摘要:

ObjectiveThe purpose of this study was to investigate the effects of salt loading on circadian patterns of blood pressure (BP) and sympathetic nervous activity.Subjects and methodsSeventy-six patients with essential hypertension were hospitalized and placed on a low-salt diet (2 g/day) for 7 days followed by a high-salt diet (20–23 g/day) for another 7 days. On the last day of each salt diet, 24 h ambulatory BP, plasma noradrenaline concentrations, urinary noradrenaline excretion, plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were measured. Patients whose average mean BP was increased by more than 10% by salt loading were assigned to the salt-sensitive (SS) group (n= 44); the remaining patients, whose mean BP was increased by less than 10%, were assigned to the non-salt-sensitive (NSS) group (n= 32).ResultsSalt loading converted the circadian pattern of BP from dippers, whose mean BP during the night-time was decreased by more than 10% from the daytime BP, to non-dippers in the SS group but not in the NSS group. A nocturnal decrease in plasma noradrenaline concentration was unaffected after salt loading in the NSS group but dampened in the SS group. The night-time/daytime ratio of urinary noradrenaline excretion, which was increased after salt loading in the SS group only, was greater in the SS group than in the NSS group under the high-salt diet. The salt-induced suppression rate of PRA and PAC was similar between the SS and NSS groups.ConclusionBP fails to fall during the night under the high-salt diet in patients with the SS type of essential hypertension. This may be related to the lack of nocturnal decrease in sympathetic nervous activity.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

AimWistar fatty rats (WFR) develop mild hypertension associated with obesity, hyperglycaemia and hyperinsulinaemia, and are thus assumed to be a good model of insulin resistance-related hypertension. We determined whether the activity of the sympathetic nervous system and its baroreflex-mediated regulation are involved in the development of hypertension in this strain.MethodsRenal sympathetic nerve activity (RSNA) was recorded in pre-hypertensive WFR (n= 8, age 12 weeks) and Wistar lean rats (WLR) (n= 8) during changes in arterial pressure by phenylephrine and nitroprusside infusion in the conscious state. Baroreflex control of RSNA and heart rate were examined by logistic function analysis.ResultsThe mean arterial pressure (MAP) of WFR was similar to that of WLR (108 ± 4 versus 101 ± 2 mmHg, not significant). Basal RSNA was elevated in WFR compared with WLR (86 ± 2 versus 51 ± 2% maximum,P< 0.01). Baroreflex control of RSNA was shifted to higher pressure levels (mid-range, 119 ± 4 versus 99 ± 4 mmHg,P< 0.05) in WFR compared with WLR, in spite of similar MAP. However, baroreflex sensitivity concerning RSNA was greater in WFR than WLR (3.07 ± 0.15 versus 1.63 ± 0.12% maximum/mmHg,P< 0.01). Baroreflex control of heart rate was also shifted to higher pressure levels (mid-range 129 ± 4 versus 100 ± 5 mmHg,P< 0.01) and its sensitivity was increased in WFR compared with WLR (4.62 ± 0.51 versus 3.16 ± 0.10 bpm/mmHg,P< 0.05).ConclusionThese results suggest that baroreflex is not impaired in spite of elevation of blood pressure and that the raised sympathetic nerve activity may contribute to the development of hypertension in WFR.J Hypertens1999, 17:959–964 © Lippincott Williams & Wilkins.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveNormotensive rats fed a high fructose diet (HFD) develop hypertriglyceridemia, hyperinsulinemia and hypertension. The glomerular changes observed in the kidneys of these animals are similar to those observed in diabetic rats. The aim of this study was to evaluate whether lacidipine could be effective not only in preventing, but also in inducing the regression of hypertension, and renal and cardiac damage in rats fed HFD.MethodsThirty male Wistar–Kyoto (WKY) rats received HFD for 1 month; thereafter, five rats were sacrificed (Group 1) and the other 25 rats were divided into three groups: Group 2 (five rats) received HFD plus placebo, Group 3 (10 rats) HFD plus lacidipine 3 mg/kg per day, and Group 4 (10 rats) HFD plus hydralazine 10 mg/kg per day. At the end of the second month all animals were sacrificed. Kidneys and hearts were immediately removed. Renal deposits of collagen I, collagen IV, fibronectin and cardiac deposits of collagen III were assessed by means of immunohistochemistry.ResultsIn the rats receiving HFD plus placebo, blood pressure was increased after the first and the second month of diet. This increase was reversed by lacidipine and hydralazine but, although both drugs normalized blood pressure, only lacidipine was effective in reducing renal and cardiac damage.ConclusionsThese data suggest that lacidipine is effective in reversing hypertension and reducing target organ damage induced by HFD. Moreover, this protective effect on target organs appears to be not simply a consequence of blood pressure reduction, but seems to be connected to the type of hypotensive drug administered.