Very low frequency blood pressure variability is modulated by myogenic vascular function and is reduced in stroke-prone rats

Stauss, Harald M.; Petitto, Carlo Emanuel; Rotella, Diane L.; Wong, Brett J.; Sheriff, Don D.

doi:10.1097/hjh.0b013e3282fb81c8

Cited by 11 publications

(12 citation statements)

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“…Over a decade ago, it had been suggested that the renin-angiotensin aldosterone system may contribute importantly to VLF BPV (7,20,21). Furthermore, studies from our laboratory demonstrated that VLF BPV depends on L-type Ca 2ϩ channels (16) and suggested that myogenic vascular function contributes significantly to VLF BPV (31). One importance of these findings is that cerebrovascular myogenic function normally protects the brain from hemorrhagic stroke and that a loss of myogenic vascular function [e.g., in chronic renal failure (15,18)] constitutes an important risk factor for hemorrhagic stroke (25,26).…”

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confidence: 92%

“…Indeed, VLF BPV is reduced in stroke-prone spontaneously hypertensive rats compared with stroke-resistant spontaneously hypertensive rats (31). However, the concept that VLF BPV primarily reflects myogenic vascular function and/or autoregulation of blood flow and, therefore, predicts hemorrhagic stroke in subjects with reduced VLF BPV is currently not generally accepted (12).Specifically, a limitation of our laboratory's previous studies (16,31) was that the conclusion that myogenic vascular function contributes significantly to VLF BPV was based on experiments utilizing the L-type Ca 2ϩ channel blocker nifedipine. As pointed out in our laboratory's previous papers (16, 31), L-type Ca 2ϩ channels are also involved in the vascular actions of vasoactive substances, such as catecholamines.…”

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confidence: 95%

“…Due to the postulated contribution of myogenic vascular function to VLF BPV (31), increased risk for hemorrhagic stroke may be detected by reduced VLF BPV. Indeed, VLF BPV is reduced in stroke-prone spontaneously hypertensive rats compared with stroke-resistant spontaneously hypertensive rats (31). However, the concept that VLF BPV primarily reflects myogenic vascular function and/or autoregulation of blood flow and, therefore, predicts hemorrhagic stroke in subjects with reduced VLF BPV is currently not generally accepted (12).…”

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confidence: 98%

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Frequency response characteristics of whole body autoregulation of blood flow in rats

Stauss

Rarick²,

Deklotz³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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Previously, we demonstrated that very low-frequency (VLF) blood pressure variability (BPV) depends on voltage-gated L-type Ca(2+)-channels, suggesting that autoregulation of blood flow and/or myogenic vascular function significantly contributes to VLF BPV. To further substantiate this possibility, we tested the hypothesis that the frequency response characteristic of whole body autoregulation of blood flow is consistent with the frequency range of VLF BPV (0.02-0.2 Hz) in rats. In anesthetized rats (n = 11), BPV (0.016-0.5 Hz) was induced by computer-regulated cardiac pacing while blood pressure, heart rate, and cardiac output (CO) were recorded during control conditions (NaCl, 1 ml/h iv) and during alpha(1)-adrenergic receptor stimulation (phenylephrine, 1 mg.ml(-1).h(-1) iv) that has been reported to facilitate myogenic vascular function. Baroreceptor-heart rate reflex responses were elicited to confirm a functional baroreflex despite anesthesia. During control conditions, transfer function analyses between mean arterial pressure (MAP) and CO, and between MAP and total vascular conductance (CO/MAP) indicated autoregulation of blood flow at 0.016 Hz, passive vascular responses between 0.033 and 0.2 Hz, and vascular responses compatible with baroreflex-mediated mechanisms at 0.333 and 0.5 Hz. Stimulation of alpha(1)-adrenergic receptors extended the frequency range of autoregulation of blood flow to frequencies up to 0.033 Hz. In conclusion, depending on sympathetic vascular tone, whole body autoregulation of blood flow operates most effectively at frequencies below 0.05 Hz. This frequency range overlaps with the lower end of the frequency band of VLF BPV in rats. Baroreceptor reflex-like mechanisms contribute to LF (0.2-0.6 Hz) but not VLF BPV-induced vascular responses.

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confidence: 92%

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confidence: 98%

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Frequency response characteristics of whole body autoregulation of blood flow in rats

Stauss

Rarick²,

Deklotz³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…Our choice to analyze DBP and its variability, in a previous work (2) and in this paper as well, is based on the relationship between the diastolic decay and TPR (27,31), and on the observation that DBP spectral power is mostly concentrated in the low-frequency (LF, ϳ0.1 Hz) band, i.e., the band of vasomotor and resistance fluctuations. Therefore, DBP was assumed to be specifically sensitive to vasomotor tone, and modulations in the LF band were assumed to reflect baroreflex-mediated regulation of vascular resistance, whereas autoregulation phenomena may be confined to slower oscillations, typical of the very low-frequency band (VLF; f Ͻ 0.04 Hz), as shown by Stauss et al (43). The choice of SBP as the input to the arterial baroreflex-related component of the model was consistent with typical approaches to the assessment of cardiac baroreflex, which use SBP as the input, since it is known to convey both the phasic and tonic dynamic features to which baroreceptors are sensitive, and heart rate or R-R as the output.…”

Section: Methodsmentioning

confidence: 99%

Short-term variability of blood pressure: effects of lower-body negative pressure and long-duration bed rest

