bradykinin, decreasing the dose producing half-maximal response (ED50) of bradykinin 18-fold and 5-fold, respectively, without changing the maximal venodilatory response. Captopril 16-25 kininogen 1 Homo sapiens 55-65 9951431-5 1999 Enalaprilat and captopril increased the sensitivity to bradykinin, decreasing the dose producing half-maximal response (ED50) of bradykinin 18-fold and 5-fold, respectively, without changing the maximal venodilatory response. Captopril 16-25 kininogen 1 Homo sapiens 129-139 9734886-11 1998 In the patient receiving the ACE-inhibitor captopril, bradykinin concentration was very high at 47 fmol/mL during an acute attack of angio-oedema, but normal at 3.2 fmol/mL in remission after withdrawal of the drug. Captopril 43-52 kininogen 1 Homo sapiens 54-64 9734886-13 1998 Although the differences between patients in remission and healthy controls did not reach statistical significance, there were substantial rises in bradykinin during acute attacks of hereditary, acquired, or captopril-induced angio-oedema. Captopril 208-217 kininogen 1 Homo sapiens 148-158 8930174-8 1996 Both ACE inhibitors dramatically, equally potentiated the vasodepressor response to bradykinin; the bradykinin dose required to decrease mean arterial pressure 15 mm Hg or increase pulse 20 bpm was 50-fold lower in ACEI-treated than in placebo-treated subjects (10 +/- 0 and 12.1 +/- 2.1 ng/kg/min in captopril and quinapril groups vs. 567 +/- 109 ng/kg/min in the placebo group; P < .005). Captopril 301-310 kininogen 1 Homo sapiens 100-110 9383175-6 1997 In the presence of 3 micromol/l of the ACE inhibitor captopril, however, bradykinin significantly enhanced the release of noradrenaline in human atrium. Captopril 53-62 kininogen 1 Homo sapiens 73-83 9383175-8 1997 Captopril (3 micromol/l) potentiated the facilitatory effect of bradykinin in rat atrium. Captopril 0-9 kininogen 1 Homo sapiens 64-74 9066005-4 1997 Bradykinin was infused in seventeen hypertensive patients randomized to treatment with the ACEIs captopril and quinapril or with placebo. Captopril 97-106 kininogen 1 Homo sapiens 0-10 7669485-11 1995 Captopril (10(-7) M) significantly potentiated the pressor effect of bradykinin on the human placental circulation (n = 6). Captopril 0-9 kininogen 1 Homo sapiens 69-79 8749030-6 1995 Captopril, the angiotensin-converting enzyme inhibitor, decreased pulmonary vasoconstrictor responses to angiotensin I and enhanced vasodilator responses to bradykinin, but did not significantly change pressor responses to L-163,491. Captopril 0-9 kininogen 1 Homo sapiens 157-167 7586370-9 1995 In the presence of captopril, bradykinin (0.1 nmol/L, n = 6) markedly accelerated LV relaxation (significantly more than captopril alone), whereas bradykinin alone (0.1 nmol/L, n = 6) had no effect. Captopril 19-28 kininogen 1 Homo sapiens 30-40 7586370-10 1995 CONCLUSIONS: These data indicate that the ACE inhibitor captopril causes an acute and selective enhancement of LV relaxation independent of changes in coronary flow, probably via an endogenous bradykinin/nitric oxide pathway. Captopril 56-65 kininogen 1 Homo sapiens 193-203 7669485-17 1995 We suggest that the toxic effects of captopril on the foetus, rather than reflecting an inhibition of angiotensin II formation, may instead be related to a potentiation of the vasoconstrictor effect of bradykinin on the foetal placental circulation, thereby reducing blood flow and causing foetal damage. Captopril 37-46 kininogen 1 Homo sapiens 202-212 7896012-0 1995 Captopril increases skin microvascular blood flow secondary to bradykinin, nitric oxide, and prostaglandins. Captopril 0-9 kininogen 1 Homo sapiens 63-73 7896012-2 1995 This study was designed to test whether the ACEI captopril increases skin microvascular blood flow by a bradykinin-dependent mechanism. Captopril 49-58 kininogen 1 Homo sapiens 104-114 7896012-7 