Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.11.18 (MAP)
 7,412 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The "effective" contribution of angiotensin II in blood pressure regulation was investigated in 6 patients on maintenance hemodialysis who were hypertensive at the time of the study (MAP 133 +/- 5 mmHg). Saralasin, a specific angiotensin II inhibitor, was infused at 0.5 and 2.5 microgram/kg/mn three hours before andone hour after hemodialysis. Before hemodialysis, a mean arterial pressure decrease of 13.2 to 19 p. 100 was obtained in 5 patients, arterial pressure being normalized in three of them. After hemodialysis, saralasin induced a normalization of arterial pressure in these 5 subjects. One patient, who was resistant to the saralasin infusion before and after the hemodialysis procedure, can be considered as purely volume-dependent. The renin-angiotensin system is probably one of the primary determinant of dialysis-resistant hypertension. However, a negative response to saralasin should encourage to control hypertension by more vigorous ultrafiltration during dialysis.
Arch Mal Coeur Vaiss 1978 Jul
PMID:[Arterial hypertension and maintenance hemodialysis: effects of specific inhibition of angiotensin II by saralasin acetate]. 10 Nov 76

We investigate the effect of a new angiotensin-converting enzyme inhibitor: Perindopril (IRIS) on regression of left ventricular hypertrophy (LVH), coronary blood flow and mechanical performance of isolated papillary muscle in renovascular hypertensive (Goldblatt 2 kidneys-1 clip) Sprague-Dawley male rats. Sham operated rats (G1) and half of hypertensive rats (G2) were studied after 8 weeks. The other half of 8 weeks long hypertensive rats (G3) were treated during 8 weeks with Perindopril in drinking water at a dosage adjusted to maintain blood pressure (BP) measured with tail cuff method under 140 mmHg. The study of each rat included 1) coronary blood flow and resistance measurements under resting conditions and after coronary dilation by carbochrome infusion (9 mg/kg) using left atrial injection of radioactive microspheres (method of Wicker and Tarazi) 2) the study of mechanical performance of the isolated papillary muscle 3) weight of left ventricle after separation of septum and free wall whose subendocardial and subepicardial layers were counted separately. Results (mean +/- SD): (table; see text) MAP: mean pressure. LV/BW: left ventricular mass (mg) per gram of body weight; CR (C): minimal coronary resistance after carbochrome (mmHg/ml/min/100 mg); DL/Dt: peak velocity of shortening at L max preload; Vrelax: peak velocity of relaxation; THR: time of half relaxation; p less than 0.05; p less than 0.01 compared to SHAM. In this model, hypertension induced a 50 p. 100 LVH whose regression was nearly complete after 8 weeks of treatment with Perindopril. Minimal coronary resistance after carbochrome were higher in hypertensive rats compared to sham and return to normal after regression of LVH.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1987 Jun
PMID:[Effects of perindopril on left ventricular hypertrophy, coronary reserve and mechanical properties of the papillary muscle of the rat with renovascular arterial hypertension]. 295 35

Deterioration of renal function may be elicited by converting enzyme inhibition (CEI) in patients with bilateral (BI) or solitary kidney (SK) renal artery stenosis, but the determinants of this complication are not clearly delimited. The effect of acute administration of captopril on arterial pressure, glomerular filtration rate (GFR) and effective renal plasma flow was assessed in 10 BI and 10 SK hypertensive patients with a mean GFR of 64 +/- 5 ml/min. CEI induced a decrease in MAP of 8 +/- 2 p. 100 and a fall in GFR of 25 +/- 8 p. 100; GFR fell by more than 20 p. 100 in 5/10 BI and 8/10 SK. Filtration fraction (FF) decreased by 16 +/- 5 p. 100. CEI-induced change in GFR was not related to the change in MAP, but was inversely correlated with pre-C FF; GFR always fell when FF was higher than 0.28. Surgical correction of the stenosis suppressed the C-induced decrease in GFR in 5 SK patients in whom it initially fell. In conclusion, basal FF, a probable index of intrarenal angiotensin II activity, rather than a fall in systemic blood pressure, is the main predictor of acute deterioration of renal function after converting enzyme inhibition.
Arch Mal Coeur Vaiss 1987 Jun
PMID:[Determinant factors in the acute functional deterioration caused by the inhibition of the conversion enzyme in reno-vascular arterial hypertension]. 311 87

Three groups of 11 male subjects with the same mean age were studied: normotensives (group I), patients with sustained essential hypertension (group II) and patients with borderline hypertension (group III). M-mode echocardiography provided a measure of aortic root systolic diameter (D) and left ventricular mass index (LVMi, g/m2). We have used a 4 MHz pulsed doppler velocity meter with spectral analysis to measure instantaneous ascending aortic blood velocity. Measurements values were averaged during 10 s and included: stroke volume (SV, cm3 = integrated velocity over one cardiac cycle.aortic cross sectional area (3.14D2/4)), cardiac output (CO, cm3 = SV.heart rate), systemic vascular resistance (SVR, mmHg/cm3.s-1 = MAP/co) and maximal aortic acceleration (MA, cm/s2). (Table: see text). Stroke volume and cardiac output were similar in three groups. SVR was higher in group II than in group I. The myocardial contractility appreciated from the maximal aortic acceleration (Bennett et al, Cardiovasc Res 1984; 18: 632-8) was increased in patients with borderline hypertension and remained within the normal range in patients with sustained essential hypertension despite and increase in cardiac mass.
Arch Mal Coeur Vaiss 1988 Jun
PMID:[Non-invasive measurement by Doppler pulse of cardiac output and maximal aortic acceleration in essential arterial hypertension]. 314 28

