Angiotensin II and phorbol ester enhance isoproterenol- and vasoactive intestinal peptide (VIP)-induced cyclic AMP accumulation in vascular smooth muscle cells

Nabika, Toru; Nara, Yasuo; Yamori, Yukio; Lovenberg, Walter; Endo, Jiro

doi:10.1016/0006-291x(85)91765-6

Cited by 97 publications

(26 citation statements)

References 12 publications

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“…This can be seen for the studies on pinealocytes [83 -851, ROS 17/23 osteosarcoma cells [86] and vascular smooth muscle cells [87] where elevations of intracellular cyclic AMP concentrations are markedly transient in nature, indicating either the action of cyclic AMP phosphodiesterase activity or extrusion of cyclic AMP from the cell. Thus, whilst the marked potentiation of ligand-stimulated cyclic AMP accumulation may reflect enhanced adenylate cyclase activity, it is equally likely to be due to inhibition of either phosphodiesterase activity or extrusion: indeed, more than one action may well be occurring.…”

Section: Cellular Systems Used To Investigate Of Adenylate Cyclase Acmentioning

confidence: 87%

‘Crosstalk’: a pivotal role for protein kinase C in modulating relationships between signal transduction pathways

Houslay

1991

European Journal of Biochemistry

328

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Over the past 20 years we have seen a phenomenal increase in our understanding ofthe diversity and the molecular mechanism of action of signal transduction systems. Now we are faced with a cell being provided with a myriad of cell surface receptors, each connected to particular signal transduction systems. The very complexity of such systems, together with the need of the cell to monitor and respond to a variety of external stimuli, poses the question as to what overall controls are placed upon these various transduction mechanisms and how they might relate to each other. At one extreme, we can envisage that pathways might be isolated completely from each other and thus function in an an apparent 'vacuum'. On the other hand, we can envisage 'cross-talk' between the various pathways linking each into an adaptable network array. Such a network, linking distinct signalling systems, would offer the cell a sophisticated ability to sense multiple environmental signals impinging upon it, thus providing a means of adapting or regulating its response to a particular range of effectors. In this way the cell might respond to the relative concentrations of various signals, taking into account the particular point in time when it first experienced a specific signal, together with the absolute length of time it was exposed to it. Such parameters having markedly different effects on cellular behaviour. Thus one might envisage that both the 'quantity' and the 'quality' of information flowing through any particular signal transduction system might be altered by the functioning of other transduction systems which were linked to form such an interactive network. A cell controlled in such a fashion could be regarded as being capable of 'learning', Correspondence to

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Section: Cellular Systems Used To Investigate Of Adenylate Cyclase Acmentioning

confidence: 87%

‘Crosstalk’: a pivotal role for protein kinase C in modulating relationships between signal transduction pathways

Houslay

1991

European Journal of Biochemistry

328

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“…It has been shown that PMA, as well as inositol phosholipidturnover-activating hormones, potentiate the cAMP accumulation induced by adenylate cyclase activators (6,(28)(29)(30). Thus, the synergism of forskolin and PMA may be due either to potentiation by PMA of the forskolin-induced cAMP synthesis or to simultaneous phosphorylation of cytoskeletal proteins by cAMP-dependent protein kinases and protein kinase C. The polymorphous response pattern of adult HAECs may be due either to differences in cAMP metabolism and protein phosphorylation systems or to differences in the cytoskeleton organization of the large, multinuclear ECs.…”

Section: Resultsmentioning

confidence: 99%

Morphological alterations in endothelial cells from human aorta and umbilical vein induced by forskolin and phorbol 12-myristate 13-acetate: a synergistic action of adenylate cyclase and protein kinase C activators.