1995 The responses to bradykinin or captopril were abolished by coinjecting a bradykinin antagonist, a specific bradykinin B2 receptor antagonist, or inhibitors of NOS or cyclooxygenase. Captopril 31-40 kininogen 1 Homo sapiens 73-83 7896012-10 1995 The results indicate that captopril increases skin microvascular blood flow in rabbits and humans secondary to an increase in endogenous tissue bradykinin; this stimulates B2 receptors with subsequent release of prostaglandins and nitric oxide. Captopril 26-35 kininogen 1 Homo sapiens 144-154 8067439-6 1994 Decreases in systemic arterial pressure and in hindquarters perfusion pressure in response to bradykinin were enhanced by the angiotensin-converting enzyme inhibitors captopril and enalaprilat. Captopril 167-176 kininogen 1 Homo sapiens 94-104 8292848-8 1993 The best inhibitor found in this study, Ala2,6-des-Pro3-bradykinin, has an apparent Ki of 30.2 nM, compared to an apparent Ki of 94 nM for des-Pro3-bradykinin, which was reported to be a better inhibitor of angiotensin-converting enzyme than captopril. Captopril 242-251 kininogen 1 Homo sapiens 56-66 7517646-9 1994 Responses to BK were enhanced by captopril, indicating that BK is rapidly inactivated by kininase II in the lung. Captopril 33-42 kininogen 1 Homo sapiens 13-15 7517646-9 1994 Responses to BK were enhanced by captopril, indicating that BK is rapidly inactivated by kininase II in the lung. Captopril 33-42 kininogen 1 Homo sapiens 60-62 8174845-8 1994 In these four groups, oral administration of captopril (2.0 mmol.kg-1) significantly increased insulin sensitivity indices, and a concomitant increase in plasma bradykinin concentrations was observed. Captopril 45-54 kininogen 1 Homo sapiens 161-171 8292848-8 1993 The best inhibitor found in this study, Ala2,6-des-Pro3-bradykinin, has an apparent Ki of 30.2 nM, compared to an apparent Ki of 94 nM for des-Pro3-bradykinin, which was reported to be a better inhibitor of angiotensin-converting enzyme than captopril. Captopril 242-251 kininogen 1 Homo sapiens 148-158 8389325-0 1993 Captopril inhibits endothelin-1 secretion from endothelial cells through bradykinin. Captopril 0-9 kininogen 1 Homo sapiens 73-83 8389325-5 1993 In addition, enhancement of nitric oxide production induced by either captopril or bradykinin was inhibited by D-Arg,[Hyp3,Thi5,8,D-Phe7]-bradykinin. Captopril 70-79 kininogen 1 Homo sapiens 138-148 1629199-9 1992 Bradykinin, a natural substrate of NEP, was in part metabolized by NEP, in the presence of captopril, since 50% of the formation of the major metabolite bradykinin 1-7 was inhibited by thiorphan. Captopril 91-100 kininogen 1 Homo sapiens 0-10 8386065-11 1993 Endothelium dependent relaxation to lisinopril and captopril was also observed in human coronary arteries treated with bradykinin (> or = 10(-7) M), but not in those treated with substance P (10(-8) M). Captopril 51-60 kininogen 1 Homo sapiens 119-129 8448072-0 1993 A comparison of the effects of captopril and enalapril on skin responses to intradermal bradykinin and skin blood flow in the human forearm. Captopril 31-40 kininogen 1 Homo sapiens 88-98 8448072-8 1993 Compared with placebo, captopril significantly augmented the cutaneous vasodilator effects of bradykinin, measured by LDF and erythema area, at 2 h and the weal responses at 2 and 6 h. Enalapril enhanced the vasodilator responses to bradykinin at 2 and 6 h and the weal responses at 2, 6 and 24 h. Neither captopril nor enalapril significantly affected forearm skin blood flow. Captopril 23-32 kininogen 1 Homo sapiens 94-104 8448072-8 1993 Compared with placebo, captopril significantly augmented the cutaneous vasodilator effects of bradykinin, measured by LDF and erythema area, at 2 h and the weal responses at 2 and 6 h. Enalapril enhanced the vasodilator responses to bradykinin at 2 and 6 h and the weal responses at 2, 6 and 24 