Sympathetic nerve traffic and baroreflex function in optimal, normal, and high-normal blood pressure states.

OBJECTIVE: Adrenergic activation and baroreflex dysfunction are common in established essential hypertension, elderly hypertension, masked and white-coat hypertension, resistant hypertension, and obesity-related hypertension. Whether this autonomic behavior is peculiar to established hypertension or is also detectable in the earlier clinical phases of the disease, that is, the high-normal blood pressure (BP) state, is still largely undefined, however. METHODS: In 24 individuals with optimal BP (age: 37.1  ±  2.1 years, mean  ±  SEM) and in 27 with normal BP and 38 with high-normal BP, age matched with optimal BP, we measured clinic, 24-h and beat-to-beat BP, heart rate (HR), and muscle sympathetic nerve activity (MSNA) at rest and during baroreceptor stimulation and deactivation. Measurements also included anthropometric as well as echocardiographic and homeostasis model assessment (HOMA) index. RESULTS: For similar anthropometric values, clinic, 24-h ambulatory, and beat-to-beat BPs were significantly greater in normal BP than in optimal BP. This was the case when the high-normal BP group was compared to the normal and optimal BP groups. MSNA (but not HR) was also significantly greater in high-normal BP than in normal BP and optimal BP (51.3  ±â€Š 2.0 vs. 40.3  ±  2.3 and 41.1 ±â€Š2.6  bursts per 100  heartbeats, respectively, P < 0.01). The sympathetic activation seen in high-normal BP was coupled with an impairment of baroreflex HR control (but not MSNA) and with a significant increase in HOMA Index, which showed a significant direct relationship with MSNA. CONCLUSION: 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.

Neuroadrenergic disarray in pseudo-resistant and resistant hypertension.

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.

Regional differences in sympathetic activation in lean and obese normotensive individuals with obstructive sleep apnoea.

OBJECTIVE: Obstructive sleep apnoea (OSA) is characterized by a marked sympathetic overdrive, as documented by the elevated sympathetic nerve firing rate detected in peripheral muscle nerves. No data are available, however, on the behaviour of sympathetic drive in vascular regional districts other than the muscle circulation. DESIGN AND METHODS: In 66 middle-aged normotensive individuals classified according to BMI, waist-to-hip ratio and apnoea-hypopnea index as lean individuals without (n = 20) or with (n = 14) OSA and as obese individuals without (n = 13) or with (n = 19) OSA, we measured blood pressure, heart rate, muscle sympathetic nerve activity (MSNA) and skin sympathetic nerve activity (SSNA), respectively, via microneurography. Measurements also included SSNA responses to an emotional stimulus. RESULTS: The four groups were matched for age, sex and blood pressure values. Both in lean and obese individuals, presence of OSA was accompanied by MSNA values significantly greater than those found in non-OSA individuals. In contrast, no significant difference was found in SSNA values between OSA and non-OSA patients both in the lean and in the obese groups. This was the case also for the SSNA responses to an emotional arousal. CONCLUSION: 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.

Muscle and skin sympathetic nerve traffic during physician and nurse blood pressure measurement.

OBJECTIVE: Previous studies have shown that blood pressure assessment by a nurse markedly attenuates the pressor and tachicardic responses triggered by the physician blood pressure measurement. Whether and to what extent this attenuation reflects a different pattern of the neuroadrenergic responses to doctor or nurse blood pressure evaluation is unknown. METHODS: In 19 lean untreated mild essential hypertensive patients (age 39.1 ±â€Š2.4 years, mean ±â€ŠSEM), we measured beat-to-beat mean arterial pressure (Finapres), heart rate (ECG), and efferent postganglionic muscle and skin sympathetic nerve traffic [muscle sympathetic nerve activity (MSNA) and skin sympathetic nerve activity (SSNA), respectively, by microneurography], before, during, and following a 10-min sphygmomanometric BP measurement by a doctor or by a nurse unfamiliar to the patients. Measurements were repeated at a 30-min interval to obtain, in separate periods, muscle and skin sympathetic nerve traffic recordings. Both the sequences (doctor vs. nurse and muscle vs. skin sympathetic nerve traffic) were randomized. RESULTS: A doctor visit induced sudden, marked, and prolonged blood pressure and heart rate increases, accompanied by a muscle sympathetic nerve traffic inhibition (average response: -18.1 ±â€Š4.3%, P < 0.01) coupled with a skin sympathetic nerve traffic excitation (average response: +46.1 ±â€Š5.5%, P < 0.01). In contrast, a nurse visit elicited blood pressure and heart rate responses markedly and significantly reduced (-72.1 ±â€Š11 and -81.7 ±â€Š13% respectively, P < 0.01) as compared with those seen during the doctor's visit. This was the case also for muscle and skin sympathetic neural responses (-44.3 ±â€Š9 and -65.6 ±â€Š13%, P < 0.01). CONCLUSION: 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.

Structural alterations of the retinal microcirculation in the "prehypertensive" high- normal blood pressure state.

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.