摘要:

BackgroundSympathetic activation induced by cold pressor test or cigarette smoking is accompanied by a marked reduction of radial artery distensibility. It is not known, however, whether arterial distensibility is under tonic sympathetic restraint, or whether this restraint involves arteries greater than the radial one in both normal and pathological conditions.MethodsWe studied the distensibility of radial artery by continuous ultrasonographic assessment of the changes in arterial diameter over the diasto-systolic pressure range (finger pressure measurement) in eight patients with a Dupuytren disease before and 20 min after ipsilateral brachial plexus anaesthesia. We also studied ultrasonographic distensibility of femoral artery in seven subjects before and 20 min after ipsilateral subarachnoid anaesthesia, performed before arthroscopic surgery, and in five patients with claudicatio intermittens before and 1 month after ipsilateral removal of the lumbar sympathectomy chain. In all three conditions, the contralateral artery served as control.ResultsThe three interventions did not cause any significant alteration in blood pressure and heart rate. Radial artery distensibility was markedly increased by ipsilateral anaesthesia of the brachial plexus(+36%,P< 0.01). This was the case also for femoral artery distensibility both following ipsilateral subarachnoid anaesthesia in healthy subjects (+47%,P< 0.05) or ipsilateral sympathetic gangliectomy in patients with peripheral artery disease (+26%,P< 0.05). In all three instances, the distensibility of the contralateral artery remained unaffected.ConclusionsThese data indicate that the sympathetic nervous system exerts a marked tonic restraint of arterial distensibility. This restraint involves medium-size and large muscular arteries and can also be seen in subjects with peripheral artery disease. This stiffening influence may increase the traumatic effect of intravascular pressure on the vessel wall and favour atherosclerosis.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveTwo hypotheses concerning mechanisms of weight gain and of blood pressure elevation in obesity were tested. The first hypothesis is that in human obesity sympathetic nervous system underactivity is present, as a metabolic basis for the obesity. The second hypothesis, attributable to Landsberg, is that sympathetic nervous activation occurs with chronic overeating, elevating blood pressure. These are not mutually exclusive hypotheses, since obesity is a heterogeneous disorder.Design and methodsWhole body and regional sympathetic nervous system activity, in the kidneys and heart, was measured at rest using noradrenaline isotope dilution methodology in a total of 86 research voluteers in four different subject groups, in lean and in obese people who either did, or did not, have high blood pressure.ResultsIn the lean hypertensive patients, noradrenaline spillover for the whole body, and from the heart and kidneys was substantially higher than in the healthy lean volunteers. In normotensive obesity, the whole body noradrenaline spillover rate was normal, mean renal noradrenaline spillover was elevated (twice normal), and cardiac noradrenaline spillover reduced by approximately 50%. In obesity-related hypertension, there was elevation of renal noradrenaline spillover, comparable to that present in normotensive obese individuals but not accompanied by suppression of cardiac noradrenaline spillover, which was more than double that of normotensive obese individuals (P< 0.05), and 25% higher than in healthy volunteers. There was a parallel elevation of heart rate in hypertensive obese individuals.ConclusionsThe sympathetic underactivity hypothesis of obesity causation now looks untenable, as based on measures of noradrenaline spillover, sympathetic nervous system activity was normal for the whole body and increased for the kidneys; the low sympathetic activity in the heart would have only a trifling impact on total energy balance. The increase in renal sympathetic activity in obesity may possibly be a necessary cause for the development of hypertension in obese individuals, although clearly not a sufficient cause, being present in both normotensive and hypertensive obese individuals. The discriminating feature of obesity-related hypertension was an absence of the suppression of the cardiac sympathetic outflow seen in normotensive obese individuals. Sympathetic nervous changes in obesityrelated hypertension conformed rather closely to those expected from the Landsberg hypothesis.