h. Neither captopril nor enalapril significantly affected forearm skin blood flow. Captopril 23-32 kininogen 1 Homo sapiens 233-243 8448072-8 1993 Compared with placebo, captopril significantly augmented the cutaneous vasodilator effects of bradykinin, measured by LDF and erythema area, at 2 h and the weal responses at 2 and 6 h. Enalapril enhanced the vasodilator responses to bradykinin at 2 and 6 h and the weal responses at 2, 6 and 24 h. Neither captopril nor enalapril significantly affected forearm skin blood flow. Captopril 306-315 kininogen 1 Homo sapiens 94-104 8448072-10 1993 This study showed that captopril and enalapril potentiated the effects of intradermal bradykinin both with respect to blood flow changes and weal formation in keeping with effective kininase II inhibition and the time course of these changes are consistent with enalapril being a longer acting drug than captopril. Captopril 23-32 kininogen 1 Homo sapiens 86-96 8448072-10 1993 This study showed that captopril and enalapril potentiated the effects of intradermal bradykinin both with respect to blood flow changes and weal formation in keeping with effective kininase II inhibition and the time course of these changes are consistent with enalapril being a longer acting drug than captopril. Captopril 304-313 kininogen 1 Homo sapiens 86-96 8388656-3 1993 Most of the bradykinin-degrading activity in cell monolayers could be inhibited in a concentration-dependent manner by the ACE inhibitors lisinopril, ramiprilat, and captopril. Captopril 166-175 kininogen 1 Homo sapiens 12-22 8436153-0 1993 Cutaneous blood flow changes and weal induced by intradermal bradykinin following pretreatment with indomethacin and captopril. Captopril 117-126 kininogen 1 Homo sapiens 61-71 8436153-5 1993 Captopril 25 mg significantly potentiated the increase in local cutaneous blood flow measured by LDF, but not erythema area, and weal volume induced by bradykinin. Captopril 0-9 kininogen 1 Homo sapiens 152-162 8436153-7 1993 The enhanced cutaneous effects of bradykinin following administration of captopril are in keeping with effective kininase II inhibition in the tissues. Captopril 73-82 kininogen 1 Homo sapiens 34-44 1629199-9 1992 Bradykinin, a natural substrate of NEP, was in part metabolized by NEP, in the presence of captopril, since 50% of the formation of the major metabolite bradykinin 1-7 was inhibited by thiorphan. Captopril 91-100 kininogen 1 Homo sapiens 153-163 1462860-2 1992 Captopril enhanced BK release, but did not suppress the increase of AII release. Captopril 0-9 kininogen 1 Homo sapiens 19-21 1558194-1 1992 Experiments were designed to study the effects of converting-enzyme inhibitors (captopril and S 10211) on the endothelium-dependent relaxation to bradykinin in isolated porcine arteries. Captopril 80-89 kininogen 1 Homo sapiens 146-156 1339590-8 1992 Bradykinin, a natural substrate of NEP, was in part metabolized by NEP, in presence of captopril, since 50% of the formation of the major metabolite bradykinin 1-7 was inhibited by thiorphan. Captopril 87-96 kininogen 1 Homo sapiens 0-10 1339590-8 1992 Bradykinin, a natural substrate of NEP, was in part metabolized by NEP, in presence of captopril, since 50% of the formation of the major metabolite bradykinin 1-7 was inhibited by thiorphan. Captopril 87-96 kininogen 1 Homo sapiens 149-159 1728438-10 1992 Captopril, but not Ro 42-5892, increased forearm blood flow (2.4 +/- 0.8 versus 1.9 +/- 0.8 ml/min/100 ml, p less than 0.01) and significantly enhanced the increase of forearm blood flow to brachial artery infusions of bradykinin (0.15, 1.5, 5, 15, and 50 ng/min/100 ml; 5 minutes each) from 744 +/- 632% to 1,383 +/- 514% (p less than 0.01). Captopril 0-9 kininogen 1 Homo sapiens 219-229 1728438-11 1992 Furthermore, repeat bradykinin infusions resulted in further decreases of blood pressure (from mean pressure