Biomedical subjects

Francesco Scopelliti

Publications and source records attributed to Francesco Scopelliti.

5 recordsLinked to original sources

PubMed2007

Excessive sympathetic activation in heart failure with obesity and metabolic syndrome: characteristics and mechanisms.

Congestive 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.

Aged↗

PubMed2006

Angiotensin-sympathetic system interactions in cardiovascular and metabolic disease.

BACKGROUND: Blood pressure, as well as blood volume homeostasis, depends to a large extent on humoral influences stemming from the renin-angiotensin axis and the sympathetic nervous system. Evidence has been provided that a large part of this homeostatic modulation is effected by the complex interactions between the two systems. OBJECTIVES: The present review will focus on three major issues. First it will examine the physiological and pathophysiological relevance of angiotensin-sympathetic crosstalk discussing possible sites, mechanisms and effects of the interaction. It will then address the clinical relevance of these inter-relationships by reviewing data collected in cardiovascular and non-cardiovascular diseases. Finally, the influences of angiotensin II on adrenergic function will be examined as possible targets of cardiovascular drug treatment. CONCLUSIONS: By interrupting the influences of angiotensin II on sympathetic function, therapeutic interventions aimed at blocking the renin-angiotensin system exert favourable effects on the haemodynamic, metabolic and renal profile. This has important implications for the treatment of hypertension, congestive heart failure, renal insufficiency and metabolic syndrome.

Angiotensin II↗

PubMed2006

Hypertension and the heart.

The interactions linking high blood pressure with hypertensive heart disease are reciprocal. Hypertension can be regarded as a source of adverse effects on myocardial structure and function by favoring the development and progression of left ventricular hypertrophy and of left ventricular dysfunction and failure in the advanced phases of the disease. Conversely, the heart can be regarded as a source of reflex influences on the cardiovascular system, which appear to be deranged in the hypertensive state. The clinical relevance of this reflex dysfunction is based on the evidence that these alterations may favor the occurrence of an increased sympathetic vasoconstrictor drive, thereby promoting the development of the1 hypertensive state. Both phenomena have important clinic and therapeutic implications potentiating the cardiovascular risk profile of the hypertensive patient.

Antihypertensive Agents↗

PubMed2003

Comparative effects of candesartan and hydrochlorothiazide on blood pressure, insulin sensitivity, and sympathetic drive in obese hypertensive individuals: results of the CROSS study.

OBJECTIVE: The increase in blood pressure that accompanies the obese state is almost invariably associated with alterations in metabolism (insulin resistance and dyslipidaemia) and the neurohumoral profile (activation of the renin-angiotensin system, sympathetic overactivity), which potentiate the cardiovascular risk associated with hypertension. However, debate remains as to the antihypertensive drug on which treatment of obesity-related hypertension should be based. The CROSS (Candesartan Role on Obesity and on Sympathetic System) study was undertaken to examine the antihypertensive, neuroadrenergic, and metabolic effects of an angiotensin II receptor blocker in comparison with a diuretic in obese hypertensive individuals. METHODS: In 127 obese hypertensive individuals aged 50.7 +/- 5.1 years (mean +/- SD), we measured clinic blood pressure, heart rate, plasma glucose, and insulin at rest and during an oral glucose load before and 12 weeks after treatment with either candesartan cilexetil (8-16 mg once daily) or hydrochlorothiazide (HCTZ, 25-50 mg once daily), administered orally in accordance with a double-blind, randomized, placebo-controlled, two-parallel-groups study design. Insulin sensitivity was expressed as insulin resistance index (IRI), calculated as the ratio of the area under the curve (AUC) for glucose to that for insulin. In a subgroup of patients, measurements also included direct microneurographic recording of muscle sympathetic nerve activity (MSNA) in the peroneal nerve. RESULTS: Candesartan cilexetil caused a significant (P < 0.01) reduction in both mean blood pressure (from 114.2 +/- 5.1 to 99.6 +/- 6.0 mmHg) and MSNA (from 51.0 +/- 12.3 to 40.4 +/- 12.5 bursts per 100 heart beats), and a significant (P < 0.02) increase in insulin sensitivity (AUC IRI: from -23.2 +/- 22.1 to -17.6 +/- 12.2). In contrast, HCTZ did not significantly affect MSNA and worsened insulin sensitivity, while achieving blood pressure reductions similar to those produced by candesartan cilexetil. CONCLUSIONS: These data provide evidence that, in obese hypertensive individuals, treatment with candesartan cilexetil has an antihypertensive effect similar to that of HCTZ. Unlike diuretic treatment, however, treatment with candesartan cilexetil improves insulin sensitivity and exerts sympathoinhibitory effects.

Adolescent↗

PubMedDate not supplied

Baroreflex function in hypertension: consequences for antihypertensive therapy.

Studies performed in experimental animal models of hypertension as well as in human hypertension have unequivocally shown that reflex cardiovascular control undergoes profound changes with high blood pressure and participates throughout direct and indirect mechanisms at the development and progression of hypertension-related target organ damage. This explains why investigation of the effects of antihypertensive drugs on neural cardiovascular control has a significant impact on hypertension treatment. This review will examine the main features of cardiovascular reflex control in hypertension and the effects of the different classes of antihypertensive drugs in uncomplicated and complicated hypertension.

Antihypertensive Agents↗