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveTo investigate the nature and time course of autonomic nervous system changes elicited by a 21-week ad libitum high-fat diet (HFD) in dogs.ResultsThe HFD increased body weight (+22.0 ± 2.8% at week 21) with an abdominal circumference gain significantly more elevated than the thoracic one. The increases in insulin and free fatty acid plasma levels were correlated with body weight changes. Systolic and diastolic blood pressures and heart rate significantly increased (+23 ± 6, +28 ± 5 and 19 ± 9% respectively). Arterial hypertension was characterized by an increase in cardiac output (+22.3 ± 7.7%), in left ventricular mass (+18.1 ± 5.0% at week 21) and a decrease in spontaneous baroreflex efficiency (−55 ± 6%). The time course of autonomic changes (using spectral analysis of systolic blood pressure and heart rate) showed the existence of time-dependent modifications, which were linked with food intake. The initial rise in arterial blood pressure during body weight increment (observed between the 1st and 8th week of HFD) was associated with a transient increase in the low frequency band of systolic blood pressure variability and noradrenaline plasma levels associated with a long-lasting decrease in the high frequency band of heart rate variability. Early changes in short-term variability were significantly correlated with free fatty acid plasma levels. In contrast, the steady-state of obesity-related hypertension was associated with a decreased high frequency band of heart rate variability, without significant changes in noradrenaline plasma levels.ConclusionsThis study shows that the HFD induces abdominal obesity, hyperinsulinaemia and arterial hypertension, with a left ventricular hypertrophy associated with a biphasic changes in autonomic activity: an early and long-lasting decrease in parasympathetic nervous system activity and an early but transient increase in sympathetic activity. The present data suggest that autonomic nervous system changes are dependent on the time course of obesity development.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveTo evaluate the effects of angiotensins acting at the rostral ventrolateral medulla (RVLM) on the cardiovascular adjustments following haemorrhage.DesignChanges in mean arterial pressure (MAP) and heart rate (HR) produced by micro-injections of angiotensin II (Ang II) and angiotensin (Ang)-(1–7) and different angiotensin antagonists into the RVLM of anaesthetized rats submitted to haemorrhage, were determined.MethodsExperiments were performed in 79 urethaneanaesthetized male Wistar rats. Ang-(1–7) (2.5 and 25 pmol), Ang II (25 pmol), [Sar1, Thr8]-Ang II (non-selective angiotensin antagonist, 0.2 nmol), A-779 (Ang-(1–7) antagonist, 0.1 nmol), losartan (AT1Ang II receptor antagonist, 0.2 nmol) or vehicle (200 nl) were bilaterally micro-injected into the RVLM under basal conditions or 30 min after blood withdrawal (0.6 ml/100 g bodyweight). In additional groups, [Sar1, Thr8]-Ang II, A-779, losartan or vehicle were micro-injected into the RVLM 10 min before bleeding to uncover a possible role of endogenous peptides during haemorrhage.ResultsThe pressor effect produced by Ang II microinjection was not altered by haemorrhage. Conversely, haemorrhage significantly increased the magnitude and duration of the pressor effect of Ang-(1–7) at the RVLM. The fall in MAP induced by haemorrhage was similar after micro-injection of vehicle or A-779. However, microinjection of [Sar1, Thr8]-Ang II significantly reduced the fall in MAP after haemorrhage. A similar finding was obtained with micro-injection of losartan. In addition, while RVLM micro-injection of [Sar1, Thr8]-Ang II or losartan 30 min after blood withdrawn produced MAP changes that were similar to that observed in control animals, micro-injection of A-779 did not significantly alter baseline MAP.ConclusionsThese results suggest that changes in the RVLM reactivity to Ang-(1–7) but not Ang II may contribute to the haemodynamic adjustments triggered by acute reductions in blood volume. The data obtained with [Sar1, Thr8]-Ang II and losartan suggest a primary inhibitory role for endogenous Ang II at the RVLM during haemorrhage.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundIn hypertensive patients, the relationships between glucose tolerance and left ventricular hypertrophy (LVH) and left ventricular diastolic function (LVDF) have been described in several reports.ObjectiveIn this study, we examined the relationships between insulin resistance and LVH and LVDF in hypertensive patients from the therapeutic perspective.Methods and resultsThe study participants were essential hypertensive patients with impaired glucose tolerance (IGT-HT,n= 26), hypertensive patients with normal glucose tolerance (NGT-HT,n= 39), and normotensive control individuals (n= 18). Insulin resistance was evaluated by the insulin suppression test by use of the steady-state plasma glucose (SSPG) level. Left ventricular mass index (LVMI) and LVDF, which was determined by the E: A ratio, were estimated by echocardiography. Temocapril, an angiotensin-converting enzyme inhibitor, was administered in an open, non- randomized manner with a mean dose of 2.8 ± 0.2 mg/ day, and the mean administration period was 18 weeks. The systolic and diastolic blood pressure, the LVMI, and the SSPG level were significantly higher in the hypertensive patients than in the control individuals. The mean systolic and diastolic blood pressures were significantly decreased by treatment with Temocapril.Before treatment, stepwise regression analysis showed that SSPG is an independent predictor for LVMI and LVDF. After treatment, the changes in LVMI (D-LVMI; %) (−15.1 ± 1.5), the changes in LVDF (D-E: A; %) (−38.2 ± 4.1), and the changes in insulin resistance (DSSPG; %) (−13.7 ± 1.7) were significantly higher in the IGT-HT group than in the NGT-HT group (−11.4 ± 1.1, −18.1 ± 1.7, −9.4 ± 1.4, respectively), and the D-SSPG was an independent predictor for D-LVMI and D-E: A.ConclusionsThe results of this study indicate that insulin resistance is an important factor affecting LVH and LVDF.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundIt has been suggested that hyperinsulinemia and insulin resistance participate in the pathogenesis of hypertension, in part by activating sympathetic activity.ObjectiveWe aimed to examine the relationship between insulin resistance and cardiac sympathetic nervous function in patients with essential hypertension using123Imetaiodobenzylguanidine (MIBG) cardiac scintigraphy.Methods and resultsTwenty-eight patients (18 men) with essential hypertension and 11 (seven men) control individuals with a mean age of 55.8 ± 3.3 years were recruited. Patients with diabetes mellitus, congestive heart failure or coronary artery disease were excluded from this study. To evaluate insulin resistance, we used steady-state plasma glucose (SSPG; mg/dl) levels measured by the SSPG method. To evaluate cardiac sympathetic nervous function, we calculated the heart-to-mediastinum ratio from the delayed MIBG image (H:M-D) and the mean washout rate (WOR,%). There were significant differences (P< 0.01) in SSPG, H:M-D and WOR between the essential hypertension and control individual groups (125 versus 103 mg/dl, 2.2 versus 2.4, and 32 versus 23%, respectively). Stepwise regression analysis showed that SSPG and plasma norepinephrine level are independent predictors for the cardiac sympathetic nervous function obtained from MIBG scintigraphy.ConclusionsThese findings indicate that insulin resistance is significantly related to activation of the cardiac sympathetic nervous function associated with left ventricular hypertrophy in patients with essential hypertension.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveThe prospective association of insulin and hypertension has been under debate in the context of the development of the insulin resistance or multiple metabolic syndrome. We examined the predictive associations of fasting serum insulin with incident hypertension occurring alone or as part of the multiple metabolic syndrome.DesignAnalyses were restricted to 5221 middle-aged participants of the Atherosclerosis Risk in Communities Study cohort who were free of component disorders of the multiple metabolic syndrome (hypertension; diabetes; high triglycerides and/or low HDL cholesterol (dyslipidaemias)) at baseline.OutcomeA total of 1018 individuals developed hypertension, 801 in the absence of components of the metabolic syndrome and 217 in combination with diabetes or dyslipidaemias, between 1987 and 