ISSN:0263-6352    

出版商:OVID    

年代:2000

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

Arterial baroreflex function in humans is commonly assessed through a number of laboratory tests based on quantification of the reflex responses in heart rate or blood pressure to external stimuli applied to the cardiovascular system. Evidence is available that these laboratory estimates of baroreflex sensitivity have both pathophysiological and clinical relevance. Indeed, a number of studies have shown that the sensitivity of the baroreceptor–heart rate reflex may have a prognostic value in myocardial infarction, heart failure and diabetic patients, where mortality seems to be inversely related to the sensitivity of cardiac baroreflex modulation. A deeper insight into the features of daily-life baroreflex cardiovascular control has been offered more recently by techniques based on computer analysis of spontaneous blood pressure and heart rate fluctuations. This innovative approach allows spontaneous baroreflex sensitivity to be assessed in real life conditions, with no need for external stimulation of the patient as required by the older laboratory techniques. This review will briefly survey the methods most widely used to assess baroreflex function in humans, in the laboratory and in daily life.

ISSN:0263-6352    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

ObjectiveThe circadian rhythm of blood pressure in patients with aldosterone-producing adenoma (APA) is not well understood. We evaluated the circadian blood pressure rhythm in such patients by comparison with that in patients with essential hypertension (EHT). The latter are characterized by a nocturnal blood pressure decline, the so called ‘dipping’ blood pressure pattern.Design and methodsA total of 12 patients with APA and 36 patients with EHT who were matched by age and sex, and who had no severe organic disorders, were hospitalized to control their diet (low sodium) and activities. Ambulatory blood pressure monitoring was conducted for 24 h. The 24-h blood pressure was divided into waking blood pressure (0600–2130 h) and sleeping blood pressure (2200–0530 h).ResultsThe two groups showed no significant differences in age, sex, serum creatinine, plasma glucose, daily urinary sodium excretion, and left ventricular mass index. Although the 24-h mean blood pressure was higher in APA (112 ± 8 mmHg) than EHT (102 ± 12 mmHg), the dipping mean blood pressure ratio (%), which was calculated from the sleeping and waking blood pressures, did not differ significantly between the two groups (93.2 ± 5.4 versus 92.8 ± 5.9).ConclusionThe dipping ratio of blood pressure in patients with APA resembled that of patients with EHT. Variables that would influence the circadian rhythm of blood pressure were controlled during study. The results suggest that a circadian blood pressure in patients with APA is of the dipping type, characterized by a nocturnal blood pressure decline, when a low sodium diet is ingested.

ISSN:0263-6352    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

ObjectiveBlood pressure changes during menopausal transition have not been studied previously using a biracial sample. We invesigated whether menopausal transition was associated with change in blood pressure in African-American or white women.Design, setting and participantsThe prospective multicenter study, the Atherosclerosis Risk In Communities (ARIC) Study (1987–95) was utilized. Included were never-users of hormone replacement therapy (3800 women, 44% of the original sample).Main outcome measureChanges in blood pressure were adjusted for baseline age and body mass index, baseline blood pressure, antihypertensive use, ARIC field center and weight change. The menopausal transition group was compared to the non-transition group, separately, by ethnicity.ResultsResults Women undergoing the menopausal transition did not differ significantly in regard to systolic blood pressure change [5.2, 95% confidence interval (CI) 4.0–6.4] from non-transitional women (4.6, 95% CI 4.0–5.2); adjustment for age, baseline systolic blood pressure and other factors did not alter this finding. Transitional women had significantly less diastolic blood pressure change (−0.5, 95% CI −1.1 to 0.2) than non-transitional women (−2.0, 95% CI −2.4 to −1.7,P= 0.000) but, after adjustment for other covariates, the result was not significant. African-American women had significantly (P= 0.003) higher systolic blood pressure change compared to white women, but this difference became non-significant (P= 0.21) after restricting the sample to women younger than 55 years of age. Interactions between menopausal transition and ethnicity were not significant, either in systolic blood pressure or diastolic blood pressure change.ConclusionMenopausal transition is not associated with significant blood pressure change in African-American or white women.