Whether the decrease in large artery compliance, observed in hypertensive patients (HT), is due to an increase in distending pressure or to intrinsic alterations of the vascular wall remains much debated. We determined the diameter-pressure curve of the common carotid artery over the systolic-diastolic range, then derived the compliance-pressure curve, in order to compare arterial compliance in normotensive subject (NT) and in HT, for a common level of distending blood pressure: 100 mmHg (isobaric compliance). Fourteen NT and 15 never treated essential HT were included in the study. The diameter-pressure curve of the common carotid artery was determined non-invasively by simultaneously and continuously recording the systolic-diastolic changes in internal diameter (using a high resolution echotracking system) and pressure waveform (using high fidelity applanation tonometry on the contralateral artery) over 4-6 cardiac cycles. The level of MAP of the carotid pressure waveform was determined electronically and set equal to mean brachial pressure. Compliance-pressure curve was then derived from the pressure-diameter curve in order to determine compliance (C) for any given level of blood pressure, particularly MAP (CMAP) and 100 mmHg (C100). Despite the considerable differences in blood pressure, the compliance-pressure curve of HT was not different from that of NT. CMAP decreased with aging (p < 0.001) and MAP (p < 0.001). According to age, CMAP was reduced in HT as compared to NT (84 +/- 49 vs 116 +/- 52 mm2.mmHg.10(-3) p < 0.01). C100 decreased with aging (p < 0.05) but not with MAP. According to age, C100 was not reduced in hypertensives.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1994 Aug
PMID:[Arterial compliance is not diminished in hypertensive patients when compared at the same level of blood pressure]. 775 61

Twenty-five normotensive men without any cardiac or arterial pathology, aged 22 to 68 years, 12 less than 45 year old, 13 over 45 years, underwent cardiac catheterisation and angiography. The following parameters were calculated: 1) a global index of arterial function (Ea) and its determining factors (Ea = LVESP/SV where LEVSP = left ventricular end systolic pressure and SV = left ventricular stroke volume); Ea = (HR x SVR) + Ea' where HR = heart rate, SVR = total systemic vascular resistance and Ea' = (LVESP - MAP/SV) (MAP = mean arterial pressure); 2) an index of global left ventricular pump function: ELV (ELV = LVESP/LVESV, where LVEDV = left ventricular end systolic volume; 3) an index of LV-arterial coupling: the Ea/ELV ratio. With aging, both Ea (by increase in SVR) and Ea' and ELV increased significantly. Ea/ELV (inverse of the ejection fraction-1) increased with age but ELV less than Ea. Ea/ELV was significantly higher in patients over 45 years of age but the correlation between ejection fraction and age was not statistically significant (p = 0.10). These results suggest that with aging, the improvement in LV pump function approximately corresponds to the degradation in arterial transport function: the left ventricular-arterial coupling as assessed by the Ea/ELV ratio (and therefore the ejection fraction) is maintained in the majority of cases.
Arch Mal Coeur Vaiss 1993 Aug
PMID:[Effects of aging on left ventricle-arterial coupling in man]. 812 7

The influence of nonspecific blockade of endothelin receptors by bosentan (30 mg/kg per day, gavage) was assessed on hypertension induced by infusion of angiotensin II (AngII 200 ng/kg/min sc for 10 days) in rats. Tail-cuff pressure was measured before and every second day of AngII-infusion period. At the end of experiments, mean arterial pressure (MAP, mmHg), cardiac output (CO ml/min/kg body weight) and renal blood flow (RBF ml/min/g kidney weight) were determined (microspheres technique) in conscious rats, and total peripheral and renal vascular resistances were calculated (TPR = MAP/CO and RVR = MAP/RBF). [table: see text] Tail-cuff pressure increased from 126 +/- 4 to 164 +/- 8 mmHg in rats infused with AngII alone whereas it did not change (basal: 132 +/- 3 and final: 135 +/- 3 mmHg: p = NS) when bosentan was coadministered with AngII. At the end of study in conscious rats, the AngII-induced rise in MAP was accompanied by a reduction in CO and RBF and a marked increased in TPR and RVR. In AngII-perfused rats, CO, RBF, TPR and RVR were restored by bosentan to values observed in untreated rats. These results indicate that blockade of endothelin A and B receptors by bosentan prevents the development of AngII-induced hypertension through attenuation of the effect of AngII on vascular tone and suggest that endothelin is an important mediator of the vasoconstrictor action of angiotensin II in rats.
Arch Mal Coeur Vaiss 1997 Aug
PMID:[Bosentan attenuates the hypertensive effect of angiotensin II in rats]. 940 19