1993.ResultsElevated fasting insulin (top quartile versus lowest quartile) was associated with overall incident hypertension in European Americans [hazard rate ratio (HRR) 2.0, 95% confidence interval (CI) 1.7–2.4] but the results were inconclusive in African Americans (HRR 1.3, 95% CI 0.9–1.8) after adjustment for age, gender and study centre. Among European Americans, body mass index and abdominal girth only partly explained the observed association. Elevated fasting insulin was more strongly predictive of hypertension occurring as a component of the multiple metabolic syndrome (HRR 2.4, 95% CI 1.5–3.9) than of hypertension occurring alone (HRR 1.3, 95% CI 1.0–1.7) adjusting statistically for age, gender, study centre, body mass index and abdominal girth.ConclusionsThe results are consistent with the concept of an aetiological heterogeneity for hypertension and may explain previously reported inconsistent findings on the association of insulin with incident hypertension.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveTo determine plasma levels of the endogenous bufodienolide Na+/K+ATPase inhibitor, marinobufagenin-like factor (MBG), in normotensive pregnancy and in preeclampsia, to compare changes of MBG with that of ouabain-like compound (OLC), and to characterize the purified MBG immunoreactive factor from preeclamptic plasma.Design and methodsConsecutive sample study. The levels of MBG and OLC compounds were measured in extracted plasma by solid phase fluoroimmunoassays. MBG and ouabain immunoreactive materials were partially purified from preeclamptic plasma via reverse-phase high-performance liquid chromatography (HPLC) and studied for their ability to cross react with MBG and ouabain antibodies, and to inhibit the Na+/K+ATPase from human mesenteric arteries. Vasoconstrictor effect of authentic MBG was studied in isolated rings of human umbilical arteries.ResultsIn 11 nonpregnant control individuals, plasma concentrations of MBG and OLC were 0.190 ± 0.04 nmol/l and 0.297 ± 0.037 nmol/l, respectively. In the third trimester of noncomplicated pregnancy (n= 6), plasma MBG increased (0.625 ± 0.067 nmol/l,P< 0.05), and OLC did not (0.32 ± 0.07 nmol/l). In 15 patients with preeclampsia, plasma levels of both MBG and OLC increased dramatically (2.63 ± 0.10 nmol/l and 0.697 ± 0.16 nmol/l, respectively,P< 0.01 versus both control groups). When fractionated by reverse phase HPLC, OLC was eluted by 18% acetonitrile, and MBG by 48% acetonitrile. Serially diluted samples of MBG and OLC immunoreactive materials from HPLC fractions reacted with MBG and ouabain antibody in solid phase immunoassay in a concentration dependent fashion. Authentic MBG caused contractile responses of isolated rings of human mesenteric arteries in a concentration-dependent manner. Similarly to the authentic MBG, HPLC purified MBG immunoreactive material from preeclamptic plasma inhibited Na+/K+ATPase purified from human mesenteric artery.ConclusionsOur observations demonstrate the coexistence of two endogenous cardiotonic steroids in preeclamptic plasma, a more polar OLC and a less polar MBG-like compound. Substantial increases in plasma OLC and MBG immunoreactivity in preeclampsia, along with the vasoconstrictor properties of authentic MBG and Na+, K+ATPase inhibitory activity of human MBG immunoreactive factor, suggest, that in preeclampsia, plasma concentrations of MBG are enough to substantially inhibit the sodium pump in cardiovascular tissues, and are in accordance with the views attributing endogenous digitalis-like factors a pathogenic role in the preeclamptic hypertension.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveTo study the effects of isradipine or metoprolol on insulin sensitivity and lipid profiles as well as on blood pressure and umbilical vascular resistance in preeclamptic women in the third trimester of pregnancy.DesignA single-centre, prospective, randomized, doubleblind, double-dummy and parallel-group study.SettingHelsinki University Central Hospital, a tertiary referral centre.PatientsTwenty-four previously healthy pregnant women with normal findings in an oral glucose-tolerance test who were hospitalized for preeclampsia, of whom 17 completed the study.InterventionsBetween 29 and 39 weeks of gestation, measurements were made of insulin sensitivity (the minimal model), magnitude of proteinuria, and the fasting levels of serum uric