ISSN:0263-6352    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

ObjectivesTo compare the effects of a highly β1-selective adrenoceptor antagonist bisoprolol with those of atenolol and placebo on endurance exercise capacity in young, healthy male volunteers.DesignTwelve subjects randomly received oral placebo, atenolol (100 mg/day) or bisoprolol (10 mg/day) for 3 weeks, following a double-blind cross-over design.MethodsAt the end of each period, the subects performed an endurance exercise test on the bicycle ergometer at 70% of maximal aerobic power. Cardiac output was measured by means of an automated CO2-rebreathing method. Venous blood was sampled before, during and after exercise.ResultsExercise duration was not significantly different between the two drugs tested. Total exercise duration was significantly reduced by bisoprolol (−19.4 ± 6.7%,P< 0.01) (mean ± SEM) and by atenolol (−29.8 ± 6.6%,P< 0.001), compared with placebo. Atenolol and bisoprolol were equally effective in lowering resting plasma renin activity, heart rate and systolic blood pressure. Resting and exercise stroke volume were significantly increased by both drugs, so that cardiac output was not significantly affected. Both drugs induced significant decreases in plasma-free fatty acid concentrations during recovery and blunted the exercise-induced increase. There were no significant relationships between the reduction of exercise duration and the haemodynamic changes or the degree of impairment of the exercise-induced increase in free fatty acid release resulting from β-blockade.ConclusionsIt is concluded that both drugs affect endurance exercise capacity in young, normotensive men, with a tendency to a smaller reduction during bisoprolol treatment. Haemodynamic variables are unlikely to be involved in the reduction of endurance exercise capacity. The role of the reduced availability of plasma free fatty acids remains unclear.

ISSN:0263-6352    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

ObjectiveEpidemiological studies indicate that a reduced birth weight and enlarged placenta increase the likelihood of human cardiovascular disease later in life. The relative importance of fetal versus maternal factors in these phenomena is not known. To assess the relative role of genotypic versus environmental factors in this effect, we examined whether the altered fetal and placental growth rates and amniotic fluid volume of spontaneously hypertensive rat (SHR) fetuses of the Okamoto strain, are modified by gestation in normotensive Wistar–Kyoto (WKY) rat mothers and vice versa.DesignOne-day-old SHR embryos were gestated for 16 days in either SHR or WKY recipients. Similarly, 1-day-old WKY rat embryos were gestated for 16 days in either SHR or WKY surrogates. At 16 days, fetal and placental weights were recorded. Paternal and maternal donor and recipient blood pressures, maternal body weight and average litter size within the four groups were also studied.MethodsOne cell SHR and WKY embryos were harvested from timed matings and transferred to psuedopregnant mothers of the same or opposite strain. Timed matings required routine vaginal smears for the detection of proestrus and the presence of sperm following overnight matings. Harvested embryos were temporarily maintained in culture medium in a 37°C incubator until injection into the oviduct of recipients. Blood pressures were meaured using indirect, tail-cuff plethysmography and a computerized data acquisition system.ResultsSHR fetal and placental weights at 16 days gestation were significantly lower than WKY fetal and placental weights, irrespective of maternal strain. At 16 days of gestation, the fetal and placental weights of SHR fetuses gestated in WKY rat surrogate mothers (0.21 ± 0.01 g and 0.19 ± 0.01 g, respectively) were not significantly different from those of SHR gestated in a surrogate SHR mother (0.21 ± 0.01 g and 0.18 ± 0.01 g, respectively). Similarly, the fetal and placental weights of WKY fetuses gestated in a WKY rat (0.27 ± 0.01 g and 0.25 ± 0.01 g, respectively) were unaltered by gestation in a SHR recipient (0.25 ± 0.01 g and 0.23 ± 0.01 g, respectively). The amniotic fluid volumes of SHR gestated in WKY rats and those of WKY fetuses gestated in SHR were not significantly different to each other (0.37 ± 0.01 ml versus 0.38 ± 0.01 ml, respectively) and were intermediate between the values for SHR and WKY fetuses gestated in a mother of the same strain (0.34 ± 0.01 ml versus 0.44 ± 0.02 ml, respectively).ConclusionThe SHR fetus exhibited reduced growth rate and placental size irrespective of maternal surrogate strain, suggesting that these measures are likely to be determined by the fetus or the placenta and, presumably, are independent of maternal blood pressure or altered electrolyte and hormonal milieu.