Antonov¹,

Lukashev²,

Romanov³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

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The morphological effects on human endothelial cells of phorbol 12-myristate 13-acetate (PMA) and of agents that increase intracellular cAMP concentration were studied. The adenylate cyclase activator forskolin (10 IAM), the cyclic nucleotide phosphodiesterase inhibitor methylisobutylxanthine (100 ,uM), dibutyryl-cAMP (10 IAM), histamine (10 IAM), and PMA (0.1 ,LM) significantly altered the morphology of human aortic and umbilical vein endothelial cells in primary cultures. These effects reached a maximum 40-80 min after the effector addition and became negligible 30-60 min after its removal. PMA and forskolin were strongly synergistic in altering endothelial cell morphology. All the effects of cAMPelevating compounds and ofPMA were abolished completely by 1 ,uM colchicine. In explants taken from human adult or child aortas, forskolin and PMA produced alterations in endothelial morphology qualitatively identical to those observed in endothelial cell cultures. Endothelium in these preparations closely resembled that found in zones of expected altered hemodynamic stresses of human aorta. Our data suggest that the morphology of endothelium in vivo may be regulated by separate or synergistic action of hormone-dependent adenylate cyclase and of inositol phospholipid turnover systems and might be important for maintenance of endothelial monolayer integrity under normal physiological and pathological conditions. MATERIALS AND METHODSMedium 199 (Earle salts), fetal calf serum, Dulbecco's phosphate-buffered saline (PBS), L-glutamine, penicillin, streptomycin, and sodium pyruvate were from GIBCO. Dispase (neutral protease from Bacillus polymixa) was from Boehringer Mannheim. Phorbol 12-myristate 13-acetate (PMA), 4a-phorbol 12,13-didecanoate, histamine, 1-methyl-3-isobutylxanthine, N6,02-dibutyryl-cAMP (Bt2cAMP), colchicine, bovine serum albumin (BSA, essentially fatty acid free) were supplied by Sigma. Forskolin was from Calbiochem. Drugs were dissolved in dimethylsulfoxide or ethanol (Merck) and stored as stock solutions in aliquots at -80°C. Prior to use the aliquots were diluted with medium 199 and 0.5% BSA or with growth medium [medium 199 supplemented with 25 mM Hepes, 2 mM L-glutamine, 1 mM pyruvate, penicillin at 100 units/ml, streptomycin at 100 ,ug/ml, 10% (vol/vol) fetal calf serum] and sterilized by filtration through 0.22-,um filters (Nalgene).Primary cultures of human umbilical vein endothelial cells (HUVECs) and human aortic endothelial cells (HAECs) were obtained as described (15,16), with minor modificationdispase was used instead of collagenase. Seeding density was 5-8 X 104 cells per cm2. Only confluent (7-9 days after seeding) cultures were used for experiments. The main characteristics of these cultures have been reported (16). For morphometry, cultures were stained with silver nitrate (17) and photographed. Cell shape was analyzed using a MOP-3 digitizer (Reichert, Jung, Vienna) and described in terms of shape index (SI), where SI = 4r x area/(perimeter)2. All the experiments were performe...

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“…15,33,34 ACE inhibitors may generate bronchoactive mediators, such as prostaglandins, 15 and then may decrease the bronchodilator effects of vasoactive intestinal peptide or ␤-agonist by preventing the accumulation of cAMP in smooth muscle. 35 On the other hand, bradykinin plays an important role in the cardiovascular system, affecting blood pressure regulation, cell proliferation, and matrix synthesis by fibroblasts. 15,18 By coupling to G proteins, the bradykinin B 2 receptor triggers the activation of phospholipase C and/or phospholipase A 2 that accompanies increased intracellular levels of Ca 2ϩ , NO, cGMP, and/or cAMP.…”

