Contrasting effects of phentolamine and nitroprusside on neural and cardiovascular variability

Borne, Philippe van de; Rahnama, Mohsen; Mezzetti, Silvia; Montano, Nicola; Porta, Alberto; Degaute, Jean Paul; Somers, Virend K.

doi:10.1152/ajpheart.2001.281.2.h559

Cited by 42 publications

(30 citation statements)

References 31 publications

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“…In conditions of baroreflex unloading, such as with sodium nitroprusside, increases in sympathetic activity and R-R interval are accompanied by clear increases in LF power of these measurements (118). In the same experiment, during hypotension after ␣ 1 -selective blockade (by phentolamine), LF power in cardiovascular variability is attenuated, despite the reflex tachycardia and increased sympathetic nerve traffic, suggesting that ␣-adrenergic transmission within the baroreflex loop appears to contribute importantly to LF oscillation.…”

Section: Arterial Baroreflex and Cardiovascular Variabilitymentioning

confidence: 79%

“…An LF rhythm, which could be independent from neural inputs, has also been described in the vasomotor tone in animals as well as in humans (98,118). In conditions of baroreflex unloading, such as with sodium nitroprusside, increases in sympathetic activity and R-R interval are accompanied by clear increases in LF power of these measurements (118).…”

Section: Arterial Baroreflex and Cardiovascular Variabilitymentioning

confidence: 96%

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Arterial baroreflex function and cardiovascular variability: interactions and implications

Lanfranchi

Somers

2002

American Journal of Physiology-Regulatory, Integrative and Comp

251

183

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The arterial baroreflex contributes importantly to the short-term regulation of blood pressure and cardiovascular variability. A number of factors (including reflex, humoral, behavioral, and environmental) may influence gain and effectiveness of the baroreflex, as well as cardiovascular variability. Many central neural structures are also involved in the regulation of the cardiovascular system and contribute to the integrity of the baroreflex. Consequently, brain injuries or ischemia may induce baroreflex impairment and deranged cardiovascular variability. Baroreflex dysfunction and deranged cardiovascular variability are also common findings in cardiovascular disease. A blunted baroreflex gain and impaired heart rate variability are predictive of poor outcome in patients with heart failure and myocardial infarction and may represent an early index of autonomic activation in left ventricular dysfunction. The mechanisms mediating these relationships are not well understood and may in part be the result of cardiac structural changes and/or altered central neural processing of baroreflex signals.

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Section: Arterial Baroreflex and Cardiovascular Variabilitymentioning

confidence: 79%

Section: Arterial Baroreflex and Cardiovascular Variabilitymentioning

confidence: 96%

Arterial baroreflex function and cardiovascular variability: interactions and implications

Lanfranchi

Somers

2002

American Journal of Physiology-Regulatory, Integrative and Comp

251

183

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“…BP variability, and more specifically LF SBP , is influenced by a multitude of physiological factors (17), which in the short-term include excitatory vasoconstrictive neural mechanisms, modulatory effects of baroreflex, and local effects of the nitric oxide system (16,24,27,34). However, despite this composite origin, LF SBP is commonly considered a marker of overall sympathetic influence to the vascular system (23).…”

Section: Cardiovascular Variability and Amsmentioning

confidence: 99%

Autonomic cardiovascular regulation in subjects with acute mountain sickness

Lanfranchi¹,

Colombo²,

Cremona³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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The aims of this study were 1) to evaluate whether subjects suffering from acute mountain sickness (AMS) during exposure to high altitude have signs of autonomic dysfunction and 2) to verify whether autonomic variables at low altitude may identify subjects who are prone to develop AMS. Forty-one mountaineers were studied at 4,559-m altitude. AMS was diagnosed using the Lake Louise score, and autonomic cardiovascular function was explored using spectral analysis of R-R interval and blood pressure (BP) variability on 10-min resting recordings. Seventeen subjects (41%) had AMS. Subjects with AMS were older than those without AMS (P Ͻ 0.01). At high altitude, the lowfrequency (LF) component of systolic BP variability (LFSBP) was higher (P ϭ 0.02) and the LF component of R-R variability in normalized units (LFRRNU) was lower (P ϭ 0.001) in subjects with AMS. After 3 mo, 21 subjects (43% with AMS) repeated the evaluation at low altitude at rest and in response to a hypoxic gas mixture. LFRRNU was similar in the two groups at baseline and during hypoxia at low altitude but increased only in subjects without AMS at high altitude (P Ͻ 0.001) and did not change between low and high altitude in subjects with AMS. Conversely, LFSBP increased significantly during short-term hypoxia only in subjects with AMS, who also had higher resting BP (P Ͻ 0.05) than those without AMS. Autonomic cardiovascular dysfunction accompanies AMS. Marked LFSBP response to short-term hypoxia identifies AMS-prone subjects, supporting the potential role of an exaggerated individual chemoreflex vasoconstrictive response to hypoxia in the genesis of AMS.hypoxia; autonomic nervous system; heart rate; blood pressure ACUTE MOUNTAIN SICKNESS (AMS) is a complex syndrome characterized by headache, gastrointestinal symptoms, weakness, insomnia, and certain neurological signs, including ataxia and changes in mental status (1). It may occur in subjects ascending to Ͼ2,500 m and is reported in 53% of those at Ͼ4,000-m altitude (6,22).AMS is generally harmless and transient but may occasionally progress to the more serious life-threatening cerebral and pulmonary forms of mountain sickness, i.e., high-altitude cerebral and pulmonary edema (1, 6).The exact mechanism causing AMS is unknown, although the prevailing hypothesis points to a process within the central nervous system (1), possibly an altered adaptation to the neurohumoral and hemodynamic adjustments during hypoxia (8). A marked increase in peripheral sympathetic activity is a common feature of mountain sickness (4, 11) and has also been suggested to contribute to the genesis of high-altitude pulmonary edema (4). Whether autonomic hyperactivation may play a role in the genesis of AMS is not known.The autonomic nervous system plays a role in the modulation of the oscillatory behavior of the cardiovascular system (23, 32a). Spectral analysis of variability in the R-R interval is a recognized tool that allows quantification of the oscillatory components, which in short-term recordings appear mainly organized...