acid, lipids and lipoproteins. Subsequently, treatment with isradipine 2.5 mg (n= 9) or metoprolol 50 mg (n= 8) twice daily was started, and these women were reinvestigated 5–7 days later. Blood pressure was recorded during 24 h by automated ambulatory blood pressure measurement. Umbilical artery resistance index was measured by Doppler ultrasound.Main outcome measuresInsulin sensitivity, uric acid, degree of proteinuria, lipids and lipoproteins, blood pressure, umbilical artery resistance index.ResultsIsradipine or metoprolol did not affect insulin sensitivity, degree of proteinuria, blood pressure, or the umbilical artery resistance index. Serum uric acid increased in both groups (P< 0.05). High-density lipoprotein2cholesterol increased 15.6% in the isradipine group (P< 0.05), but no significant changes appeared in other lipids and lipoproteins in either group.ConclusionsIn this study, short-term antihypertensive treatment with isradipine or metoprolol in preeclampsia had no detrimental effect on serum lipid and lipoprotein levels or insulin sensitivity.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveTo evaluate whether prostaglandin inhibition with the non-steroidal anti-inflammatory drug (NSAID), indomethacin (I) interacts synergistically with different doses of salt (NaCl) in elevating systolic blood pressure (SBP).Design and methodsThis randomized, placebocontrolled, double-blind, crossover study examined the interaction between NaCl and the prostaglandin inhibitor,Iin 31 healthy elderly individuals with a mean age (± SD) of 68.7 ± 5.7 years (range 61–85 years). Participants aged more than 60 years on a 140 mmol/day NaCl dose for 6 weeks were chosen with normal blood pressure [24-h SBP < 148 mmHg, diastolic blood pressure (DBP) < 85 mmHg on the Takeda Ambulatory Blood Pressure Monitor (TABPM);n= 15] and isolated systolic hypertension (ISH), [24-h SBP >148 mmHg, 24-h DBP < 85 mmHg on TABPM;n= 16]. Exclusion criteria included uncontrolled hypertension (SBP >220 mmHg and/or DBP >110 mmHg), cardiac disease, creatinine clearance < 60 ml/min, dementia and recent cerebrovascular accident or secondary hypertension. A 2 ± 2 Latin square design was structured using four treatment groups [low salt (NaCl = 90 mmol/day) +Iplacebo, high salt (NaCl = 240 mmol/day) +Iplacebo, low salt +I(25 mg three times daily) and high salt +I] for 2 weeks each, balanced and interspersed with 2 week washout periods to minimize carryover effects. Twentyfour hour SBP, DBP and heart rate were measured and summarized using a moving interval averaging technique. The mean change in 24-h SBP, DBP, heart rate, urinary Na+, K+, protein and creatinine, creatinine clearance and serum electrolytes were compared across treatments in the total cohort and in ISH and control groups separately using ANCOVA (SAS).ResultsIn the total cohort, compared with low NaCl, chronic high NaCl increased mean SBP (5.76 mmHg;P= 0.0002) and DBP (3.36 mmHg;P= 0.002). Indomethacin significantly increased mean SBP (2.66 mmHg,P= 0.015) but not DBP (0.31 mmHg,P= 0.419). High salt andIwere additive (SBP↑, DBP↑) but there was no interaction (P= 0.795 andP= 0.739, respectively). Additionally, chronic high NaCl increased serum Na (P= 0.0001) and 24-h urinary Na (P= 0.0001) as expected. Indomethacin significantly decreased mean heart rate (P= 0.018). The effects of NaCl andIon SBP, DBP and heart rate were not modified by age, alcohol intake, serum K+, body mass index or treatment order. In the ISH group, NaCl dose significantly elevated SBP (9.87 mmHg;P= 0.0001) and DBP (5.26 mmHg,P= 0.006) but did not significantly alter blood pressure in the normotensive group. Indomethacin significantly elevated SBP (P= 0.03) in normotensive individuals but had no effect on blood pressure in the ISH group.ConclusionsChronic high salt diet elevated blood pressure more thanIin the total cohort of elderly individuals. No interaction was demonstrated and their effects were additive. In the ISH group, chronic high salt diet significantly increased SBP and DBP whileIfailed to alter blood pressure. In the normotensive group,I, but not salt, elevated SBP. Patients with ISH are sensitive to the pressor effect of NaCl but resistant to the pressor effect of prostaglandin inhibition in contrast to elderly normotensive control individuals where the reverse was found.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID