1,721,005 research outputs found
Short versus long-term effects of different dihydropyridines on sympathetic and baroreflex function in hypertension
No full textAntihypertensive treatment with dihydropyridines may be accompanied by sympathetic activation. Data on whether this is common to all compounds and similar in the various phases of treatment are not univocal, however. In 28 untreated essential hypertensives (age, 56.4±1.8 years; mean ±SEM) finger blood pressure (BP, Finapres), heart rate (HR, ECG), plasma norepinephrine (NE, high-performance liquid chromatography), and muscle sympathetic nerve traffic (MSNA, microneurography) were measured at rest and during baroreceptor manipulation (vasoactive drugs) in the placebo run-in period and after randomization to double-blind acute and chronic (8 weeks) felodipine (10 mg/d, n = 14) or lercanidipine (10 mg/d, n = 14). Acute administration of both drugs induced pronounced BP reductions and marked increases in HR, NE, and MSNA. After 8 weeks of treatment, BP reductions were similar to those observed after acute administration, whereas HR, NE, and MSNA responses were markedly attenuated (-7%, -32%, and -14%, respectively; P<0.05). There was a small residual increase in sympathetic activity in the felodipine group, whereas in the lercanidipine group, all adrenergic markers returned to baseline values. Baroreflex control of HR and MSNA was markedly impaired (-42% and -48%, respectively) after acute drug administration, with a recovery and complete resetting during chronic treatment. Thus, the sympathoexcitation induced by 2 different dihydropyridines is largely limited to the acute administration. The 2 drugs have, nevertheless, a different chronic sympathetic effect, indicating that dihydropyridines do not homogeneously affect this function. The acute sympathoexcitation, but not the small between-drugs differential chronic adrenergic effect, is accounted for by baroreflex impairment
Neural mechanisms in hypertension and the elderly
No full textExperimental animal studies carried out over the past 40 years have unequivocally shown that neurogenic mechanisms are involved in the pathogenesis of hypertension. The results of these studies also suggest that neural factors are important not only in the development but also in the maintenance of the high blood pressure condition. Whether this is the case also for human hypertension has been matter of debate for several decades. However, recent studies in man by employing sophisticated techniques for assessing sympathetic tone, i.e. the norepinephrine radiolabelled technique and microneurographic recording of sympathetic nerve traffic, support the hypothesis that alterations in sympathetic modulation of the cardiovascular system take place in hypertension and may have a pathogenetic relevance in age-related blood pressure increase
Response to sympathetic activity, heart failure, obesity, and metabolic syndrome : is there any role for sleep apnea?
No full textExcessive sympathetic activation in heart failure with obesity and metabolic syndrome : characteristics and mechanisms
No full textCongestive heart failure is characterized by sympathetic activation, which has also been described in the metabolic syndrome. No information exists, however, as to whether the sympathostimulating effects of these 2 conditions summate when heart failure is complicated by the metabolic syndrome, leading to an exceedingly high adrenergic drive. This is clinically relevant, because in heart failure sympathetic activation is closely related to mortality. We studied 48 control subjects (age: 58.4 +/- 1.6 years, mean +/- SEM) and 89 age-matched heart failure patients (New York Heart Association class II), of whom 47 were without and 42 were with metabolic syndrome. Measurements included blood pressure (Finapres), heart rate (ECG), and sympathetic nerve traffic (microneurography) at rest and during baroreceptor manipulation. Waist circumference, blood pressure, and metabolic variables were greater in heart failure with metabolic syndrome than in heart failure without metabolic syndrome and in control subjects. Left ventricular ejection fraction and end-diastolic diameter were similarly altered in the 2 heart failure groups. Compared with control subjects, sympathetic nerve activity was greater in heart failure patients without metabolic syndrome (64.7 +/- 3.2 versus 45.8 +/- 2.9 bursts/100 heartbeats; P < 0.01), a further pronounced increase being detected in those with metabolic syndrome (80.9 +/- 3.2 bursts/100 heartbeats; P < 0.01). In the multivariate analysis, waist circumference and body mass index were the variables most closely related to sympathetic activation. Compared with control subjects, baroreflex responses were significantly attenuated in the 2 heart failure groups, the impairment being more marked in the group with than without metabolic syndrome. Thus, obesity and metabolic syndrome potentiate the sympathetic activation characterizing heart failure. This potentiation is likely to mainly depend on metabolic and baroreflex mechanisms
Effect of chronic angiotensin converting enzyme inhibition on sympathetic nerve traffic and baroreflex control of the circulation in essential hypertension
No full textHuman studies have shown that the blood pressure lowering effects of angiotensin converting enzyme inhibitors are accompanied by a reduction in plasma norepinephrine levels. Whether this is due to central or peripheral mechanisms is unknown, however
Sympathetic activation in congestive heart failure : Reproducibility of neuroadrenergic markers
No full textObjective: To assess the reproducibility of the two markers of adrenergic drive, venous plasma norepinephrine (NE) and efferent postganglionic muscle sympathetic nerve activity (MSNA), in reflecting the sympathetic activation characterizing congestive heart failure (CHF).