of 71.4 +/- 8.5 to 63.2 +/- 7.6 mm Hg, p less than 0.01) only after captopril. Captopril 177-186 kininogen 1 Homo sapiens 20-30 1728438-12 1992 Changes of blood pressure after captopril were unrelated to baseline plasma renin activity but correlated with captopril-induced enhancement of vasodilation to bradykinin (r = 0.68, p less than 0.05). Captopril 32-41 kininogen 1 Homo sapiens 160-170 1728438-12 1992 Changes of blood pressure after captopril were unrelated to baseline plasma renin activity but correlated with captopril-induced enhancement of vasodilation to bradykinin (r = 0.68, p less than 0.05). Captopril 111-120 kininogen 1 Homo sapiens 160-170 1462860-5 1992 These results suggest that cardioprotective effect of captopril might be dependent on local BK accumulation, but not on suppression of local AII generation. Captopril 54-63 kininogen 1 Homo sapiens 92-94 1282625-9 1992 ACE inhibition by ramipril (5 mg) or captopril (50 mg) potentiated all effects of bradykinin about 20- to 50-fold, whereas it decreased angiotensin I effects only about four- to fivefold. Captopril 37-46 kininogen 1 Homo sapiens 82-92 1721246-0 1991 Bradykinin-induced cough reflex markedly increases in patients with cough associated with captopril and enalapril. Captopril 90-99 kininogen 1 Homo sapiens 0-10 1720843-1 1991 In this study, the effect of bradykinin on coronary flow in the isolated rat heart was significantly potentiated when cysteine or the sulfhydryl-containing converting enzyme inhibitors captopril and zofenoprilat were administered simultaneously. Captopril 185-194 kininogen 1 Homo sapiens 29-39 1531690-8 1992 These differences between captopril and enalapril suggest that increases in tissue bradykinin and vasodilatory prostaglandins may play an important role in the beneficial effects of captopril. Captopril 26-35 kininogen 1 Homo sapiens 83-93 1531690-8 1992 These differences between captopril and enalapril suggest that increases in tissue bradykinin and vasodilatory prostaglandins may play an important role in the beneficial effects of captopril. Captopril 182-191 kininogen 1 Homo sapiens 83-93 2687997-4 1989 We conclude that the hyponatremia may be caused by high secretion of prostagrandin and bradykinin associated with captopril therapy. Captopril 114-123 kininogen 1 Homo sapiens 87-97 2185292-2 1990 No change in the size of wheal-and-flare reactions to histamine occurred, but the size of wheal reactions to codeine and bradykinin increased in all study subjects after ingesting the ACE inhibitor, captopril. Captopril 199-208 kininogen 1 Homo sapiens 121-131 2558508-2 1989 Each kininase activity was determined by measuring the hydrolysis of bradykinin in the presence of specific inhibitors of kininase I (2-mercaptomethyl-3-guanidinoethylthiopropanoic acid), kininase II (captopril) and NEP (phosphoramidon) in 8 normal subjects. Captopril 201-210 kininogen 1 Homo sapiens 69-79 2702034-4 1989 The cause of the damage to the alveolar-capillary membranes is still unknown and we thought that long-term administration of captopril might have contributed to the damage itself, since like all ACE-inhibitors, captopril is able to bring about tissular storage of both bradykinin and prostaglandins and therefore alter the pulmonary reactivity to phlogistic stimuli. Captopril 125-134 kininogen 1 Homo sapiens 269-279 2702034-4 1989 The cause of the damage to the alveolar-capillary membranes is still unknown and we thought that long-term administration of captopril might have contributed to the damage itself, since like all ACE-inhibitors, captopril is able to bring about tissular storage of both bradykinin and prostaglandins and therefore alter the pulmonary reactivity to phlogistic stimuli. Captopril 211-220 kininogen 1 Homo sapiens 269-279 2674438-4 1989 Interactions involving bradykinin include captopril-indomethacin, in which an attenuation