ISSN:0263-6352    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

ObjectiveNitric oxide (NO) may contribute to the actions of angiotensin converting enzyme (ACE) inhibitors. In contrast, angiotensin type 1 (AT1) receptor blockers (AT1B) have been considered to act exclusively by inhibiting angiotensin II actions. However, recent experimental findings suggest that AT1B actions may be also partly mediated by NO. In this study, we explored whether ACE inhibitors and AT1B modulate hemodynamic responses to L-arginine (L-arg), a NO precursor.MethodsSystemic (Finapres) and renal hemodynamic responses to L-arg (200 mg/kg body weight), associated with markers of systemic and renal NO production, were assessed before (control) and after 3 weeks of randomized pretreatment with the ACE inhibitor ramipril (5 mg/day for 3 weeks) or the AT1B losartan (50 mg/day for 3 weeks) in nine healthy male subjects (33 ± 2 years; body mass index 25.5 ± 0.5 kg/m2).ResultsControl L-arg did not influence mean arterial pressure (MAP) (92 ± 5 versus 90 ± 5 mmHg; not significant). In contrast, L-arg decreased MAP when administered after pretreatment with ramipril (89 ± 5 versus 83 ± 4 mmHg;P< 0.01) or losartan (90 ± 44 versus 86 ± 4;P< 0.05). Control L-arg infusion had no effect on renal plasma flow (RPF) (paraminohippuric acid clearance) and renal vascular resistance (RVR), whereas the glomerular filtration rate (GFR) (inulin clearance) decreased (98 ± 4 versus 89 ± 5 ml/min;P< 0.05), resulting in a decrease in filtration fraction (P< 0.05). After ramipril, L-arg induced renal vasodilation as indicated by significant changes in RPF (576 ± 41 versus 669 ± 21 ml/min;P< 0.01) and RVR (P< 0.05). The GFR did not change statistically after ramipril pretreatment (91 ± 3 versus 97 ± 4 ml/min; not significant); however, the trend was different as compared with control (F= 5.7,P< 0.05). L-Arg-induced renal vasodilation was also observed after losartan (RPF, 637 ± 34 versus 706 ± 40 ml/min;P< 0.05). Enhanced renal and systemic responses to L-arg after ACE inhibitor and AT1B were associated with a rise in plasma L-citrulline levels, which was greater than after control L-arg (P< 0.05). However, other indicators of NO activity such as plasma and urinary cyclic guanosine 3′,5′-monophosphate, and nitrates, remained unchanged throughout all experiments.ConclusionThe results indicate that ACE inhibitors and AT1B have a potential to enhance L-arg-induced vasodilation both in systemic and renal vascular beds. However, these hemodynamic responses were not associated with convincing changes in indicators of systemic or renal NO activity, suggesting a contribution of NO-independent vasodilator mechanisms.

ISSN:0263-6352    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

ObjectiveAdrenomedullin inhibits angiotensin II stimulated aldosterone productionin vitroandin vivoin experimental animals. The aim of this study was to investigate the effect of adrenomedullin on angiotensin II and adrenocorticotrophic hormone-stimulated aldosterone productionin vivoin healthy humans.Design and MethodsSeven volunteers were studied in a quiet, temperature-controlled laboratory. After 35 min of rest, an infusion of placebo or adrenomedullin (3 pmol/kg per min) was given over 60 min; 15 min after starting this first infusion, a second infusion of angiotensin II (0.96 fmol/kg per min) or adrenocorticotrophic hormone (0.1 mIU/kg per min) was co-infused and continued for 45 min.ResultsAdrenomedullin significantly inhibited angiotensin II stimulated aldosterone production: the increment in aldosterone on the placebo day was 691 pmol/l compared with 552 pmol/l on the adrenomedullin day (P < 0.004). Adrenomedullin did not inhibit adrenocorticotrophic hormone-stimulated aldosterone or cortisol release.ConclusionAdrenomedullin selectively inhibits angiotensin II-stimulated aldosterone production.

ISSN:0263-6352    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

ObjectiveTo determine the relative importance of the cardiac and vascular sympathetic components of the orthostatic response to 90° head-up tilt after N-type calcium-channel blockade in normotensive (sham renal cellophane wrap) and hypertensive (renal wrap) conscious rabbits.MethodsThe effects of N-type calcium-channel blockade with ω-conotoxin GVIA (ω-CTX, 10 μg/kg i.v. bolus) were assessed in the absence or presence of cardiac block by propranolol and methscopolamine. These were contrasted with the effects of α1-adrenoceptor antagonism (prazosin 0.5 mg/kg i.v. bolus, in the presence of cardiac block) or ganglion blockade (mecamylamine 4 mg/kg i.v. bolus).ResultsIn vehicle (0.9% saline) treatment groups, the response to tilt consisted of a small pressor effect (4 ± 2 and 7 ± 1 mmHg) and tachycardia (29 ± 6 and 17 ± 6 beats/min) in sham (n= 6) and wrap (n= 5) rabbits, respectively. After prazosin administration (with cardiac block), there were significant falls in MAP of 3 ± 1 and 7 ± 2 mmHg in sham (n= 7) and wrap (n= 6) rabbits, respectively, in response to tilt. ω-CTX caused postural hypotensive responses of 8 ± 2 and 13 ± 2 mmHg in sham (n= 6) and wrap (n= 7) rabbits, respectively, and 7 ± 1 and 14 ± 2 mmHg in sham (n= 7) and wrap (n= 7) rabbits with prior cardiac block. Similarly, mecamylamine caused falls in MAP of 8 ± 1 and 10 ± 2 mmHg in response to tilt in sham (n= 6) and wrap (n= 9) animals, respectively.ConclusionSympathetic vasoconstrictor effectors are primarily responsible for maintaining blood pressure during tilt in conscious rabbits. The postural hypotension caused by sympatholytic agents is about double in hypertensive rabbits, and N-type calcium-channel blockade is as effective as ganglion blockade at inducing this syndrome.

ISSN:0263-6352    

出版商:OVID    

年代:2000

数据来源: OVID