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M Safar

Publications and source records attributed to M Safar.

At least 55 records · Page 3Linked to original sources
PubMed2000

Extracellular signal-regulated kinase pathway is involved in basic fibroblast growth factor effect on angiotensin II-induced Ca(2+) transient in vascular smooth muscle cell from Wistar-Kyoto and spontaneously hypertensive rats.

We studied the effect of basic fibroblast growth factor (b-FGF) on different Ca(2+) mechanisms elicited by angiotensin II (Ang II) in normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). Intracellular Ca(2+) (Ca(2+)(i)) variations were studied in cultured vascular smooth muscle cells (VSMCs) isolated from the aorta of 5- to 6-week-old WKY rats and SHR. Ca(2+)(i) was assessed in Fura-2-loaded cells with fluorescent imaging microscopy. Ang II subtype 1 receptor activation by Ang II (1 micromol/L) induced a transient increase in Ca(2+)(i) that was partially attenuated by genistein, a tyrosine kinase inhibitor. Pretreatment of VSMCs with b-FGF for 24 hours markedly stimulated the Ang II-induced Ca(2+)(i) release from the internal stores in WKY rats, whereas it was without effect in SHR. This was not consequent to a change in the affinity of Ang II subtype 1 receptors or an increase in their density. Inhibition of mitogen-activated protein kinase with PD 98059 reduced this stimulatory effect of the cytokine in the WKY rats. On the other hand, b-FGF stimulated the Ang II-induced Ca(2+) influx in both strains. Similar results were observed when Ca(2+) influx was induced with thapsigargin. Genistein and PD 98059 abolished the effect of b-FGF. These results show for the first time that b-FGF regulates Ca(2+) mechanisms induced by Ang II and that this regulation is different in SHR than in normotensive control animals. The extracellular signal-regulated kinase cascade is implicated in this cross-regulation with G protein-signaling pathway at 2 levels and possibly more: 1 at the tyrosine kinases and the other downstream of the extracellular signal-regulated kinase family. These results may prove useful in understanding the interaction between these 2 pathways and their implication in genetic hypertension.

Angiotensin II↗
PubMed2000

[Are the 1999 World Health Organization-International Society of Hypertension recommendations applicable to clinical practice?].

UNLABELLED: The aim of the 1999 WHO-ISH guidelines is to help the physicians in the management of hypertensive patients. The institution of antihypertensive treatment represents an important stage of this management sometimes at the detriment of lifestyle measures (non pharmacological treatments). OBJECTIVES: To evaluate if the 1999 WHO-ISH guidelines concerning the initiation of antihypertensive treatment are applied in a hypertension clinic. METHODS: Seventy hypertensive subjects never treated by antihypertensive drugs, aged 51 +/- 13 years, managed in daily hospitalization, were included in the study. According to their level of cardiovascular risk, we evaluated the concordance between the 1999 WHO-ISH guidelines and the clinical practice in term of institution of treatment. RESULTS: A concordance of 70% between the 1999 WHO-ISH guidelines and the clinical practice was observed (50/70 subjects) and a discordance in 30% of cases (20/70). Among the discordant subjects, the treatment was instituted in 65% of cases although it was not recommended. In contrast, in the remaining 35% of cases, lifestyle measures have been proposed although an antihypertensive treatment was recommended. The principal determinants of the discordance were the grade 2 of hypertension, the presence of 1 or 2 risk factors and an enhanced cardiovascular risk (> or = 3 risk factors). Neither age, nor gender were an explicative parameter of the observed discordance. CONCLUSIONS: The 1999 WHO-ISH guidelines concerning the initiation of antihypertensive treatment are more often applied in clinical practice. However, in some cases of grade 2 hypertension drug treatment is more often prescribed than recommended by guidelines, and not enough in the presence of numerous cardiovascular risk factors.

Age Factors↗
PubMed2000

[Hypertension and pulse pressure].

Pulse pressure is an independent cardiovascular risk factor, mainly for myocardial infarction. The predictive value of pulse pressure is observed not only in hypertensive subjects above 50 years but also in patients with congestive heart failure, myocardial dysfunction and recurrent myocardial infarction. Treated hypertensive subjects are also at risk since, in many cases, diastolic blood pressure is normalized whereas systolic blood pressure remains elevated, thus leading to the picture of isolated systolic hypertension despite antihypertensive treatment.

Aged↗
PubMed2000

[Hypertension and obesity].

Hypertension is often associated with corpulence, an increased total and abdominal fatty mass. The fact of being corpulent exposes to the risk of error of measurement of the blood pressure which may be overestimated by 10 to 16 mmHg and lead to the unnecessary prescription of antihypertensive drugs. In order to analyse the nature of the corpulence, it is useful to define the condition as an increase in fatty and/or lean body mass. It is also useful to quantify the distribution of body fat. Hypertensive patients of increased corpulence, obese (BMI > 30) with an abdominal distribution of adipose tissue, have an increased risk of cardiovascular morbidity-mortality, especially from coronary artery disease: their cardiovascular risk factors consist not only of hypertension and corpulence, but also of metabolic abnormalities and the haemodynamic consequences of corpulence, that is to say diabetes, hypertriglyceridaemia, hypercholesterolaemia, left ventricular hypertrophy and increased glomerular filtration. In hypertension with increased corpulence, the nutritional objective is to decrease the corpulence, decrease the fatty mass without reducing the lean mass. Therefore, it is important to proceed by a progressive, even small, loss of weight with a realistic target because loss of weight is beneficial for the hypertension and its complications (cardiovascular and renal), all other risk factors and for cardiovascular mortality.

Blood Pressure↗
PubMed2000

Norepinephrine kinetics in the rat with tail-suspension-induced central hypervolemia, as a model of cardio-vascular deconditioning.

Tail-suspension (TS) in the rat represents an interesting experimental condition to mimic, on Earth, the microgravity-induced cardiovascular deconditioning although the rat's profile of response is partially different from human's. To investigate underlying pathophysiological mechanisms, we have speculated on a decreased activity of the sympathetic system, (sigma S) triggered by the increase of the central venous pressure (CVP) induced by TS. Thus a decreased activity of the sigma S could account, at least partly, for the deconditioning of the cardiovascular system. The sympathetic activity (sigma A) was evaluated through measurement of the norepinephrine (NE) kinetics in rats that were tail-suspended for either 6, 24 or 48 hours. Neither NE spillover rate nor metabolic clearance rate were changed during TS, as compared to control. Thus, TS for a short period of time in the rat is unlikely to trigger a decrease of the sigma A.

Animals↗
PubMed1999

[Homocysteine and cardiovascular disease: what is the connection?].

HYPERHOMOCYSTEINEMIA: There are experimental data arguing for a role of homocysteine in several processes involved in atherosclerosis. Multiple retrospective and prospective studies performed in populations with high cardiovascular risk have shown that high homocysteine levels are associated with increased risk of coronary artery disease, stroke and peripheral vascular disease. In populations free of cardiovascular disease, prospective studies have demonstrated that homocysteine is a risk factor for cardiovascular disease while in other publications, no such prognostic value is found for high serum levels of homocysteine. PERSPECTIVE AND PREVENTION: There are highly promising perspectives for prevention due to the fact that serum homocysteine levels fall off systematically after simple dietary supplementation with vitamin B. Nevertheless, there is no formal proof to date from therapeutic trials suggesting that such a supplementation would reduce the risk of cardiovascular disease. FURTHER INFORMATION REQUIRED: In terms of epidemiology and clinical expression, further research into homocysteine as a cardiovascular risk factor should not be based on case-control studies which can be expected to provide information of limited usefulness, but rather on interventional trials to determine the primary or secondary preventive effect on cardiovascular disease. A large-scale pragmatic study using diet supplementation in a wide population might provide answers to still open questions.

Arteriosclerosis↗
PubMed1999

Differential effects of tyrosine kinase inhibitors on contraction and relaxation of the aortas of normotensive and hypertensive rats.