Methods and measurements: In 19 CHF male normotensive patients (mean age: 53.0 +/- 2.1 years, NYHA classes II and III, left ventricular ejection fraction 35.9 +/- 2.9%), blood pressure (BP, Finapres), heart rate (EKG), plasma NE (HPLC assay) and MSNA (microneurography, peroneal nerve) were measured in two experimental sessions separated by a week interval. At each session, three NE samples were obtained and NE reproducibility between sessions was assessed by considering single NE samples or averaging 2-3 samples.
Results: While MSNA values showed a highly significant correlation between sessions (r = 0.85, P < 0.001), NE values based on a single blood sample evaluation did not correlate with each other (r = 0.41, P = NS). NE correlation coefficients improved and achieved statistical significance when average data from 2 and 3 blood samples were examined (r = 0.54 and r = 0.57, P < 0.02 for both).
Conclusions: In CHF, MSNA displays a better reproducibility pattern than plasma NE. The reproducibility of the NE approach, however, can be improved by performing the assay on multiple blood samples. (C) 2008 European Society of Cardiology
Effects of hypertension and obesityon the sympathetic activation of heart failure patients
No full textPrevious studies have shown that congestive heart failure is characterized by sympathetic and reflex dysfunctions. Whether these alterations are potentiated in the presence of obesity and hypertension, two conditions that also display neuroadrenergic abnormalities and markedly increase the risk of heart failure, is unknown. In 14 healthy control subjects (C; age, 55.1±3.0 years; mean±SEM), 13 lean hypertensive subjects (H), 15 obese normotensive subjects (O), 14 lean normotensive subjects with congestive heart failure (CHF, New York Heart Association class II), 14 lean hypertensive subjects with CHF (CHFH), 14 obese normotensive subjects with CHF (CHFO), and 13 obese hypertensive subjects with CHF (CHFOH), all age-matched with C, we measured mean blood pressure (Finapres), heart rate (ECG), and muscle sympathetic nerve traffic (MSNA, microneurography) at rest and during baroreflex testing. Compared with C, body mass index was similarly increased in O, CHFO, and CHFOH, whereas mean blood pressure was similarly increased in HF, CHFH, and CHFOH, and left ventricular ejection fraction (echocardiography) was similarly reduced in CHF, CHFH, CHFO and CHFOH. Compared with C, MSNA was significantly increased in O, H, and CHF (43.0±2.2 versus 54.1±2.8, 53.1±2.5, and 57.4±2.8 bursts/100 heart beats, P<0.01). When O or H was combined with CHF, the MSNA increase was significantly more pronounced and maximal when O and H were concomitantly associated with CHF. Baroreflex sensitivity was reduced in O and H, with a further reduction in CHF and a minimal value in CHFOH. These data show that the sympathetic activation characterizing CHF is markedly potentiated when O and H alone or combined together are associated with a low cardiac output state and that this may depend on an arterial baroreflex impairment
Heart rate as a sympathetic marker during acute adrenergic challenge
No full textObjective: Previous studies have shown that heart rate has a limited value in reflecting the chronic state of adrenergic overdrive characterizing several cardiovascular diseases. Whether this also applies to the ability of heart rate to reflect acute and generalized changes in sympathetic activity is unknown.
Methods: In 20 healthy young subjects (age: 25.2 ± 1.2 years, mean ± SEM) we measured beat-to-beat blood pressure (Finapres), heart rate (HR, ECG), venous plasma norepinephrine (NE, high-performance liquid chromatography) and efferent postganglionic muscle sympathetic nerve traffic (MSNA, microneurography) at rest and during a cold pressor test and two intravenous infusions of nitroprusside at increasing doses.