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveTo investigate the effect of nitrendipine on the development of renal changes in experimental diabetes.DesignStreptozotocin (STZ)-induced diabetic normotensive Wistar rats (WIS) and spontaneously hypertensive rats (SHR) were randomly allocated to nitrendipine treatment (250 mg/kg fodder) or placebo treatment for 6 months.MethodsBlood pressure was assessed by the tail-cuff method, urinary albumin excretion (UAE) was determined, and glomerular basement membrane (GBM) thickness, mesangial volume, and mean glomerular volume (MGV) were estimated by morphometric measurements.ResultsIn diabetic WIS, nitrendipine significantly reduced UAE after 2 months of treatment (P< 0.05), while no effect was was seen after 4–6 months. In diabetic SHR, no effect on UAE was seen at any time. Nitrendipine was unable to inhibit the renal and glomerular enlargement in diabetic WIS and SHR. Diabetes plus hypertension was associated with significant increase in GBM thickness, while diabetes or hypertension alone showed no significant increase in GBM. Nitrendipine treatment was unable to prevent increased GBM in diabetic SHR.ConclusionNitrendipine inhibits an early increase in UAE in normotensive, diabetic rats, but fails to sustain this effect in long-term diabetes. No effect of nitrendipine was observed in SHR.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

DesignPrevious studies that were based on daytime arterial pressure recordings indicate that lifetime treatment with captopril exacerbates the hypertensive response to a high NaCl diet in spontaneously hypertensive rats (SHR) but has no such effect in normotensive Wistar–Kyoto (WKY) rats. The present study used 24-h recording methods to examine the hypothesis that during the normal waking hours of rats (night-time) the hypertensive response to a high NaCl diet is exacerbated in SHR and induced in WKY rats treated with lifetime captopril.MethodsSHR and WKY rats were (1) untreated, (2), lifetime captopril treated or (3) lifetime captopril treated but removed from the treatment 2 weeks prior to exposure to a high (8%) NaCl diet.ResultsCompared to untreated SHR, in SHR that were continuously treated with captopril, the high NaCl diet caused a more rapid and greater rise in arterial pressure. Discontinuation of the captopril treatment did not significantly diminish this NaCl-sensitivity. In untreated WKY rats, the high NaCl diet did not alter mean arterial pressure, but in the lifetime captopril-treated WKY rats the high NaCl diet induced a rapid rise in arterial pressure. In WKY rats, discontinuation of the lifetime captopril treatment did not diminish this NaCl-induced rise in arterial pressure, even though baseline mean arterial pressure in this group is similar to that in untreated WKY rats.ConclusionsLifetime captopril treatment accelerates the hypertensive response to a high NaCl diet in SHR, and it induces a similar response in WKY rats. In both strains, the lifetime captopril treatment causes a change in the response that is not dependent on concurrent administration of the drug. This finding further suggests that lifetime captopril treatment causes a long-term resetting of cardiovascular response mechanisms.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundMicroalbuminuria has recently emerged as a strong, independent predictor of cardiovascular mortality in patients with essential hypertension, yet the pathophysiological mechanisms underlying this association remain to be elucidated.ObjectiveTo study the relationship between microalbuminuria and left ventricular geometry and function and extra-cardiac vascular changes in a group of 211 untreated hypertensive patients.MethodsAlbuminuria was evaluated as albumin-tocreatinine ratio in three non-consecutive first morning urine samples. Left ventricular mass index and function were assessed by M-B mode echocardiography and carotid wall thickness by high-resolution ultrasound scan.ResultsThe prevalences of microalbuminuria and left ventricular hypertrophy were 14 and 47% respectively. Patients in the top quartile of