Thus, independently of which BP the diagnosis is based, high-normal BP is a condition characterized by a sympathetic activation. This neurogenic alteration, which is likely to be triggered by metabolic rather than reflex alterations, might be involved, together with other factors, in the progression of the condition to established hypertension.
These data provide the first evidence that the blunted pressor and tachicardic responses to nurse's blood pressure measurements are accompanied by an attenuation of the adrenergic neural responses seen during the alerting reaction accompanying doctor's blood pressure measurement.
These data provide the first evidence that in OSA, the adrenergic overdrive seen in the muscle circulation is not detected in cutaneous circulation and thus it cannot be regarded as a generalized phenomenon affecting the whole cardiovascular system. Further studies are needed to clarify whether in OSA, sympathetic drive of other vascular districts, such as the coronary, renal or cerebral circulation, is activated or normal.
Several studies have investigated the behavior of sympathetic cardiovascular drive in essential hypertension, providing conclusive evidence of the adrenergic activation characterizing this condition. These studies have also shown the importance of neuroadrenergic overdrive in the development and progression of the hypertensive state as well as in the pathogenesis of hypertension-related end-organ damage. The information available on the sympathetic nervous system's behavior in 'pseudo-resistant' and 'true resistant' hypertension is much more scarce. This paper will review the available knowledge on this issue by examining the data collected via indirect and direct approaches to investigate adrenergic function in resistant hypertension as well as the effects of pharmacological and non-pharmacological interventions.
The high-normal blood pressure (also known as prehypertension) is a clinical condition characterized by an increased cardiovascular risk as well as by the presence of target organ damage. This include an increased left ventricular mass, an endothelial dysfunction and an early renal functional and structural damage. Whether this is the case also for alterations of retinal vessels network, which are frequently detectable in established hypertension, is still largey undefined. The present paper, after discussing the main characteristics of the high-normal blood pressure state, will review the different approaches used throughout the years for assessing retinal microcirculatory network. Data collected by our group in subjects with high normal blood pressure will be also discussed, showing that arterial venular ratio values are reduced in this individuals with high-normal blood pressure and more so in established hypertension. These data indicate that retinal microvascular alterations 1) are of early appearance in the clinical course of hypertension and 2) are of frequent detection in the high-normal blood pressure state. The possible hemodynamic and non-hemodynamic mechanisms resposible for these structural alteations of the retinal microcirculation will be also discussed.
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