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    Ritmi circadiani normali e patologici della pressione arteriosa

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    Ritmi circadiani normali e patologici della pressione arterios

    Atrial natriuretic peptide and circadian blood pressure regulation: clues from a chronobiological approach

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    A critical review of the data available in the literature today permits a better understanding of the multiple actions of atrial natriuretic peptide (ANP) on the cardiovascular system. Moreover, the results of chronobiological studies suggest a role for this peptide in the determination of the circadian rhythm of blood pressure (BP). ANP can affect BP by several mechanisms, including modification of renal function and vascular tone, counteraction of the renin-angiotensin-aldosterone system, and action on brain regulatory sites. A series of interrelated events may follow from very small changes in the plasma levels of ANP. The endpoints are blood volume and BP reduction, but they are rapidly offset (mainly by reactive sympathetic activation) as soon as blood volume or pressure is threatened. The circadian rhythms of BP and ANP are antiphasic under normal conditions and in essential hypertension. The loss in the nocturnal decrease of BP is accompanied by a comparable loss in the nocturnal surge of ANP in hypertensive renal failure and hypotensive heart failure. In the latter condition, BP and ANP variabilities correlate significantly both before and after therapy-induced functional recovery, independently of the mean BP levels. Autonomic function modulates the secretion of ANP, which seems more apt to determine only transient changes in BP levels, as suggested by the short half-life of the peptide and the buffering role of its clearance receptors. There is now sufficient evidence that ANP contributes to short-term control over BP and electrolyte balance, in contrast and in opposition to the renin-angiotensin-aldosterone system, which is involved primarily in long-term BP control. By interfering with other well-established neurohormonal factors, ANP appears to be an additional modulator of the circadian rhythm of BP

    Fatal familial insomnia: a chronobiological model of secondary hypertension

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    sistematizzazione di una nuova malattia da prione che impedisce progressivamente la produzione di attività ipnic

    Effects of the converting enzyme inhibitor quinapril on autonomic function in normotensive and essential hypertensive subjects

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    The lack of reflex tachycardia observed after quinapril administration suggests some specific influence on autonomic function. Twelve healthy volunteers and 12 patients with essential hypertension were given a single oral 20-mg dose of quinapril and a single dose of matching placebo, in a double-blind crossover design. Blood pressure and heart rate were monitored noninvasively on a beat-to-beat basis for eight hours and indexes of autonomic function at the time of maximum effect were measured. Identical results were obtained in both normotensives and hypertensives. Neither the pressor nor the chronotropic responses to the isometric exercise and the cold pressor test were influenced by quinapril. During dynamic exercise the increments in heart rate and systolic blood pressure were unchanged by quinapril. In the orthostatic test quinapril did not significantly alter the heart rate ratio. Similarly, the heart rate response to deep breathing and apneic facial immersion showed no significan..

    Endocrine Mechanisms of Blood Pressure Rhythms

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    The temporal organization of blood pressure is mainly controlled by neuroendocrine mechanisms. The monoaminergic systems appear to integrate the major driving factors of temporal variability, but evidence also indicates a role of the hypothalamic-pituitary-adrenal, hypothalamic-pituitary-thyroid, opioid, renin-angiotensin-aldosterone, and endothelial systems as well as other vasoactive peptides. Although their hormonal secretions are typically episodic, the probability of secretory episodes is "gated" by mechanisms that are coupled either to sleep or to an endogenous pacemaker which usually is predominantly (though not only) circadian. Many hormones with established actions on the cardiovascular system (arginine vasopressin, vasoactive intestinal peptide, melatonin, somatotropin, insulin, steroids, serotonin, CRF, ACTH, TRH, endogenous opioids, and prostaglandin E2) are also involved in sleep induction or arousal. Hence, physical, mental, and pathologic stimuli, which may drive activation or inhibition of these neuroendocrine effectors of biologic rhythmicity, may also interfere with the temporal blood pressure structure. On the other hand, the immediate adaptation of the exogenous components of blood pressure rhythms to the demands of the environment are modulated by the circadian-time-dependent responsiveness of the biologic oscillators and their neuroendocrine effectors. These notions may contribute to a better understanding of the pathophysiology and therapeutics of changes in blood pressure

    Going Beyond Counting First Authors in Author Co-citation Analysis

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    The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed

    Circadian rhythms of blood pressure and heart rate in fatal familial insomnia

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    We documented for the first time the progressive disruption of the circadian rhythms of blood pressure and heart rate, together with the progressive loss of sleep production, in fatal familial insomnia
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