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C Julien

Publications and source records attributed to C Julien.

At least 19 recordsLinked to original sources
PubMed1998

The arterial baroreceptor reflex of the rat exhibits positive feedback properties at the frequency of mayer waves.

1. Modelling studies have led to the proposal that Mayer waves ( approximately 0.4 Hz in rats) could result from a resonance phenomenon in a feedback control loop. In this study, we investigated the presence of a resonance frequency in the arterial baroreceptor reflex loop, i.e. a particular frequency at which arterial pressure feeds back positively to the baroreceptors. 2. Frequency responses of mean arterial pressure (MAP) to aortic depressor nerve (ADN) stimulation were studied in fifteen urethane anaesthetized, ventilated rats with cardiac autonomic blockade. The ADN was stimulated using rectangular trains of impulses (2 ms, 100 Hz) delivered at frequencies ranging from 0.1 to 1 Hz. Phase angles between impulses and MAP were calculated using cross-spectral analysis based on a fast Fourier transform algorithm. 3. Rhythmic ADN stimulation induced regular MAP oscillations at the expected frequencies that were attenuated by alpha-adrenoceptor blockade and abolished after ganglionic blockade. The relationship between impulse and MAP oscillations was characterized by a strong coherence and a positive phase shift at low frequencies, indicating that impulses led MAP with respect to the out-of-phase pattern. Deviation of the phase from the out-of-phase behaviour was mainly due to the presence of a fixed time delay ( approximately 0.8 s) between ADN stimuli and MAP changes. Phase angles fell to zero at 0.42 +/- 0.02 Hz. 4. In rats, the arterial baroreceptor reflex exhibits a resonance frequency close to the frequency of spontaneously occurring Mayer waves. The reflex therefore seems the most likely origin for the Mayer waves.

Adrenergic alpha-Antagonists↗
PubMed1998

Short-term haemodynamic variability in the conscious areflexic rat.

1. Simultaneous measurements of arterial pressure and cardiac output (n = 8), mesenteric blood flow (n = 7) or hindquarters (n = 8) blood flow were performed during 1 h periods in conscious rats, before and after acute pharmacological blockade of the autonomic, renin-angiotensin and vasopressin systems. In the latter condition (areflexic state), arterial pressure was maintained with a continuous infusion of noradrenaline. 2. In the areflexic state, spontaneous fluctuations in arterial pressure were markedly exaggerated, especially depressor episodes. At the onset of these falls in arterial pressure, there was an abrupt and transient decrease in stroke volume and cardiac output. Systemic vasodilatation then developed while cardiac output returned to normal. Regional vasodilatations were also delayed from the onset of the falls in arterial pressure and were usually large enough to maintain blood flow. 3. Both time and frequency domain analyses confirmed that changes in systemic and regional vascular conductances lagged by about 1 s behind arterial pressure changes. 4. These results indicate that, in the absence of neurohumoral influences, autoregulatory-like mechanisms become dominant in the control of systemic and regional circulations and contribute to exaggeration of the spontaneous short-term variability of arterial pressure.

Animals↗
PubMed1998

Characterization of a major slow oscillation in the mesenteric circulation of conscious rats.

1. Little is known about spontaneous slow rhythms in regional circulations. The present study was aimed at characterizing low-frequency (LF; 78-269 mHz) oscillations in the mesenteric and hindquarter circulations of conscious rats. 2. Mean arterial pressure (MAP) and indices (pulsed Doppler technique) of mesenteric (n = 25) and hindquarter (n = 23) blood flows were recorded in conscious, freely moving rats during 1 h periods. Fast Fourier transform analysis was applied to beat-to-beat data after resampling at 10 Hz of consecutive 205 s time series. 3. A major oscillation centred at 164 +/- 4 mHz was present in the mesenteric, but not in hindquarter, circulation. Consequently, LF power accounted for approximately 43% of the overall variability of mesenteric blood flow. Cross-spectral analysis performed between MAP and mesenteric blood flow indicated that fractional changes in flow were approximately two-fold of those in MAP, in pressure, at the peak frequency. 4. Acute blockade of the autonomic, renin-angiotensin and vasopressin systems combined with noradrenaline infusion (n = 7) reduced the frequency of the mesenteric blood flow oscillation (115 +/- 6 mHz) but did not change its contribution to overall flow variability (approximately 48%). A clear oscillation was still present after acute inhibition of nitric oxide (NO) synthesis with NG-nitro-L-arginine methyl ester (n = 8), but was virtually absent in chronically guanethidine-sympathectomized rats (n = 12). 5. In conclusion, the mesenteric blood flow of conscious rats exhibits a major slow oscillation that originates in the mesenteric vasculature and is not secondary to the activity of the major pressor systems or to the cyclic release of NO. Because of the strong attenuation of the oscillation in sympathectomized rats, we suggest that adrenergic vasoconstrictor tone plays a permissive role in its genesis.

Animals↗
PubMed1998

Beat-to-beat estimation of windkessel model parameters in conscious rats.

A windkessel model was applied on a beat-to-beat basis to evaluate the arterial mechanical characteristics in seven conscious rats. Ascending aortic arterial pressure (AP) and blood flow were recorded during steady-state in basal conditions, during infusions of isoprenaline, sodium nitroprusside, and phenylephrine, and after intravenous atenolol injection. For each cardiac cycle the exponential decay time constant (tau) was estimated from the aortic AP curve, peripheral resistances (R) were taken as the ratio of mean AP to cardiac output, and systemic arterial compliance (C) was calculated as tau/R. In all conditions, mean correlation coefficients of the exponential regression and approximately 70% of values in each rat were > 0.99, demonstrating the model validity. In all conditions tau and C exhibited a large spontaneous variability over time, and beat-to-beat correlations were high between tau and C (0.83 +/- 0.03). C was increased by sodium nitroprusside, decreased by isoprenaline, but not significantly decreased by phenylephrine [5.1 +/- 0.2, 3.2 +/- 0.3, and 3.9 +/- 0.2 microliters/mmHg, respectively, vs. 4.2 +/- 0.3 microliters/mmHg (baseline)]. In conclusion, the windkessel model enables tau and C to be reliably estimated in conscious rats during spontaneous and drug-induced hemodynamic variations.

Animals↗
PubMed1996

Baroreceptor modulation of regional haemodynamic responses to acute stress in rat.

We examined the effects of chronic sinoaortic denervation (SAD) on regional haemodynamic responses to acute environmental stress in rats. In conscious male intact (n = 12) and SAD (2 weeks before study, n = 7) rats, arterial pressure and blood flow velocities (pulsed Doppler probes) in the subdiaphragmatic aorta, superior mesenteric artery and distal aorta (hindquarters) were simultaneously recorded. In response to air jet stress, intact rats showed modest increases in arterial pressure that were accompanied by vasoconstriction in the mesentery and vasodilatation in the hindquarters. These regional haemodynamic changes were almost balanced, as indicated by the lack of change in the subdiaphragmatic aortic conductance. SAD markedly enhanced the pressor and mesenteric vasoconstrictor responses and blunted the hindquarters vasodilatation. After acute beta-adrenoceptor blockade with propranolol, the stress-induced hindquarters vasodilatation was strongly reduced in the intact rats and was reversed into vasoconstriction in the SAD rats. These results point to an opposing interaction between centrally-induced sympathoexcitation and arterial baroreceptor reflex activation during stress. This probably favours the hyperaemic response in the skeletal muscles at a lower metabolic cost.

Animals↗
PubMed1996

Spontaneous cardiac baroreceptor reflex and regional circulations in conscious rats.

OBJECTIVE: To determine the relationships between the activity of the spontaneous cardiac baroreceptor reflex (BRX) and regional vascular dynamics in conscious unrestrained rats. DESIGN: Simultaneous beat-to-beat recordings of blood pressure and measurements of indices of mesenteric and hindquarters blood flows were performed in seven male normotensive conscious rats under baseline conditions during 1 h. METHODS: The relationships between systolic blood pressure (SBP) and heart rate were examined using a computerized method, giving the degree of statistical dependence between values of the two parameters with the Z coefficient. This analysis permitted detection of cardiac beats related to cardiac BRX activity. Z analysis was also applied to SBP and to mesenteric or hindquarters blood flow or vascular resistance. Time-series representations were used to describe the chronological patterns corresponding to BRX spontaneous activity. RESULTS: In these rats, which presented spontaneous BRX-like patterns manifested by the Z analysis, BRX was active during approximately 15% of the time. For 80% of these patterns, cardiac BRX acted to buffer falls in SBP. These depressor events were preceded by muscular vasodilations whereas vasodilations in the mesentery were delayed. Z analysis of these spontaneous haemodynamic patterns confirmed that muscular vasodilations were strongly associated with falls in SBP, whereas vasodilations lagged behind SBP by about seven beats and were not dependent on simultaneous SBP values. CONCLUSIONS: The Z method showed that spontaneous hindquarters vasodilations were associated with cardiac BRX patterns and that mesenteric vasodilations were not concomitant with falls in SBP and may be the consequence either of a delayed central response or of a local mechanism such as myogenic autoregulation.

Animals↗
PubMed1996

Renin secretion in conscious Lyon hypertensive rats.

To characterize the renin secretory profile in Lyon hypertensive (LH) rats, renin responses to reductions of arterial pressure and beta-adrenoceptor stimulation were assessed in conscious unrestrained LH (n = 13) and Lyon normotensive (LN, n = 14) rats under normal-salt diet. Mean arterial pressure (MAP) in the infrarenal aorta was recorded beat to beat for 3 h. Then, plasma renin concentration (PRC) was measured 1) in basal conditions, 2) during 10-mmHg stepwise reductions of MAP down to 60 mmHg using a chronically implanted aortic inflatable cuff, and 3) during isoprenaline infusion (62.5, 125, and 250 ng.kg-1.min-1 iv). Compared with LN, LH rats had an elevated MAP (146 +/- 3 vs. 111 +/- 1 mmHg, P < 0.001) and decreased PRC [4.2 +/- 0.6 vs. 8.2 +/- 0.8 ng angiotensin (ANG) I.ml-1.h-1, P < 0.001] and kidney renin content (216 +/- 14 vs. 1,149 +/- 103 micrograms ANG I.h-1.g-1, P < 0.001). Pressure-dependent renin release occurred below 90 mmHg in LN rats and below 80 mmHg in LH rats, and its sensitivity in the low-pressure range did not differ between strains. Isoprenaline-induced increases in PRC were weaker (P < 0.01) in LH than in LN rats. In additional LH and LN rats (n = 6-8), acute ANG II AT1-receptor blockade with losartan (20 mg/kg, followed by 10 mg.kg-1.h-1 iv for 2 h) induced lesser (P < 0.001) PRC increases in LH than in LN rats. Renin responses to isoprenaline remained blunted (P < 0.01) during losartan infusion in LH rats. We conclude that, in LH rats, renin secretion is independent of MAP in the range of its spontaneous variations and is poorly responsive to beta-adrenoceptor stimulation, the alteration of which cannot be explained by an enhanced feedback inhibition by ANG II.

Adrenergic beta-Agonists↗
PubMed1995

Involvement of vasodilator mechanisms in arterial pressure lability after sino-aortic baroreceptor denervation in rat.

1. To examine the regional haemodynamic basis of arterial pressure lability seen after sino-aortic baroreceptor denervation (SAD), simultaneous beat-to-beat recordings of arterial pressure and indices of regional blood flows (Doppler probes around the subdiaphragmatic and lower abdominal aortae and the superior mesenteric artery) were performed in the same conscious rats (n = 7) before, 1 and 14 days after SAD. 2. Acute SAD increased arterial pressure, decreased regional blood flows and vascular conductances, and potentiated the depressor and vasodilator effects of ganglionic blockade with trimethaphan, suggesting sympathetic overactivity. All parameters chronically returned to or near normal. 3. Both acute and chronic SAD increased the variability of arterial pressure and of regional conductances. Arterial pressure lability was characterized by a mixture of depressor and pressor events which were associated with regional vasodilatations and vasoconstrictions, respectively. This haemodynamic pattern was not affected by acute beta-adrenoceptor blockade with propranolol. 4. In conscious rats, the baroreceptor reflex acts to buffer the spontaneous variability of regional vascular conductances and thereby stabilizes arterial pressure. Sino-aortic baroreceptor denervation-induced arterial pressure lability does not depend on the level of sympathetic activation, and is determined by the relative contribution of depressor and pressor events accompanied by extensive vasodilatations and vasoconstrictions, respectively. Vasodilatations are not caused by the stimulation of vascular beta 2-adrenoceptors.

Animals↗
PubMed1995

Hemodynamic analysis of arterial pressure oscillations in conscious rats.

This study examined the contribution of rhythmic fluctuations of regional blood flow and vascular conductance to the genesis of low- (LF, 0.27-0.74 Hz) and high- (HF, 0.76-5 Hz) frequency oscillations of arterial pressure. In conscious 15-week-old male intact (n = 11), guanethidine-sympathectomized (n = 8) and chronically sinoaortic denervated (n = 7) rats, arterial pressure and regional blood flow velocities (pulsed Doppler probes) were simultaneously recorded. Indices of subdiaphragmatic aortic, hindquarters and superior mesenteric conductances were calculated on a beat-to-beat basis over a 60-min period. Spectral power was calculated in the LF and HF bands using a fast Fourier transform algorithm. Transfer function analysis was also performed to calculate coherence and phase between arterial pressure and regional flows and conductances. In the LF band, spectral power of arterial pressure was decreased by approx. 85% in sympathectomized and approx. 54% in sinoaortic denervated rats. In the HF band, spectral power did not differ between the groups. In the three groups of rats, relations between arterial pressure and blood flow were characterized by a significant coherence in the HF band with little or no phase delay (synchronous oscillations). Relations between arterial pressure and vascular conductance were characterized in intact rats by a significant coherence in the LF band and a phase delay tending to pi radians (opposite oscillations), whereas in both sympathectomized and sinoaortic denervated rats, coherence did not reach significance. It is concluded that LF oscillations of arterial pressure are mostly secondary to rhythmic fluctuations in the vasomotor sympathetic tone in several regional circulations. Part of these oscillations originate from the synchronizing influence of the baroreceptor reflex. The study also suggests that the respiratory (HF) oscillations of arterial pressure involve fluctuations in cardiac output of purely mechanical origin.

Animals↗
PubMed1995

How sympathetic tone maintains or alters arterial pressure.

After chronic sympathectomy or sinoaortic denervation (SAD), arterial pressure (AP) becomes extremely unstable, especially because of movement-related depressor episodes. The simultaneous measurement of AP and regional blood flows in sympathectomized and SAD rats indicates that these depressor episodes are accompanied by strong regional vasodilations, possibly involving an autoregulatory component. The sympathetic nervous system, mainly through baroreflex modulation of its activity, overrides these responses and thereby, considerably limits the AP variability. In the conscious unrestrained rat, AP fluctuates in a narrow range (variation coefficients calculated over 1-hour beat-to-beat recordings are typically approximately 5%). This variability of AP involves sympathetically-mediated pressor episodes that are coupled to behavior and alerting environmental stimuli. Regarding the latter, studies in SAD rats point to an opposing interaction between centrally-induced sympathoexcitation and baroreflex activation. Another component of normal AP variability appears as an oscillation centered around 0.4 Hz. Spectral analysis of AP and regional hemodynamic variables indicates that this oscillation is secondary to rhythmic fluctuations in the vasomotor sympathetic tone that are synchronized by the arterial baroreceptor reflex. It is concluded that both stability and normal variability of AP critically depend on the baroreflex control of the sympathetic vascular tone.

Animals↗
PubMed1994

Hemodynamic analysis of arterial pressure lability in sympathectomized rat.

Male Sprague-Dawley rats, treated with either saline (n = 14) or guanethidine (n = 12) from 1 to 13 wk of age, were instrumented for the measurement of mean arterial pressure (MAP) and indexes of regional blood flows (pulsed Doppler flow probes) in the subdiaphragmatic aorta, superior mesenteric artery, and distal aorta (hindquarters). Hemodynamic parameters were simultaneously recorded in the conscious rats on a beat-to-beat basis by a computer. Chronic sympathectomy did not change the MAP level but nearly doubled its spontaneous variability, mainly due to large decreases in MAP associated with regional vasodilations that were slightly delayed with respect to the onset of the decreases in pressure, especially in the aortic and mesenteric circulations. In the hindquarters vascular bed, the onset of vasodilations sometimes coincided with the onset of the decreases in MAP. During depressor episodes, blood flow varied little (aortic and mesenteric circulations) or even increased (hindquarters). This hemodynamic pattern was not affected by acute beta-adrenoceptor blockade. We conclude that chronic sympathectomy sensitizes the cardiovascular system to decreases in arterial pressure mainly by unmasking local autoregulatory responses of regional circulations. The sympathetic control of vascular tone overrides these responses and considerably limits the MAP variability.

Adrenergic beta-Antagonists↗
PubMed1994

Pressure-dependent renin release and arterial pressure maintenance in conscious rats.

The relationship between pressure-dependent renin release and mean arterial pressure (MAP) level was assessed in normotensive intact (n = 10), sympathectomized (guanethidine at 1-13 wk of age; n = 8), and renal-denervated (1 wk before the study; n = 6) rats under normal-salt diet. MAP was recorded beat-to-beat for 2 h in conscious animals. Then plasma renin concentration (PRC) responses to graded reductions of MAP were determined using an aortic inflatable cuff. Neither sympathectomy nor renal denervation altered baseline MAP level and PRC. Lowering MAP below a threshold pressure induced large increases in PRC. Threshold pressure did not differ between intact (87 +/- 1 mmHg), sympathectomized (88 +/- 2 mmHg), and renal-denervated (83 +/- 2 mmHg) rats. MAP frequently fell below threshold pressure in sympathectomized but not in intact and renal-denervated rats. We conclude that in conscious normotensive quiet rats under normal-salt diet the pressure-dependent renin release is not activated spontaneously and is therefore unlikely to play a role in MAP maintenance. This regulatory mechanism develops and operates normally in the absence of sympathetic nerves.

Animals↗
PubMed1993

Role of vasoconstrictor tone in arterial pressure lability after chronic sympathectomy and sinoaortic denervation in rats.

In both chronically sympathectomized (SNX) and sinoaortic denervated (SAD) rats, removal of vasoconstrictor influences decreases mean arterial pressure (MAP) and its variability in parallel. This study examined if this decrease in arterial pressure lability is solely a result of decreasing vascular tone. In conscious 14-week-old male sympathectomized (guanethidine at 1-13 weeks of age) and sinoaortic denervated (2 weeks before study) rats, arterial pressure was recorded beat-to-beat during 30-min consecutive periods; control; ganglionic blockade in sinoaortic denervated rats and angiotensin converting enzyme inhibition plus vasopressin antagonism in sympathectomized rats; and restoration of the initial arterial pressure with continuous infusions of phenylephrine and angiotensin II. Sympathectomized and, even more, sinoaortic denervated rats had increased pressure variability. Neural or humoral blockade markedly reduced arterial pressure and its liability in both groups of rats and subsequent restoration of the arterial pressure with vasoconstrictor infusions returned lability to levels either slightly above (sympathectomy) or below (sinoaortic denervation) control values. In basal conditions, an increased frequency of occurrence of depressor episodes was evidenced in sympathectomized rats whereas a variable ratio of pressor to depressor events was observed in sinoaortic denervated rats. During vasoconstrictor infusions, blood pressure lability was mainly due to depressor events in both groups of rats. It is concluded that the background vascular tone provided by endogenous pressor systems is necessary for the expression of the depressor component of blood pressure lability in sinoaortic denervated and in sympathectomized rats. The study also suggests that in sympathectomized rats, humoral influences act to limit rather than enhance blood pressure lability, whereas in sinoaortic denervated rats, the sympathetic nervous system may directly generate part of the lability.

Angiotensin II↗
PubMed1993

Do thymic-neuroendocrine interactions play a role in the antihypertensive effect of neonatal thymectomy in Lyon hypertensive rats?

Previous studies showed that neonatal thymectomy prevented the spontaneous increase in blood pressure in genetically hypertensive rats (LH) of the Lyon strain, leaving untouched that of their normotensive controls (LN). As the thymus is connected to the neuroendocrine system through secretion of hormonal factors, we investigated the possible role played by these factors in hypertension of LH rats. To that end we studied, in sham-operated and neonatally thymectomized LH rats, the blood pressure effects of thymostimulin, a partially purified thymus extract and examined whether changes in major neuroendocrine factors of blood pressure regulation occurred in thymectomized LH rats. Thymostimulin (1 or 10 mg/kg/48 h) did not modify blood pressure in sham-operated LH rats and failed to consistently increase it in neonatally thymectomized animals. Urinary mineralocorticoids, catecholamines and their metabolites, and plasma renin levels were not altered by neonatal thymectomy. Plasma testosterone was decreased to a similar degree by neonatal thymectomy in LH and normotensive controls. These results do not favor a pressor role of thymic hormonal factors in LH rats and show that the antihypertensive effect of neonatal thymectomy is not secondary to a decreased secretion of catecholamines, renin, mineralocorticoids, and testosterone. They therefore suggest that the role of the thymus in genetically hypertensive LH rats is more likely mediated by cellular immune mechanisms than by hormonal processes.

Animals↗