Section: Discussionmentioning

confidence: 99%

Bradykinin B ₂ Receptor Gene Polymorphism Is Associated With Angiotensin-Converting Enzyme Inhibitor–Related Cough

et al. 2000

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Abstract-The appearance of cough in association with angiotensin-converting enzyme (ACE) inhibitors is thought to be related to bradykinin, and it has been speculated that the elicitation of adverse effects is genetically predetermined. Several polymorphisms of the human bradykinin B 2 receptor gene may be involved in ACE inhibitor-related cough. To investigate this possibility, we identified the Ϫ58 thymine (T)/cytosine (C) polymorphism in subjects with ACE inhibitor-related cough. We classified the study population into 4 groups: subjects with and without cough that were treated with ACE inhibitors (nϭ30/30), nontreated essential hypertensive subjects (nϭ100), and normotensive subjects (nϭ100). The Ϫ58T/C was genotyped by the polymerase chain reaction single-strand conformation polymorphism method. The frequencies of the CC genotype and C allele of Ϫ58T/C were significantly higher in the nontreated hypertensive subjects than in the normotensive subjects. Conversely, the frequencies of the TT genotype and T allele were significantly higher in the subjects with cough than in the subjects without cough. These tendencies were more pronounced in females. Among the promoter assays of the human bradykinin B 2 receptor, Ϫ58T was found to have a higher transcription rate than that of Ϫ58C. This finding seems to suggest that the transcriptional activity of promoter might be involved in the appearance of ACE inhibitor-related cough. A genetic variant of the bradykinin receptor is involved in the elicitation of ACE inhibitor-related cough. It may be possible to predict the side effects of ACE inhibitors in advance. Key Words: bradykinin Ⅲ genes Ⅲ polymorphism Ⅲ promoter A ngiotensin-converting enzyme (ACE) inhibitors have been widely used in therapy for hypertension, congestive heart failure, and myocardial infarction, and several large clinical trials have confirmed that ACE inhibitors reduce mortality and morbidity in patients with congestive heart failure. [1][2][3][4][5] Several studies also suggest that ACE inhibitors are efficient in left ventricular remodeling after acute myocardial infarction and congestive heart failure. 6,7 The ability of ACE inhibitors to decrease angiotensin II production and increase kinin activity has been considered to be critically important. Reduced formation of angiotensin II seems to play a major role in the antihypertensive action of ACE inhibitors, but increased kinin levels have also been proposed to contribute to other beneficial effects of ACE inhibitors, including cardioprotection. However, ACE inhibitors also have adverse effects, the most common of which are cough and angioedema. ACE inhibitor-related cough is a side effect in Ϸ10% of treated patients, 8 -10 and in some instances, an unexplained persistent cough limits the use of these drugs. Women are more likely to have this side effect, which may occur at any time from a few days to several months after the initiation of treatment. Why ACE inhibitors cause coughing is not completely understood. Accumulation of kinins has bee...

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Angiotensin II and phorbol ester enhance isoproterenol- and vasoactive intestinal peptide (VIP)-induced cyclic AMP accumulation in vascular smooth muscle cells

Cited by 97 publications

References 12 publications

‘Crosstalk’: a pivotal role for protein kinase C in modulating relationships between signal transduction pathways

‘Crosstalk’: a pivotal role for protein kinase C in modulating relationships between signal transduction pathways

Morphological alterations in endothelial cells from human aorta and umbilical vein induced by forskolin and phorbol 12-myristate 13-acetate: a synergistic action of adenylate cyclase and protein kinase C activators.

Bradykinin B ₂ Receptor Gene Polymorphism Is Associated With Angiotensin-Converting Enzyme Inhibitor–Related Cough

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Angiotensin II and phorbol ester enhance isoproterenol- and vasoactive intestinal peptide (VIP)-induced cyclic AMP accumulation in vascular smooth muscle cells

Cited by 97 publications

References 12 publications

‘Crosstalk’: a pivotal role for protein kinase C in modulating relationships between signal transduction pathways

‘Crosstalk’: a pivotal role for protein kinase C in modulating relationships between signal transduction pathways

Morphological alterations in endothelial cells from human aorta and umbilical vein induced by forskolin and phorbol 12-myristate 13-acetate: a synergistic action of adenylate cyclase and protein kinase C activators.

Bradykinin B 2 Receptor Gene Polymorphism Is Associated With Angiotensin-Converting Enzyme Inhibitor–Related Cough

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Bradykinin B ₂ Receptor Gene Polymorphism Is Associated With Angiotensin-Converting Enzyme Inhibitor–Related Cough