The contribution of tyrosine kinase activity to vasoreactivity in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats was investigated on isolated aortic preparations by the use of two tyrosine kinase inhibitors: methyl-2,5-dihydroxycinnamate (30 microM) and genistein (30 microM). The pretreatment of endothelium denuded aorta with methyl-2,5-dihydroxycinnamate reduced the sensitivity of the rings to noradrenaline to a larger extent in SHR than in WKY. The relaxing effects evoked by methyl-2,5-dihydroxycinnamate and genistein on the sustained contraction induced by endothelin-1 were also more pronounced in SHR denuded rings. Furthermore, in presence of methyl-2,5-dihydroxycinnamate, the endothelium-independent contractile responses to equipotent doses of cyclopiazonic acid were more depressed in SHR than in WKY. In WKY and SHR endothelium-intact aortas contracted with either phenylephrine or endothelin-1, carbachol and cyclopiazonic acid evoked endothelium derived relaxing factor (EDRF)/nitric oxide (NO)-dependent relaxations which were reduced by pretreatment of the rings with methyl-2,5-dihydroxycinnamate or genistein. These inhibitory effects were larger in WKY rings and more important on the cyclopiazonic acid response. In addition, sodium orthovanadate (30 microM) potentiated the noradrenaline-mediated contractions of endothelium-denuded SHR rings and reduced the cyclopiazonic acid-induced relaxation of endothelium-intact WKY rings. The present study suggests a regulatory role for tyrosine kinase in the smooth muscle contraction and the endothelium-dependent relaxation in WKY and SHR aortas and demonstrates the existence of a different relationship in the effect of tyrosine kinase inhibitors on vasoreactivity between SHR and WKY. We propose that an increase in the tyrosine kinase activity in SHR could lead to an enhanced reactivity of Ca2+-linked contractile mechanisms. In addition, our results suggest a link between the loss of tyrosine kinase activity and the altered endothelium-dependent relaxation associated with hypertension.

Animals↗
PubMed1999

Felodipine-metoprolol combination tablet: a valuable option to initiate antihypertensive therapy?

The aim of the present study was to assess the efficacy and tolerability of a calcium antagonist/beta-blocker fixed combination tablet used as first-line antihypertesnive therapy in comparison with an angiotensin converting enzyme inhibitor and placebo. Patients with uncomplicated essential hypertension (diastolic blood pressure between 95 and 110 mm Hg at the end of a 4-week run-in period) were randomly allocated to a double-blind, 12-week treatment with either a combination tablet of felodipine and metoprolol (Logimax), 5/50 mg daily (n = 321), enalapril, 10 mg daily (n = 321), or placebo (n = 304), with the possibility of doubling the dose after 4 or 8 weeks of treatment if needed (diastolic blood pressure remaining >90 mm Hg). The combined felodipine-metoprolol treatment controlled blood pressure (diastolic < or =90 mm Hg 24 h after dose) in 72% of patients after 12 weeks, as compared with 49% for enalapril and 30% for placebo. A dose adjustment was required in 38% of patients receiving the combination, in 63% of patients allocated to placebo, and 61% of enalapril-treated patients. The overall incidence of adverse events was 54.5% during felodipine-metoprolol treatment; the corresponding values for enalapril and placebo were 51.7% and 47.4%, respectively. Withdrawal of treatment due to adverse events occurred in 18 patients treated with the combination, in 10 patients on enalapril, and 12 patients on placebo. No significant change in patients' well-being was observed in either of the three study groups. These results show that a fixed combination tablet of felodipine and metoprolol allows to normalize blood pressure in a substantially larger fraction of patients than enalapril given alone. This improved efficacy is obtained without impairing the tolerability. The fixed-dose combination of felodipine and metoprolol, therefore, may become a valuable option to initiate antihypertensive treatment.

Administration, Oral↗
PubMed1999

Systolic Hypertension in Europe (Syst-Eur) trial phase 2: objectives, protocol, and initial progress. Systolic Hypertension in Europe Investigators.

The Systolic Hypertension in Europe (Syst-Eur) trial proved that blood pressure (BP) lowering therapy starting with nitrendipine reduces the risk of cardiovascular complications in older (> or = 60 years) patients with isolated systolic hypertension (systolic BP > or = 160 mm Hg and diastolic BP < 95 mm Hg). After the completion of the Syst-Eur trial on 14 February 1997, 3506 consenting patients (93.0% of those eligible) were enrolled in phase 2 of the Syst-Eur trial. This open follow-up study aims to confirm the safety of long-term antihypertensive therapy based on a dihydropyridine. To lower the sitting systolic BP below 150 mm Hg (target BP), the first-line agent nitrendipine (10-40 mg/day) may be associated with enalapril (5-20 mg/day), hydrochlorothiazide (12.5-25 mg/day), both add-on study drugs, or if required any other antihypertensive agent. On 1 November 1998, 3248 patients were still being followed, 86 patients had proceeded to non-supervised follow-up, and 43 had died. The median follow-up in Syst-Eur 2 was 14.3 months. At the last available visit, systolic/diastolic BP in the patients formerly randomised to placebo (n = 1682) or active treatment (n = 1824), had decreased by 13.2/5.2 mm Hg and by 4.6/1.6 mm Hg, respectively, so that the between-group BP difference was 1.7 mm Hg systolic (95% Ci: 0.8 to 2.6 mm Hg; P < 0.001) and 0.9 mm Hg diastolic (95% Cl: 0.4 to 1.5 mm mm Hg; P < 0.001). At the beginning of Syst-Eur 2, the goal BP was reached by 25.4% and 50.6% of the former placebo and active-treatment groups; at the last visit these proportions were 55.9% and 63.1%, respectively. At that moment, 45.9% of the patients were on monotherapy with nitrendipine, 29.3% took nitrendipine in combination with other study drugs. Until the end of 2001, BP control of the Syst-Eur 2 patients will be further improved. Cardiovascular complications and adverse events, such as cancer or gastro-intestinal bleeding, will be monitored and validated by blinded experts.

