Oscillations In Tone Research Articles

Rhythmic Skeletal Muscle Tension Increases Heart Rate Variability at 1 and 6 Contractions Per Minute.

Breathing at the resonance frequency (~ 6 breaths per min) produces resonance effects on baroreflex gain, blood pressure, vascular tone, and therapeutic benefits. Evgeny Vaschillo and Paul Lehrer have emphasized that the stimulation frequency is critical for producing resonance effects in the cardiorespiratory system. Although clinicians overwhelmingly use paced breathing to increase HRV, other promising methods exist. Vaschillo, Lehrer, and colleagues have shown that presenting non-respiratory stimulation at 0.1Hz-pictures with an emotional valence or rhythmical muscle tensing-amplifies oscillations in heart rate, blood pressure, and vascular tone. Participants in the present study included 49 undergraduate students randomly assigned to one of six different orders of 5-min trials of 1, 6, and 12 muscle contractions per min (cpm), separated by 3-min buffer periods intended to minimize carryover. This randomized controlled trial replicated the Vaschillo et al. (Psychophysiology 48:927-936, 2011. https://doi.org/10.1111/j.1469-8986.2010.01156.x ) finding that 6-cpm RSMT can produce a PkFreq of ~ 0.10Hz, similar to 6-bpm RF breathing. RSMT at 1 and 6cpm increased five time-domain metrics (HR Max-HR Min, RMSSD, SDNN, TI, and TINN), one frequency-domain metric (LF power), and three non-linear metrics (D2, SD1, SD2) significantly more than RSMT at 12cpm. There were no differences between 1 and 6cpm on these measures. The 1-cpm rate (~ 0.02Hz) may have stimulated the hypothesized vascular tone baroreflex between 0.02 and 0.055Hz. RSMT at 1 or 6 cpm provides clients with an alternative exercise for increasing HRV for patients who find slow-paced breathing challenging or medically unsafe.

Spatial heterogeneity of cutaneous blood flow respiratory-related oscillations quantified via laser speckle contrast imaging.

LSCI technique provides experimental data which can be considered in the context of spatial blood flow coherency. Analysis of vascular tone oscillations gives additional information to ensure a better understanding of the mechanisms affecting microvascular physiology. The oscillations with different frequencies are due to different physiological mechanisms. The reasons for the generation of peripheral blood flow oscillations in the 0.14–0.6 Hz frequency band are as follows: cardio-respiratory interactions, pressure variations in the venous part of the circulatory system, and the effect of the sympathetic nervous system on the vascular tone. Earlier, we described the spatial heterogeneity of around 0.3 Hz oscillations and this motivated us to continue the research to find the conditions for the occurrence of spatial phase synchronization. For this purpose, a number of physiological tests (controlled respiration, breath holder, and venous occlusion tests) which influence the blood flow oscillations of 0.14–0.6 Hz were considered, an appropriate measurement system and the required data processing algorithms were developed. At spontaneous respiration, the oscillations with frequencies around 0.3 Hz were stochastic, whereas all the performed tests induced an increase in spatial coherence. The protocols and methods proposed here can help to clarify whether the heterogeneity of respiratory-related blood flow oscillations exists on the skin surface.

Expression of ECE1, IGFBP7 and CALR in a porcine model for von Willebrand disease (VWD) type 1 and 3

To characterise Chorionic Plate Artery (CPA) function in maternal obesity, and investigate whether leptin exposure reproduces the obese CPA phenotype in normal-BMI women.CPA responses to the thromboxane-A2 mimetic U46619 (pre/post leptin incubation), to the nitric oxide donor sodium nitroprusside (SNP) and the occurrence of tone oscillations (pre/post leptin incubation) were assessed in 46 term placentas from women of normal (18.5–24.9) or obese (>30) Body Mass Index (BMI).Area Under the dose response Curve (AUC), maximum response (Vmax), sensitivity (EC50) to U46619 (pre/post leptin) and SNP; average vessel tone, oscillation amplitude and frequency (pre/post leptin).U46619 vasoconstriction was similar between BMI categories (p > 0.05), however vasodilatation to SNP was reduced in obesity (AUC p = 0.02, Vmax p = 0.04) compared to normal-BMI women. Leptin incubation altered responses to U46619 in both normal-BMI (EC50 at 100 ng/ml leptin; p < 0.05) and obese women (AUC at 50 ng/ml; p < 0.05) but vasomotion was unaffected (p > 0.05).Maternal obesity is associated with altered placental vascular function which may adversely affect placental oxygen and nutrient transport, placing the fetus at risk. Leptin incubation altered CPA vascular function but did not reproduce the obese phenotype.

Cellular and Ionic Mechanisms of Arterial Vasomotion.

Rhythmical contractility of blood vessels was first observed in bat wing veins by Jones (Philos Trans R Soc Lond 1852:142, 131-136), and subsequently described in arteries and arterioles of multiple vascular beds in several species. Despite an abundance of descriptive literature regarding the presence of vasomotion, to date we do not have an accurate picture of the cellular and ionic basis of these oscillations in tone, or the physiological relevance of the changes in pulsatile blood flow arising from vasomotion. This chapter reviews our current understanding of the cellular and ionic mechanisms underlying vasomotion in resistance arteries and arterioles. Focus is directed to the ion channels, changes in cytosolic Ca2+ concentration, and involvement of intercellular gap junctions in the development and synchronization of rhythmic changes in membrane potential and cytosolic Ca2+ concentration within the vessel wall that contribute to vasomotion. The physiological consequences of vasomotion are discussed with a focus on the cerebral vasculature, as recent advances show that rhythmic oscillations in cerebral arteriolar diameter appear to be entrained by cortical neural activity to increase the local supply of blood flow to active regions of the brain.

Enhanced nitric oxide signaling amplifies vasorelaxation of human colon cancer feed arteries.

Inadequate perfusion of solid cancer tissue results in low local nutrient and oxygen levels and accumulation of acidic waste products. Previous investigations have focused primarily on tumor blood vessel architecture, and we lack information concerning functional differences between arteries that deliver blood to solid cancer tissue versus normal tissue. Here, we use isometric myography to study resistance-sized arteries from human primary colon adenocarcinomas and matched normal colon tissue. Vasocontraction of colon cancer feed arteries in response to endothelin-1 and thromboxane stimulation is attenuated compared with normal colon arteries despite similar wall dimensions and comparable contractions to arginine vasopressin and K+-induced depolarization. Acetylcholine-induced vasorelaxation and endothelial NO synthase expression are increased in colon cancer feed arteries compared with normal colon arteries, whereas vasorelaxation to exogenous NO donors is unaffected. In congruence, the differences in vasorelaxant and vasocontractile function between colon cancer feed arteries and normal colon arteries decrease after NO synthase inhibition. Rhythmic oscillations in vascular tone, known as vasomotion, are of lower amplitude but similar frequency in colon cancer feed arteries compared with normal colon arteries. In conclusion, higher NO synthase expression and elevated NO signaling amplify vasorelaxation and attenuate vasocontraction of human colon cancer feed arteries. We propose that enhanced endothelial function augments tumor perfusion and represents a potential therapeutic target. NEW & NOTEWORTHY Local vascular resistance influences tumor perfusion. Arteries supplying human colonic adenocarcinomas show enhanced vasorelaxation and reduced vasocontraction mainly due to elevated nitric oxide-mediated signaling. Rhythmic oscillations in tone, known as vasomotion, are attenuated in colon cancer feed arteries.

Theoretical assessment of the Ca2+ oscillations in the afferent arteriole smooth muscle cell of the rat kidney

The afferent arteriole (AA) of rat kidney exhibits the myogenic response, in which the vessel constricts in response to an elevation in blood pressure and dilates in response to a pressure reduction. Additionally, the AA exhibits spontaneous oscillations in vascular tone at physiological luminal pressures. These time-periodic oscillations stem from the dynamic exchange of Ca[Formula: see text] between the cytosol and the sarcoplasmic reticulum, coupled to the stimulation of Ca[Formula: see text]-activated potassium and chloride channels, and to the modulation of voltage-gated L-type Ca[Formula: see text] channels. The effects of physiological factors, including blood pressure and vasoactive substances, on AA vasomotion remain to be well characterized. In this paper, we analyze a mathematical model of Ca[Formula: see text] signaling in an AA smooth muscle cell. The model represents detailed transmembrane ionic transport, intracellular Ca[Formula: see text] dynamics as well as kinetics of nitric oxide (NO) and superoxide (O[Formula: see text]) formation, diffusion and reaction. NO is an important factor in the maintenance of blood pressure and O[Formula: see text] has been shown to contribute significantly to the functional alternations of blood vessels in hypertension. We perform a bifurcation analysis of the model equations to assess the effect of luminal pressure, NO and O[Formula: see text] on the behaviors of limit cycle oscillations.

Voltage-gated sodium channels are involved in vasomotion of human arteries

Voltage-gated sodium channels (Na v ) are responsible for the initiation and propagation of action potential in excitable cells. In vascular smooth muscle cells (VSMCs), usually electrically quiescent, their presence and functional impact are less well-defined, especially in human arteries. In the present study, we determined Na v channels gene expression profile and assessed the effect of Na v channel activator veratridine on human arteries. Human uterine arteries obtained from women undergoing hysterectomy were used. I Na currents were electrophysiologically recorded on isolated VSMCs. Isometric tensions were recorded ex vivo on uterine artery rings in response to Na v channel agonist (veratridine) and antagonist (tetrodotoxin, TTX) under physiological and hypoxic conditions. A TTX-sensitive and fast inactivating I Na current was recorded in VSCMs isolated from human uterine artery. Various Na v channel genes were detected, corresponding to TTX-sensitive (Na v 1.2; 1.3; 1.7) and TTX-resistant (Na v 1.5) alpha-subunit isoforms. Under hypoxic conditions, promotion of Na v channel activity by veratridine triggered rhythmic oscillations in vascular tone of uterine arterial rings similar to vasomotion. This rhythmic activity was abolished by TTX (1 to 0.01 μM) and attenuated by the calcium antagonist nifedipine (1 μM). Na v channel are present in VSMCs of human arteries where they are functionally coupled to contractile activity. Under hypoxic condition, they could initiate, ex vivo, rhythmic contractile activity reminiscent of vasomotion. This is the first demonstration of Na v channels contribution to this complex phenomenon.

Phase coherence of 0.1 Hz microvascular tone oscillations during the local heating

The origin of the mechanisms of blood flow oscillations at low frequencies is discussed. It is known that even isolated arteriole demonstrates oscillations with the frequency close to 0.1 Hz, which is caused by the synchronous activity of myocyte cells. On the other hand, oscillations with close frequency are found in the heart rate, which are associated with quite different mechanism. The main purpose of this work is to study phase coherence of the blood flow oscillations in the peripheral vessels under basal and perturbed conditions. Local heating which locally influences the microvascular tone, as one of currently elucidated in sufficient detail physiological test, was chosen. During such provocation blood flow though the small vessels significantly increases because of vasodilation induced by the local synthesis of nitric oxide. In the first part of the paper microvascular response to the local test is quantified in healthy and pathological conditions of diabetes mellitus type 1. It is obtained that regardless of the pathology, subjects with high basal perfusion had lower reserve for vasodilation, which can be caused by the low elasticity of microvascular structure. Further synchronization of pulsations of the heated and undisturbed skin was evaluated on the base of wavelet phase coherency analysis. Being highly synchronised in basal conditions 0.1 Hz pulsations became more independent during heating, especially during NO-mediated vasodilation.

Elevated C-reactive protein levels and enhanced high frequency vasomotion in patients with ischemic heart disease during brachial flow-mediated dilation.

PurposeThe physiological role of vasomotion, rhythmic oscillations in vascular tone or diameter, and its underlying mechanisms are unknown. We investigated the characteristics of brachial artery vasomotion in patients with ischemic heart disease (IHD).MethodsWe performed a retrospective study of 37 patients with IHD. Endothelial function was assessed using flow-mediated dilation (FMD), and power spectral analysis of brachial artery diameter oscillations during FMD was performed. Frequency-domain components were calculated by integrating the power spectrums in three frequency bands (in ms2) using the MemCalc (GMS, Tokyo, Japan): very-low frequency (VLF), 0.003–0.04 Hz; low frequency (LF), 0.04–0.15 Hz; and high frequency (HF), 0.15–0.4 Hz. Total spectral power (TP) was calculated as the sum of all frequency bands, and each spectral component was normalized against TP.ResultsData revealed that HF/TP closely correlated with FMD (r = −0.33, p = 0.04), whereas VLF/TP and LF/TP did not. We also explored the relationship between elevated C-reactive protein (CRP) levels and vasomotion. HF/TP was significantly increased in subjects with high CRP levels (CRP;>0.08 mg/dL) compared with subjects with low CRP levels (0.052±0.026 versus 0.035±0.022, p<0.05). The HF/TP value closely correlated with CRP (r = 0.24, p = 0.04), whereas the value of FMD did not (r = 0.023, p = 0.84). In addition, elevated CRP levels significantly increased the value of HF/TP after adjustment for FMD and blood pressure (β = 0.33, p<0.05).ConclusionThe HF component of brachial artery diameter oscillation during FMD measurement correlated well with FMD and increased in the presence of elevated CRP levels in subjects with IHD.

Chorionic plate arterial function is altered in maternal obesity

ObjectivesTo characterise Chorionic Plate Artery (CPA) function in maternal obesity, and investigate whether leptin exposure reproduces the obese CPA phenotype in normal-BMI women. Study designCPA responses to the thromboxane-A2 mimetic U46619 (pre/post leptin incubation), to the nitric oxide donor sodium nitroprusside (SNP) and the occurrence of tone oscillations (pre/post leptin incubation) were assessed in 46 term placentas from women of normal (18.5–24.9) or obese (>30) Body Mass Index (BMI). Outcome measuresArea Under the dose response Curve (AUC), maximum response (Vmax), sensitivity (EC50) to U46619 (pre/post leptin) and SNP; average vessel tone, oscillation amplitude and frequency (pre/post leptin). ResultsU46619 vasoconstriction was similar between BMI categories (p > 0.05), however vasodilatation to SNP was reduced in obesity (AUC p = 0.02, Vmaxp = 0.04) compared to normal-BMI women. Leptin incubation altered responses to U46619 in both normal-BMI (EC50 at 100 ng/ml leptin; p < 0.05) and obese women (AUC at 50 ng/ml; p < 0.05) but vasomotion was unaffected (p > 0.05). ConclusionsMaternal obesity is associated with altered placental vascular function which may adversely affect placental oxygen and nutrient transport, placing the fetus at risk. Leptin incubation altered CPA vascular function but did not reproduce the obese phenotype.

Myogenic Oscillations in Rabbit Ocular Vasculature Are Very Low Frequency

Background/Aims: In a previously described model of isolated rabbit eye, we detected myogenic intrinsic vascular tone of unknown origin in the ophthalmic artery. In order to better understand the origin of these low frequency oscillations, we analyzed their spectral characteristics using fast Fourier. Methods: Hybrid New Zealand rabbits of either sex (n = 24) were used; they were divided into 2 groups according to age. The spectral characteristics of the myogenic behaviour of the rabbit external ophthalmic artery were analyzed using the fast Fourier algorithm. Results: The frequency of the oscillations of the myogenic activity seen in the rabbit external ophthalmic artery varied between 0.033 and 0.066 Hz (mean 0.045 ± 0.012 Hz), all in the region of very low frequency (VLF) oscillations (VLF <0.07 Hz for the rabbit). The frequency of spontaneous oscillations was higher in younger animals. Conclusion: Fast Fourier analysis proved to be an adequate mathematical tool to analyze the myogenic tone oscillations, which were all in the range of VLF in the model we used. These results indicate that myogenic vascular function of ocular blood flow is composed of VLF oscillations, and they provide a new explanation for the origin of VLF in arterial spectra. They also suggest that the ocular local myogenic vascular function observed is more efficient in younger animals.

Pharmacological studies of BK and L‐type Ca2+ channel function in mesenteric arteries and veins from obese patients

Small mesenteric veins (MV) are important in regulation of blood pressure via their capacitance function, however, our previous studies showed that MV displayed heterogeneity in pharmacological responses across species. For example, the large conductance Ca2+ activated K+ (BK) channels and L‐type Ca2+ channels control basal tone and spontaneous oscillations in tone in rat but not murine MV. It is unknown if BK and L‐type Ca2+ channels function in human MV. Therefore, we tested BK and L‐type Ca2+ channel function in isolated and pressurized MA (mesenteric arteries) (60 mmHg) and MV (4 mmHg) from small segments of jejunum harvested from specimens obtained from obese subjects undergoing gastric bypass surgery. The patients reported here were female, 23–45 years old, with BMI values between 34–54, but without hypertension or diabetes. We measured drug‐induced changes in outside diameter and found that: 1) Norepinephrine (NE) dose‐response curves were similar in MA (n=4) and MV (n=4). 2) Nifedipine completely blocked Bay K 8644 (L‐type Ca2+ channel agonist)‐induced MA and MV constriction. 3) Nifedipine also blocked KCl (20–60 mM)‐induced MA, and KCl (20–40 mM)‐induced MV constriction. 4) At physiological intraluminal pressure, MV, but not MA, displayed basal tone and oscillating constrictions which were blocked by nifedipine or removing extracellular Ca2+. 5) Paxilline, a BK channel blocker, caused a 20% constriction in MA. 6) Paxilline did not constrict MV, but completely inhibited spontaneous oscillations in tone. Our results indicate that both BK and L‐type Ca2+ channels regulate human MA and MV tone, but act via blood vessel specific mechanisms. Pharmacological responses of human MV are similar to those of the rat but not the mouse.

The functional role of bestrophins and TMEM16A in rat mesenteric small arteries

Two Ca2+‐activated Cl− currents (ICl(Ca)) are present in vascular smooth muscle (VSMC). One is cGMP dependent, the other is characterized as a classical ICl(Ca). Here we downregulate bestrophin‐3 (best3) and TMEM16A, to assess their importance for the two ICl(Ca) and for the role of ICl(Ca) in vascular function.Best3 and TMEM16A were downregulated in rat small mesenteric arteries using siRNA. Knockdown was confirmed at mRNA and protein levels 3 days after transfection.Best3 downregulation suppressed the cGMP‐dependent ICl(Ca) while TMEM16A downregulation suppresed both ICl(Ca)s. Both best3 and TMEM16A downregulation suppressed oscillations in vascular tone i.e. vasomotion. Best3 downregulation was without effect on sensitivity and maximal force production to norepinephrine while TMEM16A downregulation significantly reduced both. Also the force production to 125 mM KCl was reduced by TMEM16A downregulation.We conclude that TMEM16A is essential for both ICl(Ca)s while best3 may be modifying the TMEM16A current characteristics in a subset of channels. The cGMP‐dependent ICl(Ca) is critical for vasomotion and normal expression of TMEM16 is essential for VSMC conctractility.

Requirement for Functional BK Channels in Maintaining Oscillation in Venomotor Tone Revealed by Species Differences in Expression of the β1 Accessory Subunits

We determined the possible role of large-conductance Ca2+-activated K (BK) channels in regulation of venous tone in small capacitance veins and blood pressure. In rat mesenteric venous smooth muscle cells (MV SMC), BK channel α- and β1-subunits were coexpressed, unitary BK currents were detected, and single-channel currents were sensitive to voltage and [Ca2+]i. Rat MV SMCs displayed Ca sparks and iberiotoxin-sensitive spontaneous transient outward currents. Under resting conditions in vitro, rat MV exhibited nifedipine-sensitive spontaneous oscillatory constrictions. Blockade of BK channels by paxilline and Ca2+ sparks by ryanodine constricted rat MV. Nifedipine caused venodilation and blocked paxilline-induced, KCl-induced (20 mM), and BayK8644-induced contraction. Acute inhibition of BK channels with iberiotoxin in vivo increased blood pressure and reduced venous capacitance, measured as an increase in mean circulatory filling pressure in conscious rats. BK channel α-subunits and L-type Ca2+ channel α1-C subunits are expressed in murine MV. However, these channels are not functional because murine MV lack nifedipine-sensitive basal tone and rhythmic constrictions. Murine MV were also insensitive to paxilline, ryanodine, KCl, and BayK8644, consistent with our previous studies showing that murine MV do not have BK β1-subunits. These data show that not only there are species-dependent properties in ion channel control of venomotor tone but also BK channels are required for rhythmic oscillations in venous tone.

Evidence both L-type and non-L-type voltage-dependent calcium channels contribute to cerebral artery vasospasm following loss of NO in the rat

We recently found block of NO synthase in rat middle cerebral artery caused spasm, associated with depolarizing oscillations in membrane potential (Em) similar in form but faster in frequency (circa 1Hz) to vasomotion. T-type voltage-gated Ca2+ channels contribute to cerebral myogenic tone and vasomotion, so we investigated the significance of T-type and other ion channels for membrane potential oscillations underlying arterial spasm. Smooth muscle cell membrane potential (Em) and tension were measured simultaneously in rat middle cerebral artery. NO synthase blockade caused temporally coupled depolarizing oscillations in cerebrovascular Em with associated vasoconstriction. Both events were accentuated by block of smooth muscle BKCa. Block of T-type channels or inhibition of Na+/K+-ATPase abolished the oscillations in Em and reduced vasoconstriction. Oscillations in Em were either attenuated or accentuated by reducing [Ca2+]o or block of KV, respectively. TRAM-34 attenuated oscillations in both Em and tone, apparently independent of effects against KCa3.1. Thus, rapid depolarizing oscillations in Em and tone observed after endothelial function has been disrupted reflect input from T-type calcium channels in addition to L-type channels, while other depolarizing currents appear to be unimportant. These data suggest that combined block of T and L-type channels may represent an effective approach to reverse cerebral vasospasm.

Vasomotion and insulin‐mediated capillary recruitment – part of the explanation?

Vasomotion and insulin‐mediated capillary recruitment – part of the explanation?

Vasomotion has chloride-dependency in rat mesenteric small arteries

The possibility that Ca(2+)-activated Cl(-) conductances (CaCCs) contribute to oscillations in vascular tone (vasomotion) is tested in isolated mesenteric small arteries from rats where cGMP independent (I (Cl(Ca))) and cGMP-dependent (I (Cl(Ca,cGMP))) chloride conductances are important. The effect of anion substitution and Cl(-) channel blockers on noradrenaline (NA)-stimulated tension in isometrically mounted mesenteric arteries and for chloride conductance of smooth muscle cells isolated from these arteries were assessed electrophysiologically. Cl(-) (o) replacement with aspartate blocked vasomotion while 36mM SCN(-) (o) (substituted for Cl(-)) was sufficient to inhibit vasomotion. Oscillations in tone, membrane potential, and [Ca(2+)](i) disappeared with 36mM SCN(-). DIDS and Zn(2+) blocked I (Cl(Ca,cGMP)) but not I (Cl(Ca)). Vasomotion was not sensitive to DIDS and Zn(2+), and DIDS and Zn(2+) induce vasomotion in arteries without endothelium. The vasomotion in the presence of DIDS and Zn(2+) was sensitive to 36mM SCN(-) (o). The anion substitution data indicate that Cl(-) is crucial for the V (m) and [Ca(2+)](i) oscillations underlying vasomotion. The Cl(-) channel blocker data are consistent with both CaCCs being important.

Characterisation of Tone Oscillations in Placental and Myometrial Arteries from Normal Pregnancies and Those Complicated by Pre-eclampsia and Growth Restriction

Agonist-induced tone oscillations (rhythmic contractions and relaxations) occur in vascular beds to allow acute regulation of volume flow and thus the delivery of oxygen and nutrients to the tissue. Mechanisms responsible for the control of human placental vasomotor tone and blood flow are poorly characterized. This study aimed to characterise thromboxane-induced tone oscillations in human placental and myometrial arteries. Chorionic plate and myometrial arteries obtained from biopsies at term were mounted for isometric tension measurement. Tone oscillations were observed in chorionic arteries only when exposed to sub-maximal (<1 μM) concentrations of U46619. Slow (mean ± SEM) frequency (2.6 ± 0.5 per hour), large amplitude (39 ± 7% of peak contraction) tone oscillations were elicited by 0.03 μM U46619 ( n = 18). In the presence of the nitric oxide synthase (NOS) inhibitor l-NNA (100 μM) the amplitude was significantly reduced (40 ± 13% to 18 ± 8%, P < 0.05, n = 6), frequency was unaltered and the bradykinin-dependent vasodilator response was reduced (68 ± 13% to 40 ± 19%, P < 0.05, n = 6). Myometrial arteries exposed to 1 μM U46619 developed tone oscillations within 10 min, which increased in amplitude over 30 min occurring at relatively constant frequency. The mean amplitude of oscillations at 30 min (31 ± 7%, n = 16) was similar to that in chorionic arteries but the occurrence more frequent (42.8 ± 9.7 per hour, P < 0.001). Inhibition of NOS did not alter tone oscillations in myometrial arteries. Tone oscillations in chorionic arteries from pre-eclamptic and growth restricted (FGR) pregnancies were reduced in amplitude whereas those in myometrial arteries had increased frequency. Inhibition of NOS further reduced oscillation amplitude in chorionic arteries from FGR pregnancies. The alterations may contribute to the vasculopathology of these conditions, or, may represent compensatory mechanisms to maintain a matching of materno-placental blood flow.

Antiphase oscillations of endothelium and smooth muscle [Ca 2+] i in vasomotion of rat mesenteric small arteries

The mechanisms leading to vasomotion in the presence of noradrenaline and inhibitors of the sarcoplasmic/endoplasmic reticulum calcium ATPase were investigated in isolated rat mesenteric small arteries. Isobaric diameter and isometric force were measured together with membrane potential in endothelial cells and smooth muscle cells (SMC). Calcium in the endothelial cells and SMC was imaged with confocal microscopy. In the presence of noradrenaline and cyclopiazonic acid, ryanodine-insensitive oscillations in tone were produced. The frequency was about 1 min −1 and amplitude about 70% of the maximal tone. The amplitude was reduced by indomethacin and increased with L-NAME. Vasomotion was inhibited by nifedipine and by 40 mM potassium. The frequency was increased and amplitude decreased by removal of the endothelium and by application of charybdotoxin and apamin. The vasomotion was associated with in-phase oscillations of membrane potential in endothelial cells and SMC and oscillations of [Ca 2+] i that were in near anti-phase. We suggest a working model for the generation of oscillation based on a membrane oscillator where ion channels in both endothelial cells and SMC interact via a current running between the two cell types through myoendothelial gap junctions, which sets up a near anti-phase oscillation of [Ca 2+] i in the two cell types.

Characteristics of Resonance in Heart Rate Variability Stimulated by Biofeedback

As we previously reported, resonant frequency heart rate variability biofeedback increases baroreflex gain and peak expiratory flow in healthy individuals and has positive effects in treatment of asthma patients. Biofeedback readily produces large oscillations in heart rate, blood pressure, vascular tone, and pulse amplitude via paced breathing at the specific natural resonant frequency of the cardiovascular system for each individual. This paper describes how resonance properties of the cardiovascular system mediate the effects of heart rate variability biofeedback. There is evidence that resonant oscillations can train autonomic reflexes to provide therapeutic effect. The paper is based on studies described in previous papers. Here, we discuss the origin of the resonance phenomenon, describe our procedure for determining an individual's resonant frequency, and report data from 32 adult asthma patients and 24 healthy adult subjects, showing a negative relationship between resonant frequency and height, and a lower resonant frequency in men than women, but no relationship between resonant frequency and age, weight, or presence of asthma. Resonant frequency remains constant across 10 sessions of biofeedback training. It appears to be related to blood volume.