Aletti

Ferrario

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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(LBNP) has been utilized to selectively unload cardiopulmonary baroreceptors, but there is evidence that arterial baroreceptors can be transiently unloaded after the onset of mild LBNP. In this paper, a black box mathematical model for the prediction of diastolic blood pressure (DBP) variability from multiple inputs (systolic blood pressure, R-R interval duration, and central venous pressure) was applied to interpret the dynamics of blood pressure maintenance under the challenge of LBNP and in long-duration, headdown bed rest (HDBR). Hemodynamic recordings from seven participants in the WISE (Women's International Space Simulation for Exploration) Study collected during an experiment of incremental LBNP (Ϫ10 mmHg, Ϫ20 mmHg, Ϫ30 mmHg) were analyzed before and on day 50 of a 60-day-long HDBR campaign. Autoregressive spectral analysis focused on low-frequency (LF, ϳ0.1 Hz) oscillations of DBP, which are related to fluctuations in vascular resistance due to sympathetic and baroreflex regulation of vasomotor tone. The arterial baroreflex-related component explained 49 Ϯ 13% of LF variability of DBP in spontaneous conditions, and 89 Ϯ 9% (P Ͻ 0.05) on day 50 of HDBR, while the cardiopulmonary baroreflex component explained 17 Ϯ 9% and 12 Ϯ 4%, respectively. The arterial baroreflexrelated variability was significantly increased in bed rest also for LBNP equal to Ϫ20 and Ϫ30 mmHg. The proposed technique provided a model interpretation of the proportional effect of arterial baroreflex vs. cardiopulmonary baroreflex-mediated components of blood pressure control and showed that arterial baroreflex was the main player in the mediation of DBP variability. Data during bed rest suggested that cardiopulmonary baroreflex-related effects are blunted and that blood pressure maintenance in the presence of an orthostatic stimulus relies mostly on arterial control. arterial blood pressure; variability; baroreflex; lower body negative pressure; bed rest MILD OR NONHYPOTENSIVE LOWER body negative pressure (LBNP; Ϫ20 mmHg Ͻ LBNP Ͻ 0 mmHg) has been used to selectively unload cardiopulmonary baroreceptors (25,44,46,50). However, straightforward observations of the time course of mean arterial pressure (MAP) following rapid onset of mild LBNP (17, 18) evidenced a transient decrease followed by a recovery of pre-LBNP onset values, suggesting that arterial baroreceptors are affected by mild LBNP as well. More detailed analyses of such transient decreases of MAP in LBNP (13) showed that also systolic blood pressure (SBP) and diastolic blood pressure (DBP) fall and are restored within ϳ15 heart beats, confirming a direct involvement of arterial baroreflex, consistently with previous reports (23,35,45). However, to our knowledge, the quantification of the relative dynamic contribution of arterial and cardiopulmonary baroreflex has not been addressed yet. Fu et al. (13) concluded that arterial baroreflex is engaged and unloaded by mild LBNP, but they could not determine the proportional influence of cardiopulmonary vs. arterial baroreflex on t...

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“…More recently the importance of BPV in prediction of risk of vascular events and in accounting for benefits of antihypertensive drugs, especially in prevention of stroke, was emphasized [5][6][7] . Multiple studies have investigated the roles of resting vascular tone changes, arterial pressure levels, the sympathetic nervous system, and vasoactive substances in the increased BPV after SAD [3,[8][9][10][11][12][13][14] . However, the definite mechanism by which BPV dramatically increase after SAD surgery is still unclear.…”

Section: Introductionmentioning

confidence: 99%

Role of vascular KATP channels in blood pressure variability after sinoaortic denervation in rats

Yang

Liu

et al. 2011

Acta Pharmacol Sin

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Aim: To investigate the role of ATP-sensitive potassium (K ATP ) channels on blood pressure variability (BPV) in sinoaortic denervated (SAD) rats. Methods: SAD was performed on male Sprague-Dawley rats 4 weeks before the study. mRNA expression of Kir6.1, Kir6.2 and SUR2 in aorta and mesenteric artery was determined using real-time quantitative polymerase chain reaction, and confirmed at the protein level using Western blotting and laser confocal immunofluorescence assays. Concentration-response curves of isolated aortic and mesenteric arterial rings to adenosine and pinacidil were established. Effects of K ATP channel openers and blocker on BPV were examined in conscious SAD rats. Results: Aortic SUR2 expression was significantly greater, while Kir6.1 was lower, in SAD rats than in sham-operated controls. In contrast, in the mesenteric artery both SUR2 and Kir6.1 expression were markedly lower in SAD rats than controls. For both arteries, Kir6.2 expression was indistinguishable between sham-operated and SAD rats. These findings were confirmed at the protein level. Responses of the aorta to both adenosine and pinacidil were enhanced after SAD, while the mesenteric response to adenosine was attenuated. Pinacidil, diazoxide, nicorandil, and glibenclamide significantly decreased BPV. Conclusion: These findings indicate that expression of vascular K ATP channels is altered by chronic SAD. These alterations influence vascular reactivity, and may play a role in the increased BPV in chronic SAD rats.

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Very low frequency blood pressure variability is modulated by myogenic vascular function and is reduced in stroke-prone rats

Cited by 11 publications

References 50 publications

Frequency response characteristics of whole body autoregulation of blood flow in rats

Frequency response characteristics of whole body autoregulation of blood flow in rats

Short-term variability of blood pressure: effects of lower-body negative pressure and long-duration bed rest

Role of vascular KATP channels in blood pressure variability after sinoaortic denervation in rats

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