Aged↗
PubMed1999

Associations between heart rate and other risk factors in a large French population.

OBJECTIVES: In a large general French population of 100,000 subjects, the relationship of resting heart rate with age, gender, demographic parameters, physical activity and classical risk factors was evaluated. POPULATION AND METHODS: A population composed of all the subjects who had a free health check-up at the IPC Centre between 1992 and 1995 (62,353 men and 35,371 women) was analysed. Heart rate was considered either as a continuous parameter or as a qualitative parameter. The study population was divided into four heart rate classes: < 65, 65-74, 75-84 and > or = 85 beats/min. RESULTS: Women had significantly higher heart rate values than men, and this gender difference was constant in the different age groups. In both genders, heart rate was positively associated with blood pressure, triglycerides, glycaemia and physical inactivity, and negatively with body height Heart rate was also correlated with total cholesterol but only in men. The only factor having opposite effects on heart rate in men and women was tobacco smoking (positive in men and negative in women). Among untreated hypertensive men, 21.3% had a heart rate > or = 85 beats/min compared with only 4.0% among normotensive men. In women, these percentages were 23.6 and 7.6%, respectively. Subjects with untreated mild hypertension or uncontrolled treated hypertension also showed increased rates of tachycardia compared to normotensives. CONCLUSIONS: The present analysis, performed in a large French population, shows that high heart rate is associated with several other risk factors, especially hypertension, suggesting that tachycardic subjects have a high risk profile.

Adult↗
PubMed1999

Dual effect of cicletanine on the Na+-H+ exchanger in chick embryonic cardiomyocytes.

Na+-H+ exchanger is thought to play an important role in the regulation of the intracellular pH (pHi) and in the cardiac cell injury induced by ischemia and reperfusion. The aim of this study was to assess the effect of cicletanine, an antihypertensive compound in humans, which has been reported to have cardioprotective effect under an ischemia-reperfusion process, on Na+-H+ exchanger activity in ventricular cardiomyocytes isolated from chick embryo. Na+-H+ exchanger activity was assessed by the rate of pHi recovery after an acid load. A dual effect was observed: at low concentration of cicletanine (10(-7) M), Na+-H+ exchanger activity was significantly decreased, whereas at higher concentrations (10(-6)-10(-5) M), a significant stimulation of the exchanger was observed. These results suggest that cicletanine modulates pHi recovery in cardiac cells after cellular acid load.

Animals↗
PubMed1999

ANG II-induced Ca(2+) increase in smooth muscle cells from SHR is regulated by actin and microtubule networks.

We hypothesized that the cytoskeletal network in vascular smooth muscle cells (VSMC) is critical to the signaling pathways from angiotensin (ANG) II-receptor subtype 1 (AT(1)) activation to intracellular Ca(2+) (Ca(2+)(i)) release from internal stores and Ca(2+) influx. This was tested in spontaneously hypertensive rats (SHR), in which differences were reported in cultured aortic VSMC Ca(2+)(i) regulation and G protein function compared with those in normotensive Wistar-Kyoto (WKY) rats. In cultured aortic VSMC, disorganization of actin filaments with cytochalasin D (2 micromol/l) decreased the ANG II-induced Ca(2+)(i) release from internal stores and the ANG II-induced Ca(2+) influx in SHR in a reversible fashion, whereas it was without effect in WKY rats. On the other hand, blocking the dynamic state of the microtubule network significantly reduced ANG II-induced Ca(2+)(i) release from internal stores but was without effect on Ca(2+) influx in either SHR or WKY rats. This study demonstrates for the first time that, in the SHR, actin filaments play a major role in linking AT(1)-receptor activation to both Ca(2+)(i) release mechanisms and capacitative Ca(2+) influx. Furthermore, a functionally intact microtubule system is a necessary prerequisite for ANG II-induced Ca(2+)(i) release in both strains.

Actins↗
PubMed1999

Influence of heart rate on mortality in a French population: role of age, gender, and blood pressure.

-The aim of the present study was to assess the effects of high heart rate on mortality in different subgroups in a French population according to age, gender, and blood pressure levels. We studied 19 386 subjects (12 123 men, 7263 women), aged 40 to 69 years, who had a routine health examination at the Centre d'Investigations Préventives et Cliniques (IPC) between 1974 and 1977. Heart rate (HR) measured by ECG was classified into 4 groups: HR1, <60; HR2, 60 to 80; HR3, 81 to 100; and HR4, >100 bpm. Mortality data were recorded for the period of 1974 through 1994. In both sexes, HR was a significant predictor of noncardiovascular mortality. In men, the relative risk (95% confidence interval) for cardiovascular death after adjustment for age and other risk factors in the HR2, HR3, and HR4 groups was 1.35 (1.01 to 1.80), 1.44 (1.04 to 2.00), and 2.18 (1.37 to 3.47), respectively, when compared with HR1. In women, HR did not influence cardiovascular mortality. The association of HR with cardiovascular mortality in men was (1) related to a strong association with coronary but not cerebrovascular mortality, (2) independent of age and hypertension, and (3) influenced by the level of pulse pressure; in patients with high pulse pressure (>65 mm Hg), accelerated HR was not associated with increased cardiovascular mortality. In conclusion, in a large French population, accelerated resting HR represents an independent predictor of noncardiovascular mortality in both genders, and of cardiovascular mortality in men, independent of age and the presence of hypertension. Further investigations are needed to explain the complex interactions between HR, pulse pressure, and cardiovascular complications.

Adult↗
PubMed1999

[Evaluation of the individual absolute cardiovascular risk. A mathematical equation and/or arterial measurement?].

The latest recommendations about the management of cardiovascular risk factors take into account not only the level of risk factor but also the global risk profile of the patient. The reference for the calculated estimation of absolute cardiovascular risk remains the Framingham equation. Nevertheless, this estimation has a number of operational and conceptual limitations such as geographical and historical validity and its application to individual cases. Different results in the medical literature suggest that parameters of arterial structure or function measured simply, such as arterial rigidity, could be closely related to the level of individual cardiovascular risk by the integration of the deleterious effects of different vascular risk factors over decades of exposition. They could then be better predict cardiovascular effects than the result of a mathematical equation which only integrates some of the risk factors at a given point in time. These simple, rapid and non-invasive measurements could help identify subjects at high cardiovascular risk and also help the clinician in the orientation of preventive measures in subjects with cardiovascular risk factors.

Adult↗
PubMed1999

[A new cause of resistant arterial hypertension: coprescription with anticonvulsant treatments].

UNLABELLED: This article provides two case reports about pharmacokinetic interactions with hypertensive drug therapy and anticonvulsive treatment. First, a 49-year-old patient presenting severe hypertension had a non-traumatic cerebral hemorrhage with convulsions. Extensive etiologic investigations did not find any cause of secondary hypertension. Under an association of four antihypertensive drugs regimen, associated with carbamazepine blood pressure was not controlled. Finally, blood pressure was well controlled after replacement of carbamazepine with vigabatrin. The second case reports a 64-year-old treatment-resistant essential hypertensive patient, carbamazepine was associated with antihypertensive treatment because of aggressivity attributed to Alzheimer's disease. After withdrawal of carbamazepine treatment, blood pressure reached normal values with the same antihypertensive regimen. Those case reports suggest drug-drug interactions between antihypertensive and anticonvulsive drug therapies. Following explanation can be hypothesis: several antihypertensive drugs are liver-metabolised by microsomal cytochrome P450 3A4 isoform that could explain a significantly decreased half-life in association with enzymatic inducers, such as rifampicine or antiepileptic drugs (phenobarbital, phenytoin or carbamazepine). CONCLUSION: When blood pressure is not controlled without cause of secondary hypertension, physicians must be careful with drug-drug interactions.

Anticonvulsants↗
PubMed1999

[Cellular adhesion to elements of the extracellular matrix in the hypertensive rat modulates the effect of angiotensin II].

This study was to assess the role of different components of the extracellular matrix (ECM) on the mobilization of Cai++ induced by angiotensin II in vascular smooth muscle cells (VSMC) from hypertensive (SHR) and normotensive (WKY) rats. The effect of AII (10-6 M) on Cai++ release was studied in VSMC isolated from the aorta of 5-week-old WKY and SHR using fluorescent imaging microscopy (fura-2). Cai++ mobilization was characterized by amplitude, slope of Cai++ increase and total amount of Cai++. Cells were cultured on glass coverslips (control) or coated with either collagen I, collagen IV, vitronectin, fibronectin and extracellular matrix (ECM) and studied at confluence between passage 3 and 9. A significant increase of Cai++ released by AII has been observed with cells from WKY cultured on collagen I (meam +/- SEM, amplitude: 192 +/- 12% of control values, slope: 194 +/- 13%, total amount Cai++: 173 +/- 12%, n = 270, p < or = 0.0001 for each, unpaired t-test). Conversely, response with SHR was not significatively modified. Cai++ mobilization was not significatively modified after culture of VSMC from SHR and WKY on collagen IV. A significative decrease of the slope (WKY: 66 +/- 6%, p < or = 0.0001; SHR: 83 +/- 5%, p < or = 0.03) and of the amount of Cai++ (WKY: 74 +/- 7%, p < or = 0.01; SHR: 74 +/- 5%, p < or = 0.01) has been observed after culture of VSMC from the 2 strains on vitronectin. A decrease in amplitude (53 +/- 3%, p < or = 0.0001), slope (38 +/- 4%, p < or = 0.0001) and Cai++ release (69 +/- 5%, p < or = 0.004, n = 106) has been observed in VSMC from SHR seeded on fibronectin. Conversely, in VSMC from WKY, Cai++ mobilisation has not been modified compared with control cells. Culture of VSMC from SHR on ECM induced a significative decrease of amplitude (49 +/- 2%), slope (54 +/- 4%) and Cai++ release (53 +/- 3%, p < or = 0.0001 for each, n = 122), while in WKY, ECM induced a significative stimulation of these parameters (amplitude: 157 +/- 11%, slope: 149 +/- 13% and Cai++ release: 130 +/- 9%, p < or = 0.0001 for each, n = 247). These results show that the Cai++ mobilization induced by AII is modified by the adhesion of cells to different ECM components. This suggests a modulation of the A II-associated signalling events via the focal adhesion points. Furthermore, a difference in this modulation is observed between SHR and WKY when cells are seeded on collagen I, fibronectin or ECM. These modulations of Cai++ mobilization could play a role in the regulation of growth and differentiation of cells during the development of hypertension.

Angiotensin II↗
PubMed1999

[Antihypertensive treatment can normalize the geometry and the arterial function in the aged patient].

The aging process and the elevation of arterial blood pressure (BP) have synergistic effects on the modifications of the arterial system. The effects of the treatment on these modifications are unknown. Our objective was to study the consequences of anti-hypertensive treatment on the geometry and function of the arteries in men over 70 years old. In 89 men aged 74 +/- 2 years, we measured internal diameter and intima-media thickness (IMT) of carotid and radial arteries using high resolution echography (WALL TRACK SYSTEM and NIUS-02), and carotid-femoral pulse wave velocity (PWV) by COMPLIOR. The BP was measured in supine position by Dinamap. In 28 subjects the BP was more than 140/90 mmHg (poor controlled hypertensives-HTpc); in the subjects where BP < 140/90 mmHg, 44 were normotensives (NT) without treatment and 17 were well controlled hypertensives (HTwc) on use of at least one antihypertensive. [table: see text] The PWV was increased in HTpc (20.1 m/s) in comparison with NT (14.6 m/s) and HTwc (16.1 m/s) (p < 0.05). The operational distensibility of radial artery was similar in the three groups. In conclusion, in elderly men aged more than 70 years, the anti-hypertensive treatment can normalize the functional properties and the geometry of muscular and elastic arteries. These results indicate that the arterial modifications observed in elderly hypertensives are consequence of the high blood pressure per se and not only consequent the modifications due to the aging.

Aged↗