PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 24839774-0 2014 Bradykinin stimulation of nitric oxide production is not sufficient for gamma-globin induction. Nitric Oxide 26-38 kininogen 1 Homo sapiens 0-10 29424931-16 2018 Initial release of the proteases kallikrein and trypsin from dying acinar cells can, via bradykinin generation and protease-activated receptors, induce Ca2+ signals in stellate cells which can then, possibly via nitric oxide generation, damage more acinar cells and thereby cause additional release of proteases, generating a vicious circle. Nitric Oxide 212-224 kininogen 1 Homo sapiens 89-99 26952290-0 2016 Plasma kallikrein-bradykinin pathway promotes circulatory nitric oxide metabolite availability during hypoxia. Nitric Oxide 58-70 kininogen 1 Homo sapiens 18-28 24960080-0 2014 Endothelium-derived nitric oxide (NO) activates the NO-epidermal growth factor receptor-mediated signaling pathway in bradykinin-stimulated angiogenesis. Nitric Oxide 20-32 kininogen 1 Homo sapiens 118-128 24925526-2 2014 Although BK stimulates both nitric oxide and endothelium-derived hyperpolarizing factor (EDHF) release, the role of EDHF in t-PA release remains unexplored. Nitric Oxide 28-40 kininogen 1 Homo sapiens 9-11 25130038-5 2014 Bradykinin is pharmacologically active polypeptide that can promote both cardiovascular and renal function, for example, vasodilation, natriuresis, diuresis, and release of nitric oxide (NO). Nitric Oxide 173-185 kininogen 1 Homo sapiens 0-10 23361105-1 2013 Bradykinin increases during cardiopulmonary bypass (CPB) and stimulates the release of nitric oxide, inflammatory cytokines, and tissue-type plasminogen activator (t-PA), acting through its B2 receptor. Nitric Oxide 87-99 kininogen 1 Homo sapiens 0-10 23459756-8 2013 In these vessels, the pre-incubation with the Mas antagonists A779 or d-Pro-angiotensin-(1-7) totally abolished the vasodilatory capacity of both angiotensin-(1-7) and bradykinin, which was nitric oxide mediated. Nitric Oxide 190-202 kininogen 1 Homo sapiens 168-178 21983453-6 2011 Our results demonstrate that bradykinin (BK)-simulated arteriolar dilation is mediated by nitric oxide (NO) and EDHF pathways. Nitric Oxide 90-102 kininogen 1 Homo sapiens 29-39 22110081-8 2012 RESULTS: Isolated retinal arterioles developed stable basal tone and the vasodilations to endothelium-dependent nitric oxide (NO)-mediated agonists bradykinin and L-lactate were significantly reduced only by 90 minutes of ischemia. Nitric Oxide 112-124 kininogen 1 Homo sapiens 148-158 22507330-0 2012 Exhaled nitric oxide is related to bronchial eosinophilia and airway hyperresponsiveness to bradykinin in allergen-induced asthma exacerbation. Nitric Oxide 8-20 kininogen 1 Homo sapiens 92-102 21983453-6 2011 Our results demonstrate that bradykinin (BK)-simulated arteriolar dilation is mediated by nitric oxide (NO) and EDHF pathways. Nitric Oxide 90-102 kininogen 1 Homo sapiens 41-43 21654087-6 2011 It was also observed that all the peptides related to buPRL could antagonize the vascular endothelial growth factor (VEGF) and bradykinin (BK)- dependent production of endothelial nitric oxide (NO), which is a pre-requisite for endothelial tube formation. Nitric Oxide 180-192 kininogen 1 Homo sapiens 127-137 21654087-6 2011 It was also observed that all the peptides related to buPRL could antagonize the vascular endothelial growth factor (VEGF) and bradykinin (BK)- dependent production of endothelial nitric oxide (NO), which is a pre-requisite for endothelial tube formation. Nitric Oxide 180-192 kininogen 1 Homo sapiens 139-141 21448379-11 2011 The mechanism could be either that Enalapril limits the angiotensin IIinduced production of superoxide radicals which would normally inactivate nitric oxide, or that it may increase bradykinin-mediated nitric oxide release. Nitric Oxide 202-214 kininogen 1 Homo sapiens 182-192 21295852-3 2011 In addition, both bradykinin and vascular endothelial growth factor (VEGF) stimulate nitric oxide (NO), and the VEGF and bradykinin receptors have multiple interactions that converge in the endothelial NO synthase (eNOS)-NO pathway. Nitric Oxide 85-97 kininogen 1 Homo sapiens 18-28 21555712-13 2011 Third, bradykinin, but not acetylcholine, stimulates K(+)(Ca) channel-mediated vasodilation in healthy subjects, whereas in hypercholesterolemia, K(+)(Ca) channel-mediated vasodilation compensates for the reduced nitric oxide activity. Nitric Oxide 213-225 kininogen 1 Homo sapiens 7-17 21305271-1 2011 PURPOSE: The antihypertensive effects of angiotensin-converting enzyme inhibitors (ACEi) are explained, at least in part, by enhanced bradykinin-dependent nitric oxide (NO) formation and decreased angiotensin II-induced oxidative stress and vasoconstriction. Nitric Oxide 155-167 kininogen 1 Homo sapiens 134-144 20174953-10 2010 Bradykinin, an inducer of nitric oxide, prompted two folds higher nitric oxide production along with simulated microgravity in a synergistic manner. Nitric Oxide 26-38 kininogen 1 Homo sapiens 0-10 20423727-3 2010 This study tested the hypothesis that bradykinin induces oxidative stress through a nitric oxide (NO)-dependent mechanism in the human vasculature. Nitric Oxide 84-96 kininogen 1 Homo sapiens 38-48 20174953-10 2010 Bradykinin, an inducer of nitric oxide, prompted two folds higher nitric oxide production along with simulated microgravity in a synergistic manner. Nitric Oxide 66-78 kininogen 1 Homo sapiens 0-10 19886189-3 2009 It has been shown that adenosine, bradykinin, opioid peptides, calcitonin gene-related peptide and also signaling cascade involved nitric oxide, free radicals, protein kinases, mitochondrial ATP-sensitive K+ -channel, mitochondrial permeability transition pore play an important role in the mechanism of cardioprotective action of remote preconditioning. Nitric Oxide 131-143 kininogen 1 Homo sapiens 34-44 19850828-8 2010 Nitric oxide (NO) synthase inhibitor L-NAME nearly abolished dilations to bradykinin and flow and attenuated the adenosine-induced dilation without altering the response to nitroprusside. Nitric Oxide 0-12 kininogen 1 Homo sapiens 74-84 20375905-3 2010 RESULTS: IL-6 inhibited the phosphorylation of eNOS at Ser1177 and the bradykinin-stimulated nitric oxide production; however, eNOS protein expression was not changed. Nitric Oxide 93-105 kininogen 1 Homo sapiens 71-81 22466497-6 2010 It has been postulated that angiotensin II receptor activates the bradykinin-prostaglandin-nitric oxide cascade, resulting in bradykinin-mediated side effects of ARBs such as angioedema, but the true mechanism remains largely unknown. Nitric Oxide 91-103 kininogen 1 Homo sapiens 66-76 22466497-6 2010 It has been postulated that angiotensin II receptor activates the bradykinin-prostaglandin-nitric oxide cascade, resulting in bradykinin-mediated side effects of ARBs such as angioedema, but the true mechanism remains largely unknown. Nitric Oxide 91-103 kininogen 1 Homo sapiens 126-136 19841473-0 2010 Endogenous nitric oxide contributes to bradykinin-stimulated glucose uptake but attenuates vascular tissue-type plasminogen activator release. Nitric Oxide 11-23 kininogen 1 Homo sapiens 39-49 19421072-10 2009 The nitric oxide scavenger hydroxocobalamin and the Na+-K+ ATPase inhibitor ouabain abolished the responses to bradykinin and light. Nitric Oxide 4-16 kininogen 1 Homo sapiens 111-121 19767824-0 2009 Cadmium attenuates bradykinin-driven nitric oxide production by interplaying with the localization pattern of endothelial nitric oxide synthase. Nitric Oxide 37-49 kininogen 1 Homo sapiens 19-29 19767824-2 2009 Bradykinin is a Ca-mobilizing soluble peptide that acts via nitric oxide to promote vasodilation and capillary permeability. Nitric Oxide 60-72 kininogen 1 Homo sapiens 0-10 19767824-6 2009 The results of the in vitro wound healing and tube formation assays by using EAhy 926, a transformed endothelial cell line, suggest that Cd blocked bradykinin-mediated endothelial migration and tube formation by 38% and 67%, respectively, while nitric oxide supplementation could reverse the effect of Cd on bradykinin-induced endothelial migration by 94%. Nitric Oxide 245-257 kininogen 1 Homo sapiens 148-158 19767824-7 2009 The detection of nitric oxide by using a DAF-2DA fluorescent probe, Griess assay, and ultrasensitive electrode suggests that Cd blocked bradykinin-induced nitric oxide production. Nitric Oxide 17-29 kininogen 1 Homo sapiens 136-146 19767824-7 2009 The detection of nitric oxide by using a DAF-2DA fluorescent probe, Griess assay, and ultrasensitive electrode suggests that Cd blocked bradykinin-induced nitric oxide production. Nitric Oxide 155-167 kininogen 1 Homo sapiens 136-146 19767824-8 2009 Fluorescence imaging of eNOS-GFP transfected endothelial cells, immunofluorescence, and Western blot studies of Cd and bradykinin-treated cells show that Cd interfered with the localization pattern of eNOS, which possibly attenuates nitric oxide production in part. Nitric Oxide 233-245 kininogen 1 Homo sapiens 119-129 19767824-9 2009 Additionally, Ca imaging of Cd- and bradykinin-treated cells suggests that Cd blocked bradykinin-dependent Ca influx into the cells, thus partially blocking Ca-dependent nitric oxide production in endothelial cells. Nitric Oxide 170-182 kininogen 1 Homo sapiens 86-96 18307734-10 2008 The biochemical consequences of renin inhibition differ from those of angiotensin I-converting enzyme (ACE) inhibition and Ang II antagonism, particularly in terms of angiotensin profiles and interactions with the bradykinin-nitric oxide-cyclic guanosine monophosphate pathway and possibly the (pro)renin receptor. Nitric Oxide 225-237 kininogen 1 Homo sapiens 214-224 19171072-2 2009 PRCP regulates angiotensin 1-7 (Ang 1-7) - and bradykinin (BK) - stimulated nitric oxide production in endothelial cells. Nitric Oxide 76-88 kininogen 1 Homo sapiens 47-57 19171072-2 2009 PRCP regulates angiotensin 1-7 (Ang 1-7) - and bradykinin (BK) - stimulated nitric oxide production in endothelial cells. Nitric Oxide 76-88 kininogen 1 Homo sapiens 59-61 19245678-5 2009 In microvessels from subjects aged less than 60 years, most of the bradykinin-induced relaxation was due to nitric oxide release while the rest was sensitive to cyclooxygenase (COX) blockade. Nitric Oxide 108-120 kininogen 1 Homo sapiens 67-77 19442326-2 2009 The bradykinin system is involved in the mediation and modulation of the vasoconstrictor renin-angiotensin system and the vasodilators prostaglandin, prostacyclin, and nitric oxide in regulating sodium water balance, renal and cardiac hemodynamics, and blood pressure. Nitric Oxide 168-180 kininogen 1 Homo sapiens 4-14 18789901-7 2008 Acetylcholine, bradykinin and sodium nitroprusside all caused dose-dependent vasodilatation in the presence and absence of aspirin and the "nitric oxide clamp" (P< or =0.005 for all). Nitric Oxide 140-152 kininogen 1 Homo sapiens 15-25 18052679-0 2008 Cognac polyphenolic compounds increase bradykinin-induced nitric oxide production in endothelial cells. Nitric Oxide 58-70 kininogen 1 Homo sapiens 39-49 18083112-6 2008 BK is a potent inflammatory peptide which stimulates constitutive bradykinin B2 and inducible B1 receptors to release nitric oxide and prostacyclin. Nitric Oxide 118-130 kininogen 1 Homo sapiens 0-2 18083112-6 2008 BK is a potent inflammatory peptide which stimulates constitutive bradykinin B2 and inducible B1 receptors to release nitric oxide and prostacyclin. Nitric Oxide 118-130 kininogen 1 Homo sapiens 66-76 18037911-5 2008 KEY RESULTS: Bradykinin-induced relaxation in both sets of vessels was mediated entirely by EDHF whilst that generated by acetylcholine, though principally generated by EDHF, also had contribution from prostacyclin and possibly nitric oxide in mesenteric and subcutaneous vessels, respectively. Nitric Oxide 228-240 kininogen 1 Homo sapiens 13-23 18182246-3 2008 Using an animal model of hypertension, we have demonstrated that Ang II produces a vasodilator effect through the AT2 receptor via the bradykinin (BK)-dependent activation of endothelial nitric oxide (NO) synthase. Nitric Oxide 187-199 kininogen 1 Homo sapiens 135-145 18182246-3 2008 Using an animal model of hypertension, we have demonstrated that Ang II produces a vasodilator effect through the AT2 receptor via the bradykinin (BK)-dependent activation of endothelial nitric oxide (NO) synthase. Nitric Oxide 187-199 kininogen 1 Homo sapiens 147-149 17276727-6 2007 These effects of angiotensin-converting enzyme inhibitors and AT(1) receptor blockers can be mediated by activation of bradykinin pathways, resulting in the generation of vascular endothelial growth factor, nitric oxide and, consequently, angiogenesis. Nitric Oxide 207-219 kininogen 1 Homo sapiens 119-129 18160362-4 2007 Bradykinin enhances nitric oxide and vasodilatory prostaglandins. Nitric Oxide 20-32 kininogen 1 Homo sapiens 0-10 17868792-7 2007 Although similar intensity of RAS blockade can be achieved by either combination therapy or by using high doses of an AT1-receptor antagonist given alone, the ACE inhibitor present in the combination interferes with the bradykinin-nitric oxide pathway and the N-acetyl-Ser-Asp-Lys-Pro metabolism, which both may have additional biological effects. Nitric Oxide 231-243 kininogen 1 Homo sapiens 220-230 17666194-3 2007 ACE inhibitors reduce circulating and tissue angiotensin II levels and potentiate the beneficial effects of bradykinin, including generation of nitric oxide (NO). Nitric Oxide 144-156 kininogen 1 Homo sapiens 108-118 17666198-3 2007 However, ACE inhibitors interrupt bradykinin breakdown, which in turn potentially enhances nitric oxide and prostacyclin mechanisms. Nitric Oxide 91-103 kininogen 1 Homo sapiens 34-44 17636215-2 2007 Systemic arteries, isolated from women with healthy pregnancies, relax to the endothelial-dependent agonist bradykinin via a nonprostacyclin and non-nitric oxide pathway attributable to EDHF. Nitric Oxide 149-161 kininogen 1 Homo sapiens 108-118 20527397-3 2005 Tissue ACE-I, through their high affinity to endothelium, considerably stronger prevents the local synthesis of angiotensin II (Ang II) and by inhibition of kininase II causes the subsequent increase of bradykinin level and mediated by BK2 receptor release of nitric oxide (NO), prostacycline (PGI2) and tissue type plasminogen activator (t-PA). Nitric Oxide 260-272 kininogen 1 Homo sapiens 203-213 16607560-8 2006 Maximum nitric-oxide-mediated dilation to bradykinin was significantly higher in patients with SDB who had received antihypertensive drug treatment compared to normotensive SDB patients. Nitric Oxide 8-20 kininogen 1 Homo sapiens 42-52 16957554-1 2006 BACKGROUND: Tissue kallikrein (TK) generates Lys-bradykinin, which is then converted to bradykinin and releases nitric oxide (NO) from endothelial cells via B2 receptors. Nitric Oxide 112-124 kininogen 1 Homo sapiens 49-59 16601572-8 2006 Interestingly, AT1-receptor blockade appears to stimulate the bradykinin-nitric oxide pathway by increased angiotensin II type 2 receptor activation. Nitric Oxide 73-85 kininogen 1 Homo sapiens 62-72 15895105-2 2005 To clarify the involvement of these pathways in endothelium-dependent myocyte hyperpolarization, bradykinin-induced electrical changes in endothelial cells and myocytes of porcine coronary arteries (following nitric oxide (NO) synthase and cyclooxygenase inhibition) were measured using sharp microelectrodes. Nitric Oxide 209-221 kininogen 1 Homo sapiens 97-107 16272778-3 2005 However, the role of nitric oxide (NO) in the early phase protection of preconditioning with BK is not well understood. Nitric Oxide 21-33 kininogen 1 Homo sapiens 93-95 16003073-8 2005 Furthermore, a reduction of endothelial nitric oxide formation takes place, thus decreasing microvascular reactivity to dilating agents such as bradykinin, and complement function (e.g., opsonization, chemotaxis) is impaired, despite elevations of certain complement factors. Nitric Oxide 40-52 kininogen 1 Homo sapiens 144-154 15471985-1 2005 The present study tested the hypothesis that endostatin stimulates superoxide (O2*-) production through a ceramide-mediating signaling pathway and thereby results in an uncoupling of bradykinin (BK)-induced increases in intracellular Ca2+ concentration ([Ca2+]i) from nitric oxide (NO) production in coronary endothelial cells. Nitric Oxide 268-280 kininogen 1 Homo sapiens 195-197 15910619-0 2005 The contribution of nitric oxide and vasodilatory prostanoids to bradykinin-mediated vasodilation in Type 1 diabetes. Nitric Oxide 20-32 kininogen 1 Homo sapiens 65-75 15640399-1 2005 Bradykinin (BK) is an endogenous vasoactive peptide that promotes vasodilation by stimulating the release of nitric oxide (NO) from endothelial cells via activation of endothelial NO synthase (eNOS). Nitric Oxide 109-121 kininogen 1 Homo sapiens 0-10 15640399-1 2005 Bradykinin (BK) is an endogenous vasoactive peptide that promotes vasodilation by stimulating the release of nitric oxide (NO) from endothelial cells via activation of endothelial NO synthase (eNOS). Nitric Oxide 109-121 kininogen 1 Homo sapiens 12-14 15910619-7 2005 CONCLUSIONS: This study demonstrates that bradykinin-stimulated vasodilation is mediated by both nitric oxide and prostaglandin release from the endothelium in patients with Type 1 diabetes and normoalbuminuria, and in healthy control subjects. Nitric Oxide 97-109 kininogen 1 Homo sapiens 42-52 15317600-1 2004 AIMS: The aim of this study was to evaluate the effect of acutely induced hyperglycaemia on renal sodium handling and to explore the role of the bradykinin-nitric oxide-cGMP signalling