of the antihypertensive effects of captopril is manifest. Captopril 42-51 kininogen 1 Homo sapiens 23-33 2674438-4 1989 Interactions involving bradykinin include captopril-indomethacin, in which an attenuation of the antihypertensive effects of captopril is manifest. Captopril 125-134 kininogen 1 Homo sapiens 23-33 2643280-8 1989 Captopril significantly increased plasma bradykinin, prostaglandin E2, and 6-keto-prostaglandin F1 alpha (p less than 0.05 for each). Captopril 0-9 kininogen 1 Homo sapiens 41-51 2532136-0 1989 Effect of captopril on skin blood flow following intradermal bradykinin measured by laser Doppler flowmetry. Captopril 10-19 kininogen 1 Homo sapiens 61-71 2532136-1 1989 The effect of captopril on skin response to intradermal injection of bradykinin was investigated by laser Doppler flowmetry (LDF) and weal and flare measurements in this randomised, double-blind, placebo-controlled, cross-over balanced study. Captopril 14-23 kininogen 1 Homo sapiens 69-79 2532136-6 1989 Pre-treatment with captopril significantly increased LDF output following intradermal bradykinin at t1 but not at t2. Captopril 19-28 kininogen 1 Homo sapiens 86-96 2532136-10 1989 This study showed that captopril potentiated the effects of intradermal bradykinin both with respect to blood flow changes and weal formation. Captopril 23-32 kininogen 1 Homo sapiens 72-82 2837913-3 1988 In contrast, BK produced a sustained vasodilator response after treatment with captopril. Captopril 79-88 kininogen 1 Homo sapiens 13-15 2837913-10 1988 Pretreatment with both captopril and propranolol dramatically potentiated the magnitude of the increase in protein clearance, the filtration rate, and edema formation produced by BK but failed to affect the duration of the transient increase in vascular permeability. Captopril 23-32 kininogen 1 Homo sapiens 179-181 3121350-2 1987 Therefore, we tested the following hypothesis: inhibition of Kininase II, the bradykinin (BK) degrading enzyme, by captopril may also improve glucose metabolism in NIDD. Captopril 115-124 kininogen 1 Homo sapiens 78-88 2830937-7 1988 Bradykinin (BK) was broken down and A I converted to A II by CSF, both effects being inhibited by captopril. Captopril 98-107 kininogen 1 Homo sapiens 0-10 2830937-7 1988 Bradykinin (BK) was broken down and A I converted to A II by CSF, both effects being inhibited by captopril. Captopril 98-107 kininogen 1 Homo sapiens 12-14 3121350-9 1987 Because of the described insulin-like activity of bradykinin, the concomitant accumulation of local kinins by captopril-induced inhibition of kininase II may represent an attractive hypothesis to explain the generated data sufficiently. Captopril 110-119 kininogen 1 Homo sapiens 50-60 3037886-8 1987 Captopril may also influence prostaglandin synthesis by reducing inactivation of bradykinin. Captopril 0-9 kininogen 1 Homo sapiens 81-91 2829599-3 1987 When the EC were pretreated by captopril both of basal PGI2 production and ACE activity were reduced but the enhancing effects on PGI2 generation by AI or BK were preserved. Captopril 31-40 kininogen 1 Homo sapiens 155-157 2442780-4 1987 The inhibition of water flow by bradykinin was enhanced by captopril. Captopril 59-68 kininogen 1 Homo sapiens 32-42 3301083-6 1987 Captopril increased circulating bradykinin (P less than 0.05), prostaglandin E2 (P less than 0.05) and 6-keto-prostaglandin F1 alpha (P less than 0.05). Captopril 0-9 kininogen 1 Homo sapiens 32-42 3038403-4 1987 These results suggest that the accumulation of AI or BK via the inhibition of ACE by captopril did not cause the enhancement of PGI2 generation. Captopril 85-94 kininogen 1 Homo sapiens 53-55 2442780-5 1987 These data indicate that captopril increased the amount of bradykinin in toad bladder cells resulting in the production of PGE2 which inhibited the increase in water flow induced by vasopressin. Captopril 25-34 kininogen 1 Homo sapiens 59-69 2442780-7 1987 Thus, it was concluded that captopril inhibits the vasopressin-stimulated water flow indirectly by inhibiting the degradation of bradykinin and thereby enhancing the production of PGE2, and directly at a site following the production of cyclic adenosine monophosphate by vasopressin. Captopril 28-37 kininogen 1 Homo sapiens 129-139 3513809-0 1986 Effect of captopril on bradykinin inactivation by human foetal placental circulation. Captopril 10-19 kininogen 1 Homo sapiens 23-33 3016357-5 1986 Captopril solely inhibited PGI2 generation and the reported hypothesis that captopril enhances PGI2 generation by the accumulation of AI or BK via inhibition of ACE was not confirmed in this experimental system. Captopril 76-85 kininogen 1 Homo sapiens 140-142 3513809-4 1986 Bradykinin (100 ng ml-1) was infused through the foetal placental vessels before and during captopril 4 X 10(-7) M. Bradykinin produced a transient increase in placental vascular resistance that was not potentiated by captopril. Captopril 92-101 kininogen 1 Homo sapiens 0-10 3513809-4 1986 Bradykinin (100 ng ml-1) was infused through the foetal placental vessels before and during captopril 4 X 10(-7) M. Bradykinin produced a transient increase in placental vascular resistance that was not potentiated by captopril. Captopril 92-101 kininogen 1 Homo sapiens 116-126 3513809-5 1986 Bradykinin activity was completely abolished after passage through the foetal placental circulation, and the inactivation was blocked by captopril. Captopril 137-146 kininogen 1 Homo sapiens 0-10 3544729-8 1986 Captopril (25 mg) potentiated the blood pressure lowering effect of bradykinin about 20-fold. Captopril 0-9 kininogen 1 Homo sapiens 68-78 3544729-11 1986 Inhibition of inactivation of bradykinin by captopril enhances its activity markedly. Captopril 44-53 kininogen 1 Homo sapiens 30-40 3003038-3 1985 [Des-Pro3]-bradykinin was found to have a potent inhibitory action against angiotensin-converting enzyme with a K1 of 4.5 X 10(-12) M, which is approximately 7 times more potent than Captopril. Captopril 183-192 kininogen 1 Homo sapiens 11-21 6400378-2 1984 Factor XIIf-mediated hypotension was dose-dependent and augmented by pretreatment with captopril, an inhibitor of the bradykinin-processing enzyme kininase II. Captopril 87-96 kininogen 1 Homo sapiens 118-128 3004113-2 1985 Acute effects on blood pressure, the renin-angiotensin system and blood bradykinin after a single dose of captopril. Captopril 106-115 kininogen 1 Homo sapiens 72-82 3909277-2 1985 The present study was carried out to test the hypothesis of a possible effectiveness of captopril--an enzymatic inhibitor of both angiotensin II formation and bradykinin degradation--on hypoxic pulmonary hypertension. Captopril 88-97 kininogen 1 Homo sapiens 159-169 3909277-4 1985 In our patients, captopril significantly lowered pulmonary arterial pressure and vascular resistance only when combined with oxygen, suggesting that an increase in bradykinin availability and/or a decrease in angiotensin II synthesis might be important factors in reversing pulmonary arterial hypertension only after blunting of the hypoxic stimulus on pulmonary circulation. Captopril 17-26 kininogen 1 Homo sapiens 164-174 6098010-2 1984 Factor XIIf-mediated hypotension was dose-dependent and augmented by pretreatment with captopril, an inhibitor of the angiotensin I- and bradykinin-processing enzyme. Captopril 87-96 kininogen 1 Homo sapiens 137-147 6363144-5 1983 Captopril elevated plasma bradykinin concentration (PBK) from a control value of 12.5 +/- 4.1 (mean +/- s.d.) Captopril 0-9 kininogen 1 Homo sapiens 26-36 6437780-1 1984 By inhibiting ACE, captopril blocks the conversion of AI or AII and augments the effects of bradykinin both in vitro and in vivo. Captopril 19-28 kininogen 1 Homo sapiens 92-102 6381834-0 1984 [Effect of angiotensin I converting enzyme inhibitor (captopril) on blood pressure and bradykinin in patients with excessive aldosterone secretion]. Captopril 54-63 kininogen 1 Homo sapiens 87-97 7042175-0 1982 Antihypertensive and renal effects of captopril in relation to renin activity and bradykinin-induced vasodilation. Captopril 38-47 kininogen 1 Homo sapiens 82-92 6311635-1 1983 In order to investigate the possible role of bradykinin in the hypotensive mechanism of angiotensin I converting enzyme inhibitor (Captopril) in renin-independent essential hypertension (EHT), we studied the effects of the single administration of 100 mg captopril on plasma bradykinin levels by sensitive radioimmunoassay in 21 EHT, who showed agonistic responses to 1Sar, 8Ile-angiotensin II (A IIA). Captopril 131-140 kininogen 1 Homo sapiens 45-55 6311635-10 1983 The present results suggest that bradykinin may be involved in the hypotensive action of captopril in the EHT subgroup, where the renin-angiotensin system appears to play an inert role for the elevation of blood pressure. Captopril 89-98 kininogen 1 Homo sapiens 33-43 6214858-1 1982 Captopril (Capoten; Squibb) is a specific orally active antagonist of peptidyl-dipeptide carboxyhydrolase, the enzyme which converts angiotensin I to angiotensin II and which inactivates bradykinin. Captopril 0-9 kininogen 1 Homo sapiens 187-197 6214858-1 1982 Captopril (Capoten; Squibb) is a specific orally active antagonist of peptidyl-dipeptide carboxyhydrolase, the enzyme which converts angiotensin I to angiotensin II and which inactivates bradykinin. Captopril 11-18 kininogen 1 Homo sapiens 187-197 6176105-1 1982 Captopril is a remarkably effective new antihypertensive drug designed and developed as a potent and specific inhibitor of angiotensin-converting enzyme, a zinc metallopeptidase that participates in the synthesis of a hypertensive peptide, angiotensin II, and in the degradation of a hypotensive peptide, bradykinin. Captopril 0-9 kininogen 1 Homo sapiens 305-315 6280473-2 1982 On the sodium-restricted diet, the hypotensive response to captopril was accompanied by significant increments in the metabolite of prostaglandin E2 (PGE2-M) and bradykinin and by significant decrements in angiotensin II. Captopril 59-68 kininogen 1 Homo sapiens 162-172 7018190-7 1981 Captopril (SQ 14.225) is a competitive inhibitor of peptidyl dipeptide hydrolase, also known as angiotensin converting enzyme (ACE) or kininase II, which converts angiotensin I (A I) into angiotensin II (A II), hydrolyzes des-Asp-angiotensin I to angiotensin III (A III) and inactivates bradykinin (BK) (19). Captopril 0-9 kininogen 1 Homo sapiens 287-297 6796855-1 1981 Captopril is a specific inhibitor of kininase II which is responsible for the conversion of angiotensin I into the active angiotensin II and also for the inactivation of bradykinin. Captopril 0-9 kininogen 1 Homo sapiens 170-180 6269554-3 1981 Inhibition of the conversion enzyme, notably with captopril, prevents the formation of angiotensin II from angiotensin I and also results in accumulation of a vasodilator and natriuretic peptide: bradykinin. Captopril 50-59 kininogen 1 Homo sapiens 196-206 6266379-4 1981 Captopril (SQ14225) blocks angiotensin I and potentiates bradykinin effects in vitro and in vivo. Captopril 0-9 kininogen 1 Homo sapiens 57-67 6266379-4 1981 Captopril (SQ14225) blocks angiotensin I and potentiates bradykinin effects in vitro and in vivo. Captopril 11-18 kininogen 1 Homo sapiens 57-67 7018190-7 1981 Captopril (SQ 14.225) is a competitive inhibitor of peptidyl dipeptide hydrolase, also known as angiotensin converting enzyme (ACE) or kininase II, which converts angiotensin I (A I) into angiotensin II (A II), hydrolyzes des-Asp-angiotensin I to angiotensin III (A III) and inactivates bradykinin (BK) (19). Captopril 0-9 kininogen 1 Homo sapiens 299-301