Results: Both cold pressor test and nitroprusside infusions triggered marked and significant increases in HR, plasma NE and MSNA; blood pressure showing an increase with cold pressor test and a reduction with nitroprusside. The magnitude of the responses was greater with the higher than with the lower dose of nitroprusside. The HR changes induced by cold pressor test were not significantly related to the concomitant NE and MSNA changes (r = -0.08 and r = -0.18, P = NS). This was also the case for the lower and the higher dose of nitroprusside (NE: r = -0.11 and r = 0.08; MSNA: r = 0.01 and r = -0.11, P = NS for all). In contrast NE and MSNA changes induced by cold pressor test and by the lower and the higher dose of nitroprusside were significantly related to each other (r = 0.70, r = 0.89 and r = 0.79 respectively, P < 0.01 for all).
Conclusions: In a given individual, HR responses to sympathetic challenge do not quantitatively reflect the degree of acute and generalized adrenergic activation. Qualitative information on the acute adrenergic effects of given stimuli should thus be based on the assessment of NE and MSNA rather than on HR changes
Behaviour of regional adrenergic outflow in mild-to-moderate renal failure
No full textOBJECTIVES: Chronic renal failure is characterized by a marked sympathetic activation. No information exists, however, as to whether the adrenergic overdrive is confined to selected vascular districts or is rather generalized to the whole cardiovascular system. METHODS: In 15 patients aged 60.5 ± 2.0 years (mean ± SEM) with stable chronic renal failure belonging to stage 2-3 of the Kidney Foundation classification and in 12 age-matched healthy controls, we measured arterial blood pressure (Finapres), heart rate (ECG), venous plasma norepinephrine (high-performance liquid chromatography) and postganglionic sympathetic nerve traffic in skeletal muscle and skin areas (microneurography). Muscle and skin nerve traffic measurements were made in a randomized sequence over two periods of 30 min each, spaced by a 20-30-min interval. Measurements also included evaluation of skin sympathetic responses to emotional stimuli. RESULTS: Muscle sympathetic nerve traffic was markedly and significantly greater in renal failure patients compared with controls (58.2 ± 3.6 vs. 36.8 ± 5.7 bursts/100 heart beats, P < 0.01), with this also being the case for plasma norepinephrine (380.6 ± 63 vs. 210.8 ± 29 pg/ml, P < 0.05). By contrast, skin sympathetic nerve traffic was superimposable in the two groups (11.5 ± 0.8 vs. 12.7 ± 1.7 bursts/minute, P = not significant), this being the case also for the responses to emotional arousal. CONCLUSION: These data provide the first evidence that the sympathetic activation characterizing renal failure is not generalized to the entire cardiovascular system. This may depend on the fact that the two sympathetic districts are governed by mechanisms that are differently affected by the chronic uraemic state
Multiple sampling improves norepinephrine reproducibility in essential hypertension : a comparison with the microneurographic technique
No full textObjectives Plasma norepinephrine displays a limited ability to reflect the enhanced sympathetic drive characterizing essential hypertension. Among the factors responsible, an important one is the reduced reproducibility of the norepinephrine approach. The present study aimed to determine whether increasing the number of blood samples on which norepinephrine assay is based improves norepinephrine reproducibility. This was done by taking muscle sympathetic nerve traffic recording as 'gold standard', which is characterized by an elevated short- and long-term reproducibility.
Methods In 14 untreated mild-to-moderate essential hypertensive patients, we evaluated, in two experimental sessions spaced each other by a 10-14-day interval, blood pressure (Finapres), heart rate (ECG), plasma norepinephrine (HPLC) and muscle sympathetic nerve traffic (microneurography, peroneal nerve). In the two sessions, three norepinephrine samples were obtained at 30-min intervals between each. Norepinephrine reproducibility between sessions was assessed on a single norepinephrine sample or averaging together the values obtained from second or third samples. Reproducibility of norepinephrine data was then compared with the microneurographic one.
Results Although muscle sympathetic nerve traffic values showed a highly significant correlation between sessions (r=0.79, P < 0.001), norepinephrine values derived from a single blood sample did not correlate with each other (r=0.42, PUNS). Norepinephrine correlation coefficients were consistently improved and achieved statistical significance when average data from second or third blood samples were examined (r=0.63, P < 0.03).
Conclusion In essential hypertension, the reproducibility of plasma norepinephrine as an adrenergic marker can be substantially improved by performing a norepinephrine assay on multiple blood samples
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