pathway. Nitric Oxide 156-168 kininogen 1 Homo sapiens 145-155 15516132-5 2004 With the aid of a scanning electrochemical microscope, it was possible to use the distance sensor by recording the negative feedback effect on the reduction of molecular oxygen to "guide" the nitric oxide sensor to various known distances from a layer of adherently growing human umbilical vein endothelial cells for the detection of nitric oxide released from the cells upon stimulation with bradykinin. Nitric Oxide 192-204 kininogen 1 Homo sapiens 393-403 15516132-5 2004 With the aid of a scanning electrochemical microscope, it was possible to use the distance sensor by recording the negative feedback effect on the reduction of molecular oxygen to "guide" the nitric oxide sensor to various known distances from a layer of adherently growing human umbilical vein endothelial cells for the detection of nitric oxide released from the cells upon stimulation with bradykinin. Nitric Oxide 334-346 kininogen 1 Homo sapiens 393-403 15586018-4 2005 RECENT FINDINGS: During the past year, the evidence for an AT2 receptor microvascular dilator action has been presented that is mediated by nitric oxide (NO) generation in a bradykinin-dependent or independent manner. Nitric Oxide 140-152 kininogen 1 Homo sapiens 174-184 15526242-6 2004 Bradykinin is thought to contribute to the cardioprotective effect of ACE inhibition through modification of nitric oxide release, calcium handling and collagen accumulation. Nitric Oxide 109-121 kininogen 1 Homo sapiens 0-10 14514933-0 2003 Effect of bradykinin on allergen induced increase in exhaled nitric oxide in asthma. Nitric Oxide 61-73 kininogen 1 Homo sapiens 10-20 15167831-2 2004 Myometrial resistance arteries from women with preeclampsia show a minimal, wholly nitric oxide-mediated, bradykinin-induced relaxation. Nitric Oxide 83-95 kininogen 1 Homo sapiens 106-116 12876216-1 2003 The Ca2+ mobilizing peptide, bradykinin (BK), stimulates endothelial nitric oxide synthase (eNOS)-derived cellular nitric oxide (NO) production in association with altering the subcellular distribution of the enzyme. Nitric Oxide 69-81 kininogen 1 Homo sapiens 29-39 12876216-1 2003 The Ca2+ mobilizing peptide, bradykinin (BK), stimulates endothelial nitric oxide synthase (eNOS)-derived cellular nitric oxide (NO) production in association with altering the subcellular distribution of the enzyme. Nitric Oxide 69-81 kininogen 1 Homo sapiens 41-43 12392844-4 2002 Nitric oxide (NO) bioactivity was represented by both basal and bradykinin-stimulated cellular cyclic guanosine monophosphate accumulation and L-citrulline conversion from L-arginine. Nitric Oxide 0-12 kininogen 1 Homo sapiens 64-74 12767053-6 2003 One mechanism involves the action of bradykinin, acting through bradykinin B(2) receptors, to increase nitric oxide (NO) production and ultimately enhance glucose transport. Nitric Oxide 103-115 kininogen 1 Homo sapiens 37-47 12767053-6 2003 One mechanism involves the action of bradykinin, acting through bradykinin B(2) receptors, to increase nitric oxide (NO) production and ultimately enhance glucose transport. Nitric Oxide 103-115 kininogen 1 Homo sapiens 64-74 12063315-8 2002 We conclude that H(2)O(2) mediates the non-nitric oxide-, non-prostanoid-dependent vasorelaxation to BK in the piglet pial vasculature. Nitric Oxide 43-55 kininogen 1 Homo sapiens 101-103 12052484-3 2002 Endothelial nitric oxide production was quantified as the forearm blood flow response to intra-brachial infusion of bradykinin and N(G) monomethyl-L-arginine (L-NMMA). Nitric Oxide 12-24 kininogen 1 Homo sapiens 116-126 12163339-7 2002 These results suggest that gap junctional communication is involved in the nitric oxide (NO)- and prostanoid-independent vasodilator responses to bradykinin in myometrial small arteries in normal pregnancy. Nitric Oxide 75-87 kininogen 1 Homo sapiens 146-156 12423422-8 2002 BK acts mainly indirectly, primarily through airway nerve activation, but also by the release of prostanoids, thromboxanes and nitric oxide (NO). Nitric Oxide 127-139 kininogen 1 Homo sapiens 0-2 11992135-3 2002 ACE inhibitors reduce angiotensin II and, by blocking the metabolism of bradykinin, ACE inhibitors upregulate nitric oxide and prostacycline. Nitric Oxide 110-122 kininogen 1 Homo sapiens 72-82 11791011-0 2002 Bradykinin inhibits serum-depletion-induced apoptosis of human vascular endothelial cells by inducing nitric oxide via calcium ion kinetics. Nitric Oxide 102-114 kininogen 1 Homo sapiens 0-10 11791011-4 2002 The apoptosis inhibited by bradykinin was reduced by nitric oxide inhibitor N(G)-monomethyl-L-arginine (L-NMMA) and consequently restored by combined treatment with L-NMMA and L-arginine. Nitric Oxide 53-65 kininogen 1 Homo sapiens 27-37 11791011-6 2002 Bradykinin increased nitric oxide production, which was inhibited by L-NMMA and restored by combined treatment with L-NMMA and L-arginine. Nitric Oxide 21-33 kininogen 1 Homo sapiens 0-10 11791011-9 2002 These findings suggest that bradykinin inhibits serum-depletion-induced apoptosis in HUVECs by enhancing nitric oxide production via an increase in [Ca2+]i. Nitric Oxide 105-117 kininogen 1 Homo sapiens 28-38 12152253-2 2002 Bradykinin promotes generation by endothelium such substances as endothelium-derived hyperpolarizing factor, prostacyclin and nitric oxide. Nitric Oxide 126-138 kininogen 1 Homo sapiens 0-10 11677365-9 2001 CONCLUSIONS: Ang(1-7) potentiates the vasodilating effect of bradykinin, possibly through a mechanism(s) involving nitric oxide release, in human forearm resistance vessels. Nitric Oxide 115-127 kininogen 1 Homo sapiens 61-71 11587919-3 2001 In addition, nitric oxide mediates a number of vasodilator responses in ocular vessels to agonists such as acetylcholine, bradykinin, histamine, substance P and insulin. Nitric Oxide 13-25 kininogen 1 Homo sapiens 122-132 11392475-13 2001 Furthermore, inhibition of ACE prolongs the half-life of bradykinin and stabilizes bradykinin receptors linked to the formation of nitric oxide and prostacyclin. Nitric Oxide 131-143 kininogen 1 Homo sapiens 83-93 11356600-9 2001 Thus nitric oxide- and prostaglandin-independent, bradykinin-mediated forearm vasodilation is suppressed by high intravascular K+ concentrations, indicating a contribution of EDHF. Nitric Oxide 5-17 kininogen 1 Homo sapiens 50-60 11356613-4 2001 Inhibiting nitric oxide synthase with 10(-5) M N(omega)-nitro-L-arginine methyl ester (L-NAME) blocked bradykinin-induced vasodilation but did not affect the flow-diameter relation or the maximum change in diameter from static conditions (67 +/- 10 microm in control vs. 71 +/- 8 microm after L-NAME, P = not significant). Nitric Oxide 11-23 kininogen 1 Homo sapiens 103-113 11392476-5 2001 In addition, ACE inhibition of kininase inhibits the breakdown of bradykinin, a direct stimulant of nitric oxide release from the intact endothelial cell. Nitric Oxide 100-112 kininogen 1 Homo sapiens 66-76 11551775-3 2001 Bradykinin, a nonapeptide formed by enzymatic cleavage of a plasma protein precursor, activates eNOS by an independent pathway that does not require serine phosphorylation, suggesting a complex interplay of signals in the control of endothelial formation of nitric oxide. Nitric Oxide 258-270 kininogen 1 Homo sapiens 0-10 11496234-1 2001 BACKGROUND: Endogenous nitric oxide protects against airway hyperresponsiveness (AHR) to bradykinin in mild asthma, whereas AHR to bradykinin is enhanced by inhaled allergens. Nitric Oxide 23-35 kininogen 1 Homo sapiens 89-99 11496234-10 2001 CONCLUSIONS: These data indicate that allergen exposure in asthma induces increased airway hyperresponsiveness to bradykinin through impaired release of bronchoprotective nitric oxide associated with downregulation of ecNOS. Nitric Oxide 171-183 kininogen 1 Homo sapiens 114-124 11247797-8 2001 Liberated bradykinin stimulates the endothelial cell bradykinin B2 receptor to form nitric oxide. Nitric Oxide 84-96 kininogen 1 Homo sapiens 10-20 11247797-8 2001 Liberated bradykinin stimulates the endothelial cell bradykinin B2 receptor to form nitric oxide. Nitric Oxide 84-96 kininogen 1 Homo sapiens 53-63 11715356-9 2001 In addition to their role in inhibiting the renin-angiotensin system, angiotensin-converting enzyme (ACE) inhibitors raise the activity of bradykinin, thereby leading to an increase in nitric oxide release. Nitric Oxide 185-197 kininogen 1 Homo sapiens 139-149 11137083-4 2001 The purpose of this investigation was to verify in vivo and in vitro vasoreactivity to bradykinin (BK) and serotonin (5-hydroxytryptamine; 5-HT) (endothelial dependent agonists) as well as to nitroglycerin (NTG) (exogenous nitric oxide donor) at different times after oversized balloon angioplasty intervention ranging from 1 h to 12 weeks, in normal porcine coronary arteries. Nitric Oxide 223-235 kininogen 1 Homo sapiens 87-97 11344778-3 2000 On the other hand, ACE inhibitors can increase bradykinin, and thus, nitric oxide, which may cause potent cardioprotection, inhibition of smooth muscle proliferation and attenuation of inflammation mechanisms. Nitric Oxide 69-81 kininogen 1 Homo sapiens 47-57 10681501-12 2000 This interaction of nNOS with the B2R may recruit the enzyme to allow for the effective coupling of bradykinin signaling to the nitric oxide pathway. Nitric Oxide 128-140 kininogen 1 Homo sapiens 100-110 19667535-4 2000 Oxidized lipoproteins inhibit the release of the vasodilative substance nitric oxide, and angiotensin II degrades bradykinin, a potent stimulator of nitric oxide production in endothelial cells that is known to protect against atherosclerosis. Nitric Oxide 149-161 kininogen 1 Homo sapiens 114-124 10978247-1 2000 Nitric oxide (NO) production by endothelial cells in response to bradykinin (Bk) treatment was markedly and synergistically enhanced by cotreatment with sodium orthovanadate (vanadate), a phosphotyrosine phosphatase inhibitor. Nitric Oxide 0-12 kininogen 1 Homo sapiens 65-75 10978247-1 2000 Nitric oxide (NO) production by endothelial cells in response to bradykinin (Bk) treatment was markedly and synergistically enhanced by cotreatment with sodium orthovanadate (vanadate), a phosphotyrosine phosphatase inhibitor. Nitric Oxide 0-12 kininogen 1 Homo sapiens 77-79 10916114-2 2000 Some of the effects of BK are mediated by nitric oxide (NO). Nitric Oxide 42-54 kininogen 1 Homo sapiens 23-25 10596684-0 1999 Prostaglandins mediate bradykinin-induced reduction of exhaled nitric oxide in asthma. Nitric Oxide 63-75 kininogen 1 Homo sapiens 23-33 11270506-8 2000 Quinaprilat could ameliorate both apoptosis and necrosis through the upregulation of constitutive endothelial nitric oxide synthase via an increase of bradykinin, with the resulting increase of nitric oxide. Nitric Oxide 110-122 kininogen 1 Homo sapiens 151-161 10585891-3 1999 In human subcutaneous arteries from uraemic subjects, noradrenaline- and KCl-induced vasoconstrictions were enhanced when nitric oxide (NO) production was blocked with N(G)-nitro-L-arginine methyl ester (L-NAME), but were unaffected by EPO, while acetylcholine- and bradykinin-induced concentration-dependent relaxations were markedly attenuated by L-NAME, but not by EPO. Nitric Oxide 122-134 kininogen 1 Homo sapiens 266-276 10596684-2 1999 Endogenous release of nitric oxide may inhibit BK-induced bronchoconstriction. Nitric Oxide 22-34 kininogen 1 Homo sapiens 47-49 10596684-9 1999 Inhaled bradykinin induced bronchoconstriction and a reduction in exhaled nitric oxide levels in asthmatic subjects, an effect that is partly mediated by cyclo-oxygenase products. Nitric Oxide 74-86 kininogen 1 Homo sapiens 8-18 9876291-4 1998 Although in some cases the action of bradykinin is entirely mediated by the endothelial release of nitric oxide (NO) and/or prostacyclin (PGI2), a large amount of evidence has been accumulated during the last 10 years indicating that a non-NO/PGI2 factor accounts for bradykinin-induced vasodilation in a wide variety of perfused vascular beds and isolated small arteries from several species including humans. Nitric Oxide 99-111 kininogen 1 Homo sapiens 37-47 10499558-8 1999 Beyond inhibiting the renin-angiotensin system, angiotensin-converting enzyme (ACE) inhibitors diminish the inactivation of bradykinin, thus leading to an augmentation of nitric oxide release. Nitric Oxide 171-183 kininogen 1 Homo sapiens 124-134 10384200-4 1999 The endothelium-derived hyperpolarizing factor-mediated relaxation to bradykinin was studied when endothelium-derived nitric oxide and prostaglandin I2 were inhibited with the presence of 7 micromol/L indomethacin and 300 micromol/L NG-nitro-L -arginine. Nitric Oxide 118-130 kininogen 1 Homo sapiens 70-80 10415540-0 1999 Interaction of bradykinin with angiotensin, prostacyclin, and nitric oxide in myocardial preservation. Nitric Oxide 62-74 kininogen 1 Homo sapiens 15-25 10415540-3 1999 Bradykinin appears to function as a signaling molecule by controlling the release of other intracellular modulators, such as prostacyclins and nitric oxide, which also exert beneficial effects on the ischemic myocardium. Nitric Oxide 143-155 kininogen 1 Homo sapiens 0-10 10377076-0 1999 Human coronary arteriolar dilation to bradykinin depends on membrane hyperpolarization: contribution of nitric oxide and Ca2+-activated K+ channels. Nitric Oxide 104-116 kininogen 1 Homo sapiens 38-48 10367598-0 1999 Nitric oxide decreases microvascular permeability in bradykinin stimulated and nonstimulated conditions. Nitric Oxide 0-12 kininogen 1 Homo sapiens 53-63 10397075-0 1999 The role of nitric oxide in bradykinin-induced dilation of coronary resistance vessels in patients with hypercholesterolemia. Nitric Oxide 12-24 kininogen 1 Homo sapiens 28-38 10397075-10 1999 Bradykinin-induced dilation was similar in hypercholesterolemic patients and control patients after inhibition of nitric oxide. Nitric Oxide 114-126 kininogen 1 Homo sapiens 0-10 10397075-11 1999 CONCLUSION: These results suggest that the bradykinin-mediated endothelium-dependent dilation of coronary resistance vessels may be impaired due to depressed nitric oxide production in patients with hypercholesterolemia. Nitric Oxide 158-170 kininogen 1 Homo sapiens 43-53 10361449-3 1999 On the other hand, ACEIs can increase bradykinin, and thus, nitric oxide, which may cause potent cardioprotection. Nitric Oxide 60-72 kininogen 1 Homo sapiens 38-48 10435013-8 1999 CONCLUSION: In ITA relaxations to carbachol and bradykinin were mediated via nitric oxide. Nitric Oxide 77-89 kininogen 1 Homo sapiens 48-58 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. Nitric Oxide 175-187 kininogen 1 Homo sapiens 105-115 10227752-3 1998 Previously, we showed the rise in plasma levels of prostaglandins and nitric oxide derivatives accompanied by the rise in bradykinin levels. Nitric Oxide 70-82 kininogen 1 Homo sapiens 122-132 10604529-1 1999 Bradykinin (BK) increased carotid blood flow (CBF) and jugular nitric oxide (NO) levels when administered into the common carotid artery of rabbits, and potentiated selectively, when infused together with histamine (HIST) or serotonin (5-HT), their effects on both CBF and jugular NO levels (but not vice versa). Nitric Oxide 63-75 kininogen 1 Homo sapiens 0-10 10500040-0 1999 Vasodilation to bradykinin is mediated by an ouabain-sensitive pathway as a compensatory mechanism for impaired nitric oxide availability in essential hypertensive patients. Nitric Oxide 112-124 kininogen 1 Homo sapiens 16-26 10444513-7 1999 It is concluded that endothelium-dependent vasodilation can be demonstrated with histamine and bradykinin in the fetoplacental vessels, and at least for bradykinin, this is partly mediated by release of nitric oxide. Nitric Oxide 203-215 kininogen 1 Homo sapiens 153-163 10096262-1 1999 OBJECTIVE: In arteries and veins smoking is associated with impaired nitric oxide-mediated relaxation to endothelium-dependent agonists such as bradykinin. Nitric Oxide 69-81 kininogen 1 Homo sapiens 144-154 9713849-0 1998 Nitric oxide and cyclic GMP attenuate sensitivity of the blood-tumor barrier permeability to bradykinin. Nitric Oxide 0-12 kininogen 1 Homo sapiens 93-103 9635158-1 1998 We have recently shown that isolated pulmonary resistance arteries of the fetal lamb have prostaglandin (PG) I2 based and nitric oxide (NO) based relaxing mechanisms, which are activated by oxygen (at neonatal levels) and bradykinin. Nitric Oxide 122-134 kininogen 1 Homo sapiens 222-232 9707267-5 1998 ACE inhibition of kininase II inhibits the breakdown of bradykinin, a direct stimulant of nitric oxide release from the intact endothelial cell. Nitric Oxide 90-102 kininogen 1 Homo sapiens 56-66 9688841-1 1998 Vasodilation by agents such as bradykinin and ATP is dependent on nitric oxide, the endothelium-dependent relaxing factor (EDRF). Nitric Oxide 66-78 kininogen 1 Homo sapiens 31-41 9547352-1 1998 In primary human umbilical vein endothelial cells (HUVECs), incubation with phorbol-12-myristate-13-acetate (PMA) enhanced basal and bradykinin-stimulated nitric oxide production. Nitric Oxide 155-167 kininogen 1 Homo sapiens 133-143 9717055-4 1998 Bradykinin is a vasodilator that increases the activity of constitutive nitric oxide. Nitric Oxide 72-84 kininogen 1 Homo sapiens 0-10 9717056-6 1998 Bradykinin is a very potent vasodilator that exerts its vasodilatory actions by causing endothelial release of nitric oxide, prostacyclin and/or endothelium-derived hyperpolarizing factor. Nitric Oxide 111-123 kininogen 1 Homo sapiens 0-10 9767830-4 1998 NO SYNTHESIS: Nitric oxide is synthesized from L-arginine by NO-synthetase whose activity is regulated by intracellular calcium concentration and modulated by pharmacological compounds such as acetylcholine, 5-hydroxytryptamine, bradykinin and ADP as well as the sheer forces produced by blood flow. Nitric Oxide 14-26 kininogen 1 Homo sapiens 229-239 17013240-5 1998 In clinical practice, ACE inhibitors may be preferred to angiotensin II receptor antagonists since the former, besides reducing angiotensin II synthesis, also lead to an accumulation of kinins (e.g. bradykinin), which have important cardio- and renal protective effects through liberation of prostacyclin and nitric oxide in endothelial cells and through stimulation of guanylate cyclase to form cyclic GMP. Nitric Oxide 309-321 kininogen 1 Homo sapiens 199-209 9564911-9 1998 Vascular relaxation in response to bradykinin (10[-9] to 10[-6] mol/L), which was found to induce endothelium-dependent vasodilation independent of nitric oxide production, was unaffected by magnesium removal (n=10). Nitric Oxide 148-160 kininogen 1 Homo sapiens 35-45 9597423-7 1998 Bradykinin-induced nitric oxide production is regulated by angiotensin converting enzyme located on the endothelial cell membrane; indeed, the enzyme not only activates angiotensin I into angiotensin II, but also inactivates bradykinin. Nitric Oxide 19-31 kininogen 1 Homo sapiens 0-10 9597423-7 1998 Bradykinin-induced nitric oxide production is regulated by angiotensin converting enzyme located on the endothelial cell membrane; indeed, the enzyme not only activates angiotensin I into angiotensin II, but also inactivates bradykinin. Nitric Oxide 19-31 kininogen 1 Homo sapiens 225-235 9597423-12 1998 Nitrates substitute in part for deficient endogenous nitric oxide, while angiotensin converting enzyme inhibitors increase the bradykinin induced nitric oxide and prostacyclin production. Nitric Oxide 146-158 kininogen 1 Homo sapiens 127-137 9523665-11 1998 The infusion of the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester increased the tone of the HCC tissues and significantly reduced (P < 0.01) the relaxation induced by BK (74%), Lys-BK (90%), Met-Lys-BK (87%) and acetylcholine (89%) without affecting those induced by GTN. Nitric Oxide 20-32 kininogen 1 Homo sapiens 195-197 9523665-11 1998 The infusion of the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester increased the tone of the HCC tissues and significantly reduced (P < 0.01) the relaxation induced by BK (74%), Lys-BK (90%), Met-Lys-BK (87%) and acetylcholine (89%) without affecting those induced by GTN. Nitric Oxide 20-32 kininogen 1 Homo sapiens 209-211 9475274-13 1998 In conclusion, bradykinin-induced relaxation of isolated porcine iliac arteries was mediated by endothelial bradykinin B2 receptors and mainly nitric oxide. Nitric Oxide 143-155 kininogen 1 Homo sapiens 15-25 9453327-1 1998 In the present study we tested the hypothesis whether an angiotensin AT2 receptor-mediated stimulation of the bradykinin (BK)/nitric oxide (NO) system can account for the effects of AT1 receptor antagonism on aortic cGMP described previously in SHRSP. Nitric Oxide 126-138 kininogen 1 Homo sapiens 110-120 9453327-1 1998 In the present study we tested the hypothesis whether an angiotensin AT2 receptor-mediated stimulation of the bradykinin (BK)/nitric oxide (NO) system can account for the effects of AT1 receptor antagonism on aortic cGMP described previously in SHRSP. Nitric Oxide 126-138 kininogen 1 Homo sapiens 122-124 9605596-8 1998 ACE inhibitors diminish transformation of angiotensin I (Ang I) into angiotensin II (Ang II) and prevent degradation of bradykinin [which stimulates nitric oxide (NO) and prostacyclin formation]. Nitric Oxide 149-161 kininogen 1 Homo sapiens 120-130 9208131-21 1997 These results show that BK induces endothelium-dependent relaxation in human small omental arteries via multiple mechanisms involving nitric oxide, cyclo-oxygenase derived prostanoid(s) and another factor (probably an endothelium-derived hyperpolarizing factor). Nitric Oxide 134-146 kininogen 1 Homo sapiens 24-26 9207629-0 1997 Bradykinin-induced vasodilation of human coronary arteries in vivo: role of nitric oxide and angiotensin-converting enzyme. Nitric Oxide 76-88 kininogen 1 Homo sapiens 0-10 9207629-1 1997 OBJECTIVES: The present study aimed to determine the role of nitric oxide (NO) and angiotensin-converting enzyme (ACE) in bradykinin (BK)-induced dilation of human coronary arteries in vivo. Nitric Oxide 61-73 kininogen 1 Homo sapiens 122-132 9207629-1 1997 OBJECTIVES: The present study aimed to determine the role of nitric oxide (NO) and angiotensin-converting enzyme (ACE) in bradykinin (BK)-induced dilation of human coronary arteries in vivo. Nitric Oxide 61-73 kininogen 1 Homo sapiens 134-136 9415011-0 1997 Bradykinin induced dilatation of human epicardial and resistance coronary arteries in vivo: effect of inhibition of nitric oxide synthesis. Nitric Oxide 116-128 kininogen 1 Homo sapiens 0-10 9415011-1 1997 OBJECTIVE: To clarify whether endothelium derived nitric oxide contributes to exogenous bradykinin induced dilatation of human epicardial and resistance coronary arteries in vivo. Nitric Oxide 50-62 kininogen 1 Homo sapiens 88-98 9415011-9 1997 CONCLUSIONS: Endothelium derived nitric oxide contributes to bradykinin induced dilatation of epicardial coronary arteries, but may be less important in coronary resistance vasodilatation. Nitric Oxide 33-45 kininogen 1 Homo sapiens 61-71 9235967-0 1997 Modulation of bradykinin receptor ligand binding affinity and its coupled G-proteins by nitric oxide. Nitric Oxide 88-100 kininogen 1 Homo sapiens 14-24 9138678-0 1997 Evidence that mechanisms dependent and independent of nitric oxide mediate endothelium-dependent relaxation to bradykinin in human small resistance-like coronary arteries. Nitric Oxide 54-66 kininogen 1 Homo sapiens 111-121 9124496-4 1997 Two agents that elicit EDNO production, bradykinin (BK) and carbamylcholine (Cch), increased J(H) when added to the peritubular capillary perfusate. Nitric Oxide 23-27 kininogen 1 Homo sapiens 40-50 9124496-4 1997 Two agents that elicit EDNO production, bradykinin (BK) and carbamylcholine (Cch), increased J(H) when added to the peritubular capillary perfusate. Nitric Oxide 23-27 kininogen 1 Homo sapiens 52-54 9392837-5 1997 These data suggest that vasodilator responses to T-kinin and bradykinin are mediated by kinin B2 receptor stimulated release of nitric oxide from the endothelium, but that the activation of kinin B1 receptors, the release of vasodilator prostaglandins, or the opening of K+ ATP channels are not involved in the response to T-kinin in the mesenteric vascular bed of the cat. Nitric Oxide 128-140 kininogen 1 Homo sapiens 61-71 9429844-6 1997 Bradykinin is a very potent vasodilator that exerts its vasodilatory actions by causing endothelial release of nitric oxide, prostacyclin and/or a hyperpolarising factor [endothelium-derived hyperpolarising factor (EDHF)]. Nitric Oxide 111-123 kininogen 1 Homo sapiens 0-10 9397288-10 1997 Beyond inhibiting the renin-angiotensin system, angiotensin-converting enzyme inhibitors diminish the inactivation of bradykinin, thus leading to an augmentation of nitric oxide release. Nitric Oxide 165-177 kininogen 1 Homo sapiens 118-128 8971090-4 1997 Endothelium-dependent relaxation by nitric oxide pathways stimulated after receptor activation (bradykinin and thrombin) was not different in vein rings from diabetic (n = 12) and nondiabetic patients (n = 12). Nitric Oxide 36-48 kininogen 1 Homo sapiens 96-106 8971427-2 1996 Angiotensin converting enzyme inhibitors have been suggested to act in part by potentiating the stimulatory effect of bradykinin on endothelial prostacyclin and/or nitric oxide (NO) formation. Nitric Oxide 164-176 kininogen 1 Homo sapiens 118-128 8987958-8 1996 CONCLUSION: This study provides evidence for an increase in bradykinin-mediated nitric oxide synthesis from the vascular endothelium of small arteries from the peripheral circulation of normotensive pregnant women and a relative reduction in women with preeclampsia. Nitric Oxide 80-92 kininogen 1 Homo sapiens 60-70 9115953-6 1996 Bradykinin is a direct stimulant of nitric oxide release from the intact endothelial cell. Nitric Oxide 36-48 kininogen 1 Homo sapiens 0-10 9048263-6 1996 In the hypercholesterolaemic patients compared with control subjects maximal forearm blood flow was significantly impaired after stimulation of endogenous nitric oxide synthesis by acetylcholine and bradykinin and during infusion of the nitric oxide donor sodium nitroprusside (acetylcholine: -19%, bradykinin: -29%, sodium nitroprusside: -24% versus control individuals; P < 0.05). Nitric Oxide 155-167 kininogen 1 Homo sapiens 199-209 8840871-10 1996 Suppression of ET-1 results from both removal of endogenous angiotensin II and accumulation of endogenous bradykinin/nitric oxide. Nitric Oxide 117-129 kininogen 1 Homo sapiens 106-116 9048263-6 1996 In the hypercholesterolaemic patients compared with control subjects maximal forearm blood flow was significantly impaired after stimulation of endogenous nitric oxide synthesis by acetylcholine and bradykinin and during infusion of the nitric oxide donor sodium nitroprusside (acetylcholine: -19%, bradykinin: -29%, sodium nitroprusside: -24% versus control individuals; P < 0.05). Nitric Oxide 237-249 kininogen 1 Homo sapiens 299-309 8883499-6 1996 Bradykinin-induced nitric oxide production is reduced by angiotensin-converting enzyme. Nitric Oxide 19-31 kininogen 1 Homo sapiens 0-10 8877579-3 1996 Bradykinin (BK: Gi-2 protein-independent), serotonin (5-HT: Gi-2 protein-dependent), or direct activation of the G(i-2)-protein by mastoparan increased the release of endothelium-derived nitric oxide (EDNO) from porcine arterial endothelial cells (EC). Nitric Oxide 187-199 kininogen 1 Homo sapiens 0-10 8877579-3 1996 Bradykinin (BK: Gi-2 protein-independent), serotonin (5-HT: Gi-2 protein-dependent), or direct activation of the G(i-2)-protein by mastoparan increased the release of endothelium-derived nitric oxide (EDNO) from porcine arterial endothelial cells (EC). Nitric Oxide 201-205 kininogen 1 Homo sapiens 0-10 8709736-0 1996 Randomised double-blind placebo-controlled study of the effect of inhibition of nitric oxide synthesis in bradykinin-induced asthma. Nitric Oxide 80-92 kininogen 1 Homo sapiens 106-116 8709736-1 1996 BACKGROUND: Bronchoconstriction induced by bradykinin is reduced by the release of nitric oxide (NO) in the airways of guinea pigs. Nitric Oxide 83-95 kininogen 1 Homo sapiens 43-53 8818341-2 1996 The effects of inhibitors of nitric oxide synthase and local anaesthetics were studied on changes in human nasal airway patency and albumin extravasation in response to bradykinin and histamine, in vivo. Nitric Oxide 29-41 kininogen 1 Homo sapiens 169-179 8707379-7 1996 We conclude that bradykinin relaxes these human resistance arteries in an endothelium-dependent but predominantly nitric oxide- and prostanoid-independent manner; relaxation likely depends on the action of an endothelium-derived hyperpolarizing vasodilator. Nitric Oxide 114-126 kininogen 1 Homo sapiens 17-27 8818341-18 1996 We conclude that the extravasation of plasma albumin caused by bradykinin and by histamine involves the generation of nitric oxide. Nitric Oxide 118-130 kininogen 1 Homo sapiens 63-73 8818341-19 1996 The nasal blockage induced by bradykinin involves nitric oxide generation but the nasal blockage induced by histamine does not. Nitric Oxide 50-62 kininogen 1 Homo sapiens 30-40 8964116-4 1996 Microvessels were incubated in the presence of agonists for nitric oxide production (acetylcholine and bradykinin), which caused dose-dependent increases in nitrite, a response that was blocked by NG-nitro-L-arginine methyl ester and receptor-specific antagonists (atropine and HOE 140, respectively). Nitric Oxide 60-72 kininogen 1 Homo sapiens 103-113 8856164-0 1996 Biosynthesis of endothelium-derived nitric oxide by bradykinin as endogenous precursor. Nitric Oxide 36-48 kininogen 1 Homo sapiens 52-62 8764214-3 1996 Nitric oxide synthase inhibitor (nitro-L-arginine methyl ester) caused a significant inhibition of bradykinin-induced glycoconjugate secretion, which was reversed by the addition of L-arginine. Nitric Oxide 0-12 kininogen 1 Homo sapiens 99-109 8856114-1 1996 Bradykinin causes vasodilatation by stimulating the production of vasodilator prostanoids and nitric oxide (NO). Nitric Oxide 94-106 kininogen 1 Homo sapiens 0-10 7659783-0 1995 A bradykinin antagonist inhibited nitric oxide generation and thromboxane biosynthesis in acute pancreatitis. Nitric Oxide 34-46 kininogen 1 Homo sapiens 2-12 8779918-0 1996 Flow- and bradykinin-induced nitric oxide production by endothelial cells is independent of membrane potential. Nitric Oxide 29-41 kininogen 1 Homo sapiens 10-20 8573025-3 1996 RESULTS: The vascular endothelial cell may produce nitric oxide, endothelins, prostaglandins, and renin-angiotension products in response to chemical stimuli such as acetylcholine and bradykinin, to changes in blood pressure and vessel wall stress, to changes in local oxygen levels, and to other local stimuli. Nitric Oxide 51-63 kininogen 1 Homo sapiens 184-194 9085350-7 1996 Nitric oxide production was induced by the action of different physical agents (shear stress, stretching) as well as various chemical substances agonists (bradykinin, acetylcholine, ATP). Nitric Oxide 0-12 kininogen 1 Homo sapiens 155-165 8865464-4 1996 Evidence for a role for bradykinin and nitric oxide in pancreatitis has been conflicting with some studies suggesting these agents might ameliorate pancreatic dysfunction by enhancing pancreatic blood flow and secretion in response to bradykinin-stimulated generation of nitric oxide from endothelium, while other studies suggest that nitric oxide potentiates pancreatic oxidative stress. Nitric Oxide 271-283 kininogen 1 Homo sapiens 235-245 8521563-1 1995 BACKGROUND: Bradykinin is a potent vasodilator that acts through B2 kinin receptors to stimulate the release of endothelium-derived nitric oxide, prostacyclin, and hyperpolarizing factor. Nitric Oxide 132-144 kininogen 1 Homo sapiens 12-22 7484881-7 1995 It is conceivable that these beneficial effects of chronic ACE inhibition are due, in part, to blockade of bradykinin degradation by the ACE and the increased endothelial synthesis of prostaglandins and/or the release of nitric oxide by enhanced tissue levels of bradykinin. Nitric Oxide 221-233 kininogen 1 Homo sapiens 263-273 8562468-8 1995 While ACE inhibitors inhibit activation of angiotensin I into angiotensin II and prevent the breakdown of bradykinin (which stimulates nitric oxide and prostacyclin formation), calcium antagonists inhibit the effects of vasoconstrictor hormones such as angiotensin II at the level of vascular smooth muscle by reducing calcium inflow and facilitating the vasodilator effects of nitric oxide. Nitric Oxide 135-147 kininogen 1 Homo sapiens 106-116 8846418-6 1995 The most likely is the generation of cyclic GMP within the ischemic myocardium following bradykinin-stimulated nitric oxide generation and release from endothelial cells. Nitric Oxide 111-123 kininogen 1 Homo sapiens 89-99 7890486-14 1995 ACE-inhibitors prevents the effects of Ang 1 and augment endothelium-dependent relaxation to bradykinin, which releases nitric oxide through B2 receptors. Nitric Oxide 120-132 kininogen 1 Homo sapiens 93-103 7768281-4 1995 Bradykinin induced contractions of the isolated human bronchus and umbilical artery and vein (the umbilical vessels were pretreated with indomethacin and L-nitro-arginine to inhibit prostaglandin and nitric oxide synthesis). Nitric Oxide 200-212 kininogen 1 Homo sapiens 0-10 8529790-8 1996 This is of interest, because in recent studies insulin has been suggested to elicit its actions on MBF and MGU via the accelerated release of endothelium-derived nitric oxide, the generation of which is also stimulated by BK in a concentration-dependent manner. Nitric Oxide 162-174 kininogen 1 Homo sapiens 222-224 8865464-4 1996 Evidence for a role for bradykinin and nitric oxide in pancreatitis has been conflicting with some studies suggesting these agents might ameliorate pancreatic dysfunction by enhancing pancreatic blood flow and secretion in response to bradykinin-stimulated generation of nitric oxide from endothelium, while other studies suggest that nitric oxide potentiates pancreatic oxidative stress. Nitric Oxide 271-283 kininogen 1 Homo sapiens 235-245 7558231-4 1995 The phospholipase C inhibitor U73122 (1 mumol/L) abolished bradykinin-induced, nitric oxide-mediated relaxation but did not inhibit either bradykinin-induced, EDHF-mediated relaxation or prostaglandin I2 production. Nitric Oxide 79-91 kininogen 1 Homo sapiens 59-69 7639622-9 1995 Furthermore, tracheal relaxation by, e.g., bradykinin or potassium chloride, is mediated by the release of nitric oxide. Nitric Oxide 107-119 kininogen 1 Homo sapiens 43-53 7659783-1 1995 The effect of bradykinin on nitric oxide generation and eicosanoid production in the early stage of an experimental model of acute necrotizing pancreatitis induced by sodium taurocholate has been evaluated. Nitric Oxide 28-40 kininogen 1 Homo sapiens 14-24 7659783-6 1995 Bradykinin seems to be involved in nitric oxide and thromboxane synthesis during the initial phases of acute necrohemorrhagic pancreatitis. Nitric Oxide 35-47 kininogen 1 Homo sapiens 0-10 8067439-7 1994 These results suggest that hindquarters vasodilator responses to bradykinin are mediated by activation of kinin B2 receptors and in part by the release of