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“…4,18 During reflexly induced sympathetic activation, SNA oscillations at Mayer wave's frequency are amplified when the baroreceptor reflex is normally functioning. 9,19 After acute administration of the ␣-adrenoceptor blockade, phentolamine, the baroreceptor reflex loop is opened at the vascular neuroeffector junction, and the reflex sympathetic activation occurring in response to the decrease in AP is not accompanied by a parallel increase in the amplitude of SNA oscillations at Mayer wave's frequency. On the contrary, these oscillations are strongly attenuated or even abolished, 19,20 which further favors a major role of the baroreceptor reflex in their production.…”

mentioning

confidence: 99%

“…9,19 After acute administration of the ␣-adrenoceptor blockade, phentolamine, the baroreceptor reflex loop is opened at the vascular neuroeffector junction, and the reflex sympathetic activation occurring in response to the decrease in AP is not accompanied by a parallel increase in the amplitude of SNA oscillations at Mayer wave's frequency. On the contrary, these oscillations are strongly attenuated or even abolished, 19,20 which further favors a major role of the baroreceptor reflex in their production. During centrally induced sympathetic activation, it is not known whether the amplification of SNA oscillations at Mayer wave's frequency requires the functional integrity of the baroreceptor reflex.…”

mentioning

confidence: 99%

Steady-State and Dynamic Responses of Renal Sympathetic Nerve Activity to Air-Jet Stress in Sinoaortic Denervated Rats

2004

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Abstract-This study examined the role of arterial baroreceptors in mediating the relationship between changes in the mean level and the amplitude of slow oscillations of renal sympathetic nerve activity (RSNA) during environmental stress. In 7 sham-operated (control) and 7 chronically (2 weeks before study) sinoaortic baroreceptor denervated (SAD) conscious rats, arterial pressure (AP) and RSNA were simultaneously recorded during two 15-minute periods, before and during the application of a mild environmental stressor (jet of air). Air-jet stress induced a similar degree of sympathoexcitation in both groups of rats. During stress in control rats, AP and RSNA spectral power in the mid-frequency (MF) range (0.27 to 0.74 Hz) increased, mainly as a consequence of an amplification of strongly coherent oscillations of Ϸ0.4 Hz frequency. In SAD rats, MF fluctuations of AP and RSNA were reduced but not abolished before stress, tended to increase during stress, and were linearly related under both experimental conditions. However, in the MF range, there was no well-defined oscillation at any specific frequency. At the peak coherence frequency (Ϸ0.4 Hz), the gain of the transfer function from RSNA to AP did not change during stress in control rats and was similar to that measured in SAD rats, indicating that it mainly reflected the properties of the feedforward effect of RSNA on AP (ie, vascular reactivity). In summary, the parallelism between stress-induced changes in the mean level of RSNA and the amplitude of slow RSNA oscillations requires the functional integrity of the baroreceptor reflex, which is consistent with the hypothesis that slow AP and RSNA rhythms are resonant oscillations within the baroreceptor reflex loop.

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Contrasting effects of phentolamine and nitroprusside on neural and cardiovascular variability

Cited by 42 publications

References 31 publications

Arterial baroreflex function and cardiovascular variability: interactions and implications

Arterial baroreflex function and cardiovascular variability: interactions and implications

Autonomic cardiovascular regulation in subjects with acute mountain sickness

Steady-State and Dynamic Responses of Renal Sympathetic Nerve Activity to Air-Jet Stress in Sinoaortic Denervated Rats

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