Hypertensive pregnant rats with inhibition of NO synthase are frequently considered as model of pre-eclampsia with proteinuria, hypertension and elevated endothelin (ET-1) blood levels. We describe here the cardiovascular in vivo effects of ET-1 in this rat model since ET-1 and NO are both important vasoactive mediators in uteroplacental circulation. From day 13 of gestation 2 groups of Wistar female rats were fed control (C) or nitroarginine enriched diet (0.063%, Treated: T). On gestational day 20 mean arterial pressure (MAP, mmHg) was measured via a carotid catheter in pentobarbital (60 mg/kg) anesthetized rats. After chronic NO synthase inhibition hypertension develops; MAP on day 20: 158 +/- 2.2 in T and 113 +/- 2.2 in C, p < 0.001. ET-1 bolus injection (0.1 nmol/kg) is rapidly followed by a decrease in blood pressure significantly more important in T: -46 +/- 5.1 than in C: -30 +/- 2.2. In vivo depressor effect is blocked by the specific antagonist BQ-788. After inhibition of cycloxygenase with acetylsalicylic acid (27 mumol/kg, 30 min before) the hypotension is not modified. Since NO and PGI2 productions are not expected in our conditions, vasodepressor effect can be explained by an endothelial hyperpolarazing factor (EDHF). In conclusion in vivo ET-1 hypotensive effects in pregnant rats are mediated by ETB receptors and more pronounced in hypertensive NO-deprived animals.
Arch Mal Coeur Vaiss 1998 Aug
PMID:[Hypotensive effect of endothelin-1 in a rat model of pre-eclampsia]. 974 58

Angiotensin II (Ang II) is involved in hypertension-related arterial wall hypertrophy [1]. Regulation of AT II transduction pathway in vascular smooth muscle cells (VSMC) may involve cytoskeleton and extracellular matrix (ECM) [2]. We assessed the role of components of ECM on Cai2+ increase induced by Ang II in Wistar-Kyoto (WKY) and Spontaneously Hypertensive Rats (SHR) aortic VSMC. The effect of Ang II (1 mumol) on Ca2+ mobilization was studied in cultured VSMC isolated from the aorta of 6-wk old WKY (MAP (m +/- SE) = 98 +/- 4 mmHg) and SHR (136 +/- 5 mmHg; p < 0.05), using fluorescent imaging microscopy (Fura-2 AM). Cai2+ release from internal stores and Ca2+ influx were assessed in the absence and upon reintroduction of external Ca2+ respectively. Cells were cultured on uncoated glass coverslips (control) or coated with either collagen I (10 micrograms/mL), collagen IV (7 micrograms/mL), vitronectin (0.1 microgram/mL), fibronectin (3 micrograms/mL) and extracellular matrix extract (matrigel, 1/10) and studied at confluence. Paxillin was located in cells by indirect immunofluorescence micrography. Results are expressed in % of Control. Statistical significance (p < 0.05) was assessed with Student's t-test for unpaired data. The effects on Ang II-induced Ca2+ mobilization of growing cells on ECM are in Table. Paxillin in Control cells appeared as dots at the cell boundaries. Density increased in cells grown on collagen I with a diffuse distribution in the WKY cells. On matrigel, paxillin was located in a belt-like fashion at the periphery of the cell. These effects were not linked to differences in cell cycle (flux cytometry).
Arch Mal Coeur Vaiss
PMID:[Role of extracellular matrix in angiotensin II signalling in aortic smooth muscle cells: relationship with arterial hypertension]. 1236 72

Signal transduction processes activated by Toll-like receptors (TLRs) include the important transcription factor NF-kappaB and 2 MAP kinases, p38 and Jun N-terminal kinase. These signals ultimately give rise to increased expression of a multitude of pro-inflammatory proteins. Receptor-proximal proteins involved in signalling by all TLRs include the adapter MyD88, 3 IRAKs (IRAK-4, IRAK and IRAK-2), Tollip, Traf-6 and TAK-1. Differences between signals generated by TLRs are emerging, with both TLR4 and TLR2 signalling requiring an additional adapter termed MyD88-adapter-like (Mal; also known as TIRAP). MyD88 and Mal both have a homologous Toll/IL-1 receptor (TIR) domain although they differ in their N-termini, with MyD88 possessing a death domain. In addition, structural models reveal marked differences in surface charges which, when taken with surface charge differences between TLR2 and TLR4 TIR domains, may indicate that TLR4 but not TLR2 recruits Mal directly. Another difference is that Mal can become phosphorylated. Future studies on Mal will reveal specificities in signal transduction by different TLRs, which may ultimately provide molecular explanations for specificities in the innate immune response to infection.
 ...
PMID:Mal and MyD88: adapter proteins involved in signal transduction by Toll-like receptors. 1269 20


1 2 Next >>