Arterial spontaneous rhythmic contractile activity in humans and rats: spectral analysis and regulatory mechanisms

Rizzoni, Damiano; Castellano, Maurizio; Porteri, Enzo; Bettoni, Giorgio; Muiesan, Paolo; Muiesan, M.L.; Sm, Giulini; Cinelli, Angel R.; Salvetti, Massimo; E, Agabiti Rosei

doi:10.1097/00004872-199509000-00016

Cited by 20 publications

(18 citation statements)

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“…Inhibition of NOS increases arterial pressure oscillations at low frequencies in rats (16) and dogs (15) and increases steady-state arterial pressures in humans (11,12). On the basis of this evidence and evidence that the peripheral vasculature seems to possess intrinsic rhythmicity (10,21,30), we tested the hypothesis that NO contributes importantly to the control of arterial pressure rhythms in humans. Our data confirm a primary role for NO in maintaining stable arterial pressures at rest but provide evidence against the notion that dynamic oscillations of pressure, including naturally occurring rhythms at the frequency of Mayer waves, depend critically on tonic NO activity.…”

Section: Discussionmentioning

confidence: 99%

“…With this construct, waxing and waning of arterial pressures around 0.1 Hz are likely driven by arterial baroreceptor input (9). Second, low-frequency arterial pressure rhythms have been recorded in patients with cervical spinal cord lesions (10) and in isolated mesenteric arteries (21), suggesting the possibility that the peripheral vasculature possesses intrinsic rhythmicity independent of baroreflex feedback loops. The notion that Mayer waves reflect vascular sympathetic outflow has recently been challenged (27), and therefore factors that may contribute directly to vascular rhythmicity warrant further investigation.…”

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confidence: 88%

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Does nitric oxide buffer arterial blood pressure variability in humans?

Cooke

Zhang²,

Zuckerman

et al. 2002

Journal of Applied Physiology

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. Does nitric oxide buffer arterial blood pressure variability in humans? J Appl Physiol 93: 1466-1470, 2002. First published July 12, 2002 10.1152/ japplphysiol.00287.2002.-Animal studies suggest that nitric oxide (NO) plays an important role in buffering shortterm arterial pressure variability, but data from humans addressing this hypothesis are scarce. We evaluated the effects of NO synthase (NOS) inhibition on arterial blood pressure (BP) variability in eight healthy subjects in the supine position and during 60°head-up tilt (HUT). Systemic NOS was blocked by intravenous infusion of N G -monomethyl-L-arginine (L-NMMA). Electrocardiogram and beat-bybeat BP in the finger (Finapres) were recorded continuously for 6 min, and brachial cuff BP was recorded before and after L-NMMA in each body position. BP and R-R variability and their transfer functions were quantified by power spectral analysis in the low-frequency (LF; 0.05-0.15 Hz) and highfrequency (HF; 0.15-0.35 Hz) ranges. L-NMMA infusion increased supine BP (systolic, 109 Ϯ 4 vs. 122 Ϯ 3 mmHg, P ϭ 0.03; diastolic, 68 Ϯ 2 vs. 78 Ϯ 3 mmHg, P ϭ 0.002), but it did not affect supine R-R interval or BP variability. Before L-NMMA, HUT decreased HF R-R variability (P ϭ 0.03), decreased transfer function gain (LF, 12 Ϯ 2 vs. 5 Ϯ 1 ms/mmHg, P ϭ 0.007; HF, 18 Ϯ 3 vs. 3 Ϯ 1 ms/mmHg, P ϭ 0.002), and increased LF BP variability (P Ͻ 0.0001). After L-NMMA, HUT resulted in similar changes in BP and R-R variability compared with tilt without L-NMMA. Increased supine BP after L-NMMA with no effect on BP variability during HUT suggests that tonic release of NO is important for systemic vascular tone and thus steady-state arterial pressure, but NO does not buffer dynamic BP oscillations in humans. cardiovascular control; head-up tilt; intrinsic rhythmicity LOW-FREQUENCY ARTERIAL PRESSURE oscillations or "Mayer waves" were first described in 1877 (14), yet mechanisms underlying these low-frequency rhythms have remained elusive. Because the magnitude of systolic pressure fluctuations is directly associated with severity of end-organ damage (renal, heart, and brain) and subsequent cardiovascular complications (18), understanding mechanisms of arterial blood pressure oscillations assumes clinical importance.In an effort to explain arterial pressure rhythms occurring at frequencies slower than respiration, at least two hypotheses have been advanced. First, because of intrinsic delays in effector responses to norepinephrine, increases of sympathetic nerve firings are manifested in cardiac and vascular responses with a time delay of ϳ10 s (28). With this construct, waxing and waning of arterial pressures around 0.1 Hz are likely driven by arterial baroreceptor input (9). Second, low-frequency arterial pressure rhythms have been recorded in patients with cervical spinal cord lesions (10) and in isolated mesenteric arteries (21), suggesting the possibility that the peripheral vasculature possesses intrinsic rhythmicity independent of baroreflex feedback loops. The notion that Mayer wa...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 88%

