Arterial baroreflex function and cardiovascular  variability: interactions and implications

Lanfranchi, Paola; Somers, Virend K.

doi:10.1152/ajpregu.00051.2002

Cited by 248 publications

(198 citation statements)

References 120 publications

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“…Recent evidence suggests that changes in arterial baroreflex control and the autonomous nervous system are involved in the development and maintenance of hypertension. [29][30][31] In a classic study carried out in the 1960's, Bristow et al 32 reported for the first time that the baroreflex control of HR in patients with hypertension was significantly lower than that of normotensive individuals. Herein, we have observed that baroreflex sensitivity in normotensive rats is much higher than in SHRs, which supports the previous study.…”

Section: Discussionmentioning

confidence: 99%

Brain nitric oxide production by a proline-rich decapeptide from Bothrops jararaca venom improves baroreflex sensitivity of spontaneously hypertensive rats

Lameu

Pontieri

Guerreiro³

et al. 2010

Hypertens Res

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Baroreflex sensitivity is disturbed in many people with cardiovascular diseases such as hypertension. Brain deficiency of nitric oxide (NO), which is synthesized by NO synthase (NOS) in the citrulline-NO cycle (with argininosuccinate synthase (ASS) activity being the rate-limiting step), contributes to impaired baroreflex. We recently showed that a decapeptide isolated from Bothrops jararaca snake venom, denoted Bj-PRO-10c, exerts powerful and sustained antihypertensive activity. Bj-PRO-10c promoted vasodilatation dependent on the positive modulation of ASS activity and NO production in the endothelium, and also acted on the central nervous system, inducing the release of GABA and glutamate, two important neurotransmitters in the regulation of autonomic systems. We evaluated baroreflex function using the regression line obtained by the best-fit points of measured heart rate (HR) and mean arterial pressure (MAP) data from spontaneously hypertensive rats (SHRs) treated with Bj-PRO-10c. We also investigated molecular mechanisms involved in this effect, both in vitro and in vivo. Bj-PRO-10c mediated an increase in baroreflex sensitivity and a decrease in MAP and HR. The effects exerted by the peptide include an increase in the gene expression of endothelial NOS and ASS. Bj-PRO-10c-induced NO production depended on intracellular calcium fluxes and the activation of a G i/o -protein-coupled metabotropic receptor. Bj-PRO-10c induced NO production and the gene expression of ASS and endothelial NOS in the brains of SHRs, thereby improving baroreflex sensitivity. Bj-PRO-10c may reveal novel approaches for treating diseases with impaired baroreflex function. Hypertension Research (2010Research ( ) 33, 1283Research ( -1288 doi:10.1038/hr.2010 Keywords: argininosuccinate synthase; baroreflex sensitivity; Bothrops jararaca venom; nitric oxide; proline-rich oligopeptide INTRODUCTIONThe gaseous messenger NO is involved mainly in the regulation of local and systemic vascular resistance, sodium balance and, consequently, blood pressure control, 1 but it is also a signaling molecule and modulator of brain function. 2 Recent studies relate NO with central cardiovascular control through the regulation of the cardiac and vascular autonomic system via the modulation of the central sites of cardiovascular autonomic neural integration. 3,4 NO is generated in the citrulline-NO cycle by NO synthase (NOS) using L-arginine as a substrate. Three isoforms of NOS have been described: calcium-dependent endothelial (eNOS) and neuronal (nNOS) isoforms and inducible NOS. The expression and activity

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Section: Discussionmentioning

confidence: 99%

Brain nitric oxide production by a proline-rich decapeptide from Bothrops jararaca venom improves baroreflex sensitivity of spontaneously hypertensive rats

Lameu

Pontieri

Guerreiro³

et al. 2010

Hypertens Res

View full text Add to dashboard Cite

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“…Because cardiovascular events most frequently occur in the morning hours (17)(18)(19)(20), BP elevation and the occurrence of cardiovascular events in the morning would have the same pathological background. Impaired BRS is associated with enhanced BP variability (21,22) and poor BP control in hypertensive patients (23). The reason why BRS was independently associated only with morning BP is unknown, but one possible explanation is that activation of the sympathetic nervous system, which is seen in hypertensive patients with morning hypertension, decreases BRS (24,25).…”

Section: Arterial Brs and Bp Controlmentioning

confidence: 99%

Factors Associated with Baroreflex Sensitivity: Association with Morning Blood Pressure

et al. 2007

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Baroreflex sensitivity (BRS) is a primary mechanism for acute and chronic control of blood pressure (BP).However, there are few data showing the relationship between BRS and ambulatory BP (ABP). We assessed the hypothesis that BRS specifically contributes to some specific parameters of ABP in never-treated hypertensive/normotensive subjects. We studied 128 subjects (mean age: 54.5 ± 13 years, 60% male) consisting of 92 untreated hypertensive and 36 normotensive subjects. Radial tonometric BP and simultaneous RR interval were recorded for 10 min, and the Valsalva maneuver was performed 3 times for each subject. BRS was calculated in two ways: the spontaneous-BRS by the spectral method, and the Valsalva-BRS by the slope method, using commercial software. ABP monitoring was performed on the same day as the BRS test.

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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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Arterial baroreflex function and cardiovascular variability: interactions and implications

Cited by 248 publications

References 120 publications

Brain nitric oxide production by a proline-rich decapeptide from Bothrops jararaca venom improves baroreflex sensitivity of spontaneously hypertensive rats

Brain nitric oxide production by a proline-rich decapeptide from Bothrops jararaca venom improves baroreflex sensitivity of spontaneously hypertensive rats

Factors Associated with Baroreflex Sensitivity: Association with Morning Blood Pressure

Autonomic cardiovascular regulation in subjects with acute mountain sickness

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