nitric oxide. Nitric Oxide 155-167 kininogen 1 Homo sapiens 65-75 7955144-5 1994 Pulmonary vasodilator responses under elevated-tone conditions were inhibited by N omega-nitro-L-arginine methyl ester, suggesting that des-Arg9-bradykinin stimulates the release of nitric oxide, whereas meclofenamate and U-37883A, a nonsulfonylurea ATP-sensitive K+ channel antagonist, did not alter vasodilator responses to the B1 receptor agonist. Nitric Oxide 182-194 kininogen 1 Homo sapiens 145-155 7955144-6 1994 These results suggest that vasoconstrictor responses to des-Arg9-bradykinin under low-tone conditions are mediated by the activation of kinin B1 receptors, the release of catecholamines within the lung, and the activation of alpha-adrenergic receptors, whereas vasodilator responses under elevated tone conditions are mediated by activation of B1 receptors and the release of nitric oxide from the endothelium. Nitric Oxide 376-388 kininogen 1 Homo sapiens 65-75 7620517-1 1994 Endothelium-dependent relaxations to bradykinin (BK) in U46619-contracted, indomethacin (INDO)-treated porcine coronary artery (PCA) rings are modestly attenuated by the nitric oxide (NO) synthase inhibitor, N omega-nitro-l-arginine methyl ester (L-NAME); whereas, when contracted with KCl, L-NAME abolishes BK relaxations. Nitric Oxide 170-182 kininogen 1 Homo sapiens 37-47 7620517-1 1994 Endothelium-dependent relaxations to bradykinin (BK) in U46619-contracted, indomethacin (INDO)-treated porcine coronary artery (PCA) rings are modestly attenuated by the nitric oxide (NO) synthase inhibitor, N omega-nitro-l-arginine methyl ester (L-NAME); whereas, when contracted with KCl, L-NAME abolishes BK relaxations. Nitric Oxide 170-182 kininogen 1 Homo sapiens 49-51 7620517-1 1994 Endothelium-dependent relaxations to bradykinin (BK) in U46619-contracted, indomethacin (INDO)-treated porcine coronary artery (PCA) rings are modestly attenuated by the nitric oxide (NO) synthase inhibitor, N omega-nitro-l-arginine methyl ester (L-NAME); whereas, when contracted with KCl, L-NAME abolishes BK relaxations. Nitric Oxide 170-182 kininogen 1 Homo sapiens 308-310 7833219-12 1994 The response to bradykinin, but not that to GTN, was attenuated by L-NMMA compared with noradrenaline (P < 0.05; n = 6), suggesting that bradykinin-induced vasodilatation in the forearm is mediated, at least in part, by stimulating release of nitric oxide. Nitric Oxide 246-258 kininogen 1 Homo sapiens 16-26 7833219-12 1994 The response to bradykinin, but not that to GTN, was attenuated by L-NMMA compared with noradrenaline (P < 0.05; n = 6), suggesting that bradykinin-induced vasodilatation in the forearm is mediated, at least in part, by stimulating release of nitric oxide. Nitric Oxide 246-258 kininogen 1 Homo sapiens 140-150 7867229-4 1994 Nitric oxide release occurs under basal conditions, in response to chemical stimuli (acetylcholine, bradykinin, thrombin, prostacyclin, serotonin, etc.) Nitric Oxide 0-12 kininogen 1 Homo sapiens 100-110 7835634-2 1994 The present study was undertaken to determine whether endothelial nitric oxide (NO) is involved in the endothelium-dependent vasodilation elicited by bradykinin (BK) in rings of newborn (1-7-day-old) piglet cerebral arteries precontracted with KCl (25 mM). Nitric Oxide 66-78 kininogen 1 Homo sapiens 150-160 7835634-2 1994 The present study was undertaken to determine whether endothelial nitric oxide (NO) is involved in the endothelium-dependent vasodilation elicited by bradykinin (BK) in rings of newborn (1-7-day-old) piglet cerebral arteries precontracted with KCl (25 mM). Nitric Oxide 66-78 kininogen 1 Homo sapiens 162-164 7531489-2 1994 Enhanced, superimposed EDNO release can be stimulated by various local and circulating factors, such as bradykinin, ATP, etc., but also most importantly by viscous drag-induced shear stress of the bloodstream acting on the endothelial lining. Nitric Oxide 23-27 kininogen 1 Homo sapiens 104-114 7515323-0 1994 Enhancement of cytosolic calcium, prostacyclin and nitric oxide by bradykinin and the ACE inhibitor ramiprilat in porcine brain capillary endothelial cells. Nitric Oxide 51-63 kininogen 1 Homo sapiens 67-77 8026018-10 1994 NG-Monomethyl-L-arginine, an inhibitor of nitric oxide synthesis, reduced the maximum forearm vasodilation induced by bradykinin to the same extent in patients and in healthy subjects (-29 +/- 8% versus -32 +/- 6% reduction in peak flow, P = .80), with similar maximum flows in response to bradykinin (9.2 +/- 4.0 versus 10.4 +/- 2.6 mL.min-1 x 100 mL-1, P = .35). Nitric Oxide 42-54 kininogen 1 Homo sapiens 118-128 8026018-11 1994 CONCLUSIONS: Hypercholesterolemic patients are capable of normal nitric oxide bioavailability in response to bradykinin. Nitric Oxide 65-77 kininogen 1 Homo sapiens 109-119 7517646-5 1994 The nitric oxide (NO) synthase inhibitors N omega-nitro-L-arginine benzyl ester and N omega-nitro-L-arginine reduced vasodilator responses to BK in a selective manner, indicating that responses to BK are mediated in part by the release of NO. Nitric Oxide 4-16 kininogen 1 Homo sapiens 142-144 7517646-5 1994 The nitric oxide (NO) synthase inhibitors N omega-nitro-L-arginine benzyl ester and N omega-nitro-L-arginine reduced vasodilator responses to BK in a selective manner, indicating that responses to BK are mediated in part by the release of NO. Nitric Oxide 4-16 kininogen 1 Homo sapiens 197-199 7514511-1 1994 The transient increase in [Ca2+]i in endothelial cells after stimulation with bradykinin can account for the initiation but not the sustained production of nitric oxide (NO). Nitric Oxide 156-168 kininogen 1 Homo sapiens 78-88 8206638-3 1994 Thus when contracted with KCl, bradykinin-induced relaxation of PCA rings is mediated solely by nitric oxide (NO), whereas when contracted with the thromboxane mimetic U46619, a small component of the relaxation is attributable to NO and a large component is attributable to a non-NO mechanism that is independent of cyclooxygenase activity. Nitric Oxide 96-108 kininogen 1 Homo sapiens 31-41 7515323-1 1994 We studied whether primary cultured porcine brain capillary endothelial cells (PBCEC) respond to bradykinin with an enhanced intracellular cytosolic calcium concentration [Ca2+]i with subsequent formation of nitric oxide (NO) and prostacyclin (PGI2). Nitric Oxide 208-220 kininogen 1 Homo sapiens 97-107 8012902-1 1994 To determine whether the ductus arteriosus can form endothelium-derived relaxing factor--nitric oxide, we used isolated ductal strips from near-term fetal lamb and examined their response to bradykinin (a nitric oxide stimulator), L-arginine (a nitric oxide precursor), and agents interfering with the synthesis (N omega-nitro-L-arginine) and action (methylene blue) of nitric oxide. Nitric Oxide 205-217 kininogen 1 Homo sapiens 191-201 8012902-1 1994 To determine whether the ductus arteriosus can form endothelium-derived relaxing factor--nitric oxide, we used isolated ductal strips from near-term fetal lamb and examined their response to bradykinin (a nitric oxide stimulator), L-arginine (a nitric oxide precursor), and agents interfering with the synthesis (N omega-nitro-L-arginine) and action (methylene blue) of nitric oxide. Nitric Oxide 205-217 kininogen 1 Homo sapiens 191-201 8012902-1 1994 To determine whether the ductus arteriosus can form endothelium-derived relaxing factor--nitric oxide, we used isolated ductal strips from near-term fetal lamb and examined their response to bradykinin (a nitric oxide stimulator), L-arginine (a nitric oxide precursor), and agents interfering with the synthesis (N omega-nitro-L-arginine) and action (methylene blue) of nitric oxide. Nitric Oxide 205-217 kininogen 1 Homo sapiens 191-201 8012902-4 1994 Pretreatment with nitric oxide inhibitors also prevented, in part (methylene blue, 1 microM) or in full (N omega-nitro-L-arginine, 100 microM), the relaxant effect of bradykinin. Nitric Oxide 18-30 kininogen 1 Homo sapiens 167-177 8258520-12 1993 CONCLUSIONS: Endothelium-derived nitric oxide released under basal conditions or stimulated by bradykinin significantly regulated flow to the porcine ophthalmic microcirculation. Nitric Oxide 33-45 kininogen 1 Homo sapiens 95-105 1330642-1 1992 The influence of an elevated level of cyclic AMP on the formation of nitric oxide was investigated in a neuronal cell line (108CC15; NG108-15), in which we had previously shown that nitric oxide mediates the activation of soluble guanylyl cyclase upon stimulation with the hormones bradykinin, endothelin, and serotonin. Nitric Oxide 182-194 kininogen 1 Homo sapiens 282-292 8344795-5 1993 However, all local anesthetics (10(-5)M) and bupivacaine (10(-5)-10(-6)M) reduced endothelium-dependent relaxations to bradykinin (10(-9)-10(-6)M), whereas the endothelium-independent relaxations to the nitric oxide-donor 3-morpholino-sydnonimine (SIN-1; 10(-9)-10(-5)M) were unaffected by local anesthetics. Nitric Oxide 203-215 kininogen 1 Homo sapiens 119-129 8344795-7 1993 CONCLUSION: These findings demonstrate that in porcine ciliary arteries, local anesthetics impair endothelial formation of nitric oxide from L-arginine after stimulation with bradykinin, which may contribute importantly to the reduction in blood flow to the eye during retrobulbar anesthesia. Nitric Oxide 123-135 kininogen 1 Homo sapiens 175-185 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. Nitric Oxide 28-40 kininogen 1 Homo sapiens 83-93 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. Nitric Oxide 28-40 kininogen 1 Homo sapiens 138-148 8388656-6 1993 The functional consequence of bradykinin degradation was demonstrated by the potentiating effect of ramiprilat on the generation of endothelium-derived relaxing factors nitric oxide and prostacyclin from endothelial cells. Nitric Oxide 169-181 kininogen 1 Homo sapiens 30-40 8357330-5 1993 Bradykinin is a potent activator of the L-arginine nitric oxide system (endothelium-derived relaxing factor). Nitric Oxide 51-63 kininogen 1 Homo sapiens 0-10 7512465-6 1993 Bradykinin activates endothelial bradykinin (B2) receptors, which results in the formation of nitric oxide and prostacyclin. Nitric Oxide 94-106 kininogen 1 Homo sapiens 0-10 7512465-6 1993 Bradykinin activates endothelial bradykinin (B2) receptors, which results in the formation of nitric oxide and prostacyclin. Nitric Oxide 94-106 kininogen 1 Homo sapiens 33-43 7512465-7 1993 Hence, ACE inhibitors not only prevent the formation of angiotensin II, but also increase the local levels of bradykinin and in turn nitric oxide and prostacyclin. Nitric Oxide 133-145 kininogen 1 Homo sapiens 110-120 7508046-3 1993 Bradykinin, which is rapidly degraded by ACE, stimulates the release of endothelium-derived vasodilator mediators, including nitric oxide, endothelium-derived hyperpolarizing factor, and prostacyclin. Nitric Oxide 125-137 kininogen 1 Homo sapiens 0-10 8123881-6 1993 BK interacts with multiple endogenous mesenteric vasodilator mediators, such as nitric oxide, prostacyclin, and neuropeptides. Nitric Oxide 80-92 kininogen 1 Homo sapiens 0-2 7510651-0 1993 A nitric oxide synthase inhibitor reduces desensitisation of bradykinin-induced activation of phospholipase C in sensory neurones. Nitric Oxide 2-14 kininogen 1 Homo sapiens 61-71 1467832-8 1992 Bradykinin and SIN 1 (a donor of nitric oxide) reduced contractions induced by prostaglandin F2 alpha in an additive fashion in the presence of nitro-L-arginine. Nitric Oxide 33-45 kininogen 1 Homo sapiens 0-10 1279283-1 1992 Using a chemiluminescence method in the present study, we measured nitric oxide and one-electron oxidation products of nitric oxide (NOX) released from porcine coronary artery segments in response to bradykinin, ADP, and the calcium ionophore A23187. Nitric Oxide 67-79 kininogen 1 Homo sapiens 200-210 1279283-1 1992 Using a chemiluminescence method in the present study, we measured nitric oxide and one-electron oxidation products of nitric oxide (NOX) released from porcine coronary artery segments in response to bradykinin, ADP, and the calcium ionophore A23187. Nitric Oxide 119-131 kininogen 1 Homo sapiens 200-210 1279283-1 1992 Using a chemiluminescence method in the present study, we measured nitric oxide and one-electron oxidation products of nitric oxide (NOX) released from porcine coronary artery segments in response to bradykinin, ADP, and the calcium ionophore A23187. Nitric Oxide 133-136 kininogen 1 Homo sapiens 200-210 1279283-4 1992 Bradykinin, ADP, and A23187 elicited vasorelaxation greater than that observed basally; A23187, but not bradykinin or ADP, caused additional release of NOX greater than that measured basally. Nitric Oxide 152-155 kininogen 1 Homo sapiens 0-10 1279283-6 1992 We compared the amount of nitric oxide released under basal conditions and after stimulation with bradykinin, ADP, and A23187 with the amount of authentic nitric oxide necessary to elicit a bioequivalent response. Nitric Oxide 26-38 kininogen 1 Homo sapiens 98-108 1607246-5 1992 The results show that in the human ophthalmic artery, nitric oxide is released under basal conditions and that its production can be markedly stimulated by bradykinin, acetylcholine, and particularly histamine, which cause profound vascular relaxation. Nitric Oxide 54-66 kininogen 1 Homo sapiens 156-166 1627761-2 1992 Pharmacologically, the renal vasodilation and, to some extent, the natriuresis produced by endothelium-dependent vasodilators such as acetylcholine and bradykinin are mediated by nitric oxide and also by prostaglandins. Nitric Oxide 179-191 kininogen 1 Homo sapiens 152-162 1282634-4 1992 In vitro studies demonstrate that the relaxations to bradykinin are mostly endothelium dependent and are mediated by nitric oxide, endothelium-derived hyperpolarizing factor, and/or vasodilator prostaglandins; however, these endothelium-derived relaxing factors do not always contribute simultaneously to the relaxations in every artery. Nitric Oxide 117-129 kininogen 1 Homo sapiens 53-63 1659406-0 1991 Bradykinin and ATP stimulate L-arginine uptake and nitric oxide release in vascular endothelial cells. Nitric Oxide 51-63 kininogen 1 Homo sapiens 0-10 1663586-6 1991 This endothelium-derived bradykinin can exert an autocrine function by stimulating endothelial B2-receptors with a subsequent increase in [Ca2+]i and nitric oxide formation. Nitric Oxide 150-162 kininogen 1 Homo sapiens 25-35 1655653-9 1991 These data indicate that cultured endothelial cells from different species are capable of producing and releasing bradykinin into the extracellular space in amounts that lead to a sustained stimulation of nitric oxide and prostacyclin formation, provided that bradykinin degradation is prevented by angiotensin converting enzyme inhibition. Nitric Oxide 205-217 kininogen 1 Homo sapiens 114-124 2032802-11 1991 Endothelium-derived nitric oxide is released both under basal conditions and after stimulation with acetylcholine and bradykinin. Nitric Oxide 20-32 kininogen 1 Homo sapiens 118-128 34580391-10 2021 Glucose provocation is known to cause insulin-induced vasodilation through the nitric oxide pathway, and this study indicates that this is facilitated through the interactions of the RAS (angiotensinogen) and kallikrein-kinin (kininogen-1) systems. Nitric Oxide 79-91 kininogen 1 Homo sapiens 227-238 1992790-10 1991 An endothelium-derived relaxing factor different from nitric oxide must mediate the relaxations to bradykinin and contribute to those evoked by serotonin. Nitric Oxide 54-66 kininogen 1 Homo sapiens 99-109 1719954-4 1991 The results indicate that Ca(2+)-calmodulin directly activates the endothelial nitric oxide synthase, thereby transducing agonist-induced increases in intracellular free Ca2+ concentration to nitric oxide formation from L-arginine, K(+)-induced depolarization of the endothelial cells markedly inhibited the sustained, but not initial phase of the intracellular Ca2+ response to bradykinin, indicating that K(+)-induced depolarization depresses the transmembrane Ca2+ influx. Nitric Oxide 79-91 kininogen 1 Homo sapiens 379-389 35612774-12 2022 Comorbid ADNC and mVBI appear to synergistically interact to selectively impair bradykinin-induced vasodilation in WM-penetrating arterioles, which may be related to reduced nitric oxide- and excess reactive oxygen species-mediated vascular endothelial dysfunction. Nitric Oxide 174-186 kininogen 1 Homo sapiens 80-90 3260776-7 1988 Our data provide convincing evidence that under basal, BK and ATP-stimulated conditions 1. endothelial cells release nitric oxide as free radical, 2. Nitric Oxide 117-129 kininogen 1 Homo sapiens 55-57 34291395-6 2021 Omeprazole decreased BK-induced phosphorylation of endothelial nitric oxide synthase (eNOS) at Ser1177 and tended to decrease BK-induced nitric oxide production. Nitric Oxide 137-149 kininogen 1 Homo sapiens 21-23 34291395-6 2021 Omeprazole decreased BK-induced phosphorylation of endothelial nitric oxide synthase (eNOS) at Ser1177 and tended to decrease BK-induced nitric oxide production. Nitric Oxide 137-149 kininogen 1 Homo sapiens 126-128 34074111-3 2021 Even though both drug groups block angiotensin II, ACE inhibitors typically reduce the degradation of bradykinin, which leads to the release of nitric oxide and prostaglandins with subsequent vasodilation. Nitric Oxide 144-156 kininogen 1 Homo sapiens 102-112 2889967-4 1987 It is suggested that the effect of bradykinin is mediated by the release of nitric oxide from the endothelial cells, and that nitric oxide release contributes to the non-adhesive properties of vascular endothelium. Nitric Oxide 76-88 kininogen 1 Homo sapiens 35-45