Does nitric oxide buffer arterial blood pressure variability in humans?

Cooke

Zhang²,

Zuckerman

et al. 2002

Journal of Applied Physiology

View full text Add to dashboard Cite

show abstract

“…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: 91%

“…However, phentolamine did not suppress completely the LF oscillations in cardiovascular variability, suggesting the possibility that LF vasomotor oscillations may persist even in the absence of intact neurovascular transmission. These neural-independent oscillations could either indicate the presence of "autoregulatory" properties (98) or be an expression of the modulation operated by the nitric oxide system (79), as described below.…”

Section: Arterial Baroreflex and Cardiovascular Variabilitymentioning

confidence: 99%

Arterial baroreflex function and cardiovascular variability: interactions and implications

Lanfranchi

Somers

2002

American Journal of Physiology-Regulatory, Integrative and Comp

252

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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“…Previous studies have shown that this phenomenon is not endothelium-dependent (42,43) and our findings support this view. In humans, SRC was described in coronary arteries (44), small omental arteries (45), pial arteries (46), and placental vessels (47). This phenomenon was previously described in human RA; it concerned fluctuation of blood flow through RA.…”

Section: Discussionmentioning

confidence: 99%

Analysis of Vasoreactivity of Isolated Human Radial Artery

et al. 2006

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Abstract. Radial artery (RA) is increasingly used as graft for coronary artery bypass grafting due to its good long-term patency. However, the mechanism of peri-and post-operative spasm is still unclear. Because of that, the aim of our study is to analyze the contractility of RA and to determine whether the presence of functional endothelium alters its contractile properties. Contractions of isolated RA rings were provoked by exogenously applied vasoconstrictors or by electrical field stimulation (EFS, 20 Hz). The order of vasoconstrictors potency based on their EC 50 values was as follows: angiotensin II > phenylephrine > 5-hydroxytriptamine. Presence of endothelium increased both EC 50 and maximal contraction to phenylephrine and angiotensin II, but inhibited reactivity of RA to 5-hydroxytriptamine. Spontaneous rhythmic contractions (SRC, <4 mHz) and EFS-induced contractions of RA are endothelium-independent and weaker than contractions induced by exogenously applied vasoconstrictors. Our study concludes that RA shows marked sensitivity and reactivity to angiotensin II, phenylephrine, and 5-hydroxytriptamine. Further investigations are necessary to answer why angiotensin II and phenylepehrine induce stronger contractions in the presence of endothelium. In addition, SRC as well as contractions of neurogenic origin may take part in developing vascular spasm of RA.

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Arterial spontaneous rhythmic contractile activity in humans and rats: spectral analysis and regulatory mechanisms

Cited by 20 publications

References 0 publications

Does nitric oxide buffer arterial blood pressure variability in humans?

Does nitric oxide buffer arterial blood pressure variability in humans?

Arterial baroreflex function and cardiovascular variability: interactions and implications

Analysis of Vasoreactivity of Isolated Human Radial Artery

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