albuminuria showed a higher left ventricular mass index (57 ± 1.8, 55 ± 2, 47 ± 1.4 and 48 ± 1.6 g/m2:7, respectively;P< 0.0001) as well as a higher prevalence of left ventricular hypertrophy (72, 65, 26 and 25%, respectively;P< 0.001) and especially concentric hypertrophy (56, 47, 17 and 21%, respectively;P< 0.0001) in the four quartiles of albuminuria. Microalbuminuric patients showed depressed left ventricular performance as indicated by a reduced midwall fractional shortening (15.7 ± 0.3, 15.9 ± 0.3, 16.7 ± 0.4 and 16.8 ± 0.3%, respectively;P< 0.02). Furthermore patients in the top quartile of albuminuria showed increased carotid wall thickness as compared to normoalbuminuric patients (0.78 ± 0.03, 0.7 ± 0.04, 0.65 ± 0.03 and 0.6 ± 0.03 mm, respectively;P< 0.001).ConclusionsHypertensive patients with microalbuminuria show a higher prevalence of unfavourable left ventricular geometric patterns, depressed left ventricular function and early signs of extra-cardiac vascular damage. These findings strengthen the role of microalbuminuria as an indicator of subclinical cardiovascular disease and may account for the worse outcome that is usually associated with increased urinary albumin excretion in essential hypertension.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundTo test the hypothesis that in the presence of left ventricular concentric geometry the definition of ‘normal’ ejection fraction should be reconsidered, and normality should rather be considered to have a higher than usual lower limit.MethodsM-mode echocardiographic endocardial shortening (eS) was studied in 148 hypertensive patients with left ventricular concentric geometry (relative wall thickness ≥ 0.42), 78 with normal (54 ± 10 years, 27 women) and 70 with depressed midwall shortening (mS) (53 ± 10 years, 26 women), based on normal distribution of stress-corrected mS, and compared to a reference adult population of 297 age-matched normal subjects (54 ± 8 years, 121 women) with eS ≥ 28%.ResultsPatients with low mS exhibited higher heart rates and body mass indices than control individuals (bothP< 0.01); blood pressure, left ventricular mass, relative wall thickness and peripheral resistance were higher than in patients with normal mS, whereas cardiac index was reduced (allP< 0.01). Adjustment for body mass index and race attenuated but did not eliminate the differences between the two groups of patients (0.05 <P< 0.0001). In contrast, eS was higher than normal in patients with normal midwall shortening, whereas was ‘normal’ in patients with low left ventricular midwall function. More than 80% of patients in the lowest quartile of apparently normal eS exhibited clear-cut low left ventricular midwall function.Conclusions‘Normal’ left ventricular chamber function in the presence of concentric geometry is associated with depressed midwall performance, more severe left ventricular hypertrophy, lower cardiac output and higher peripheral resistance. ‘Normal’ eS is the hallmark of normal myocardial function when left ventricular geometry is normal, but should be considered as a marker of systolic dysfunction when associated with concentric left ventricular geometry. Normal limits for eS should be therefore reset to upper values.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveEffective arterial elastance (Ea), integrating the pulsatile component of left ventricular (LV) afterload, is an estimate of aortic input impedance. We evaluated relationships of Eawith left ventricular anatomy and function in essential hypertension.DesignA cross-sectional analysis in 81 normotensive and 174 untreated hypertensive individuals enrolled in a referral hypertension centre.MethodsUsing echocardiography we determined left ventricular mass index (LVMI), relative wall thickness (RWT), stroke volume (SV), endocardial (FSe) and midwall (FSm) fractional shortening and total peripheral resistance (TPR). Carotid pressure waveforms were obtained by arterial tonometry, and end-systolic pressure (Pes) was measured at the dicrotic notch. Eaindex (EaI) was calculated as Pes/(SV index); LV elastance (Ees) was estimated as Pes/LV end-systolic volume, and ventriculoarterial coupling was evaluated by the Ea/Eesratio.ResultsEaI was higher in hypertensives than in normotensives (3.02 ± 0.63 versus 2.40 ± 0.52 mmHg/l per m2;P< 0.0001). Using the 95% upper confidence limit in normotensives, hypertensives were divided in two groups with normal or elevated EaI. The 38 hypertensives with elevated EaI had higher RWT (0.41 ± 0.06 versus 0.37 ± 0.05), lower LVMI (87.5 ± 18.5 versus 96.8 ± 19.3 g/m2), higher TPR (2247 ± 408 versus 1658 ± 371 dynes/cm s−5) and lower FSeand FSm(35 ± 5 versus 39 ± 5 and 16 ± 2 versus 18 ± 2%; allP< 0.05) than patients with normal EaI. Ea/Eesratio was increased and cardiac output was reduced in hypertensives with elevated EaI.ConclusionsHigh values of EaI identify a minority of hypertensive patients characterized by elevated TPR, left ventricular concentric remodelling, depressed left ventricular systolic function and impaired ventriculoarterial coupling.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveTo examine whether hypertension predicts the incidence of kidney stone disease.DesignProspective cohort study (the Olivetti Prospective Heart Study).SettingThe Olivetti factory in Southern Italy.SubjectsFive hundred and three male workers, aged 2168 years, with no evidence of kidney stone disease at baseline.Follow-up8 years.Main outcome measuresAnthropometry, blood pressure, biochemistry and history of kidney stone disease were evaluated at the baseline examination in 1987. Occurrence of kidney stone disease was evaluated again in 1994–1995. Hypertension was defined as systolic blood pressure ≥ 160 or diastolic blood pressure, ≥ 95 mmHg or both, or being on drug therapy for hypertension. Occurrence of kidney stone disease was defined as radiological or echographic evidence of calculi or documented passage of one or more stones.ResultsAt baseline, 114/503 men (22.7%) had hypertension and 32 were on drug treatment. After 8 years, 52 (10.3%) incident cases of kidney stone disease were detected. The majority (n = 45) had a documented passage of one or more stones. The incidence of kidney stone disease was higher in hypertensive than in normotensive men (19/114 (16.7%) versus 33/389 (8.5%);P= 0.011). Hypertensive men had a greater risk of developing kidney stones than normotensive ones (RR 1.96; 95% confidence interval 1.16–3.32). The risk was unaffected by the exclusion of treated hypertensives (2.01; 1.13–3.59) and after adjustment for age (1.89; 1.12–3.18), body weight (1.78; 1.05–3.00) or height (2.00; 1.19–3.38).ConclusionsHypertension in middle-aged men is a significant predictor of kidney stone disease rather than a consequence of renal damage caused by the kidney stones.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveTo measure the time effect profiles of a once daily administered combination tablet felodipine-metoprolol 5/50 mg (Logimax®, Astra) and amlodipine 5 mg (Norvasc®, Pfizer) on blood pressure and heart rate using 24-h ambulatory blood pressure monitoring.DesignRandomized multicentre parallel-group study with a single-blind placebo run-in period of 4 weeks duration and a 6-week double-blind active treatment period.Patients and methodsOut of 245 randomized outpatients (90 men, 155 women) with uncomplicated mild-to-moderate primary hypertension and mean sitting diastolic blood pressure (DBP) 95–115 mmHg inclusive, 212 (102 on felodipine-metoprolol, 110 on amlodipine) were eligible for analysis. 24-h ambulatory blood pressure monitoring was performed at the end of the placebo run-in (baseline) and after 6 weeks active treatment (post-treatment).ResultsBoth felodipine-metoprolol and amlodipine induced smooth and consistent reduction in DBP and systolic blood pressure throughout the 24-h period, hence not altering the diurnal rhythm. However, felodipine-metoprolol reduced all average blood pressures (24-h, day- and night-time) more than amlodipine (for 24-h average blood pressure 14:4/9:5 mmHg and 8:9/5:5 mmHg, respectively). Medians of individual diastolic trough-to-peak (T/P) ratios were similar for felodipine-metoprolol and amlodipine (54 and 50%, respectively), while for the systolic T/P ratios, the corresponding values were 74 and 35%, repectively; no significant difference between treatments was seen. As distinguished from amlodipine, both heart rate and rate pressure product were markedly decreased on felodipine-metoprolol throughout the 24-h period and even during the early morning hours. In general, both treatments were well tolerated.ConclusionsBoth felodipine-metoprolol and amlodipine achieved optimal control of blood pressure during the inter-dosing interval in line with their pharmokinetic profiles. The vasodilatory adverse events were slightly more reported with felodipine-metoprolol combination, but due to more pronounced lowering of the average blood pressures and the potent additional effect on heart rate and rate pressure product, the efficacy/tolerability balance seems to be equal to or better than that obtained with monotherapy such as amlodipine.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID