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PubMed1995

Modulation of baroreflex function by angiotensin II endogenous to the caudal ventrolateral medulla.

Neurons in the ventrolateral medulla (VLM) mainly determine the tonic sympathetic activity. The caudal VLM (CVLM) relays baroreflex signals to the rostral VLM. We have reported that endogenous angiotensin II (ANG II) contributes to the ongoing activity of the VLM neurons. In the present study, we examined if ANG II endogenous to the CVLM modulates the baroreflex function in anesthetized normotensive Sprague-Dawley rats. Changes in renal sympathetic nerve activity (RSNA) in response to changes in mean arterial pressure (MAP) induced by i.v. infusion of phenylephrine and nitroglycerin were recorded before and after bilateral microinjection of [Sar1, Thr8]-ANG II, an ANG II antagonist, into the CVLM. The ANG II antagonist injection into the CVLM significantly increased MAP and RSNA by 17.6 +/- 8.0 mmHg (mean +/- S.D.) and 36.3 +/- 18.1%, respectively. It also significantly increased the baroreflex sensitivity (BS) from -0.49 +/- 0.38 to -0.74 +/- 0.37%/mmHg during nitroglycerin infusion. In contrast, the BS examined by phenylephrine infusion was not altered by the pretreatment with ANG II antagonist. Injection of artificial CSF affected neither the baseline values of MAP and RSNA nor the BS. These results suggest that ANG II endogenous to the CVLM exert a modulating role in baroreflex control of RSNA.

Adrenergic Fibers↗
PubMed1996

Cardiac baroreflex properties in myocardial infarcted rats.

Recent studies demonstrated that chronic but not acute myocardial infarction impairs the cardiopulmonary reflex. The aim of the present study was to evaluate the baroreflex in awake rats bearing short-term (1 day) or long-term (30 days) myocardial infarction. Left ventricular infarction was produced by ligation of the anterior descending branch of the left coronary artery. In order to examine the baroreceptor reflex function by means of sigmoidal curvefitting analysis in conscious rats, reflex heart rate responses were elicited by alternate intravenous injections of phenylephrine (change, +5 to +40 mmHg) and sodium nitroprusside (change, -5 to -40 mmHg). Infarcted rats showed either hypotension plus tachycardia (1 day) or bradycardia (30 days) in resting conditions. The baroreceptor reflex gain (sensitivity) was significantly increased in 30 days (5.20 +/- 0.33 bpm/mmHg, p < 0.01) but not in 1 day (3.78 +/- 0.20 bpm/mmHg) infarcted rats when compared to sham rats (3.83 +/- 0.16 bpm/mmHg). Transmural antero-medio-lateral infarcted areas spanned over nearly 37% (1 day group) and 35% (30 days group) of the left ventricular circumference. Myocardial hypertrophy was showed in right ventricle (39%, p < 0.01) as well as in right (35%, P < 0.05) and left atria (127%, p < 0.001) in the 30 days but not in the 1 day infarcted group. The enhancement of baroreflex correlated significantly with the extent of myocardial necrosis in the 30 days infarcted group. We conclude that baroreflex control of heart rate is well preserved in short- but exaggerated in long-term myocardial infarction. The enhancement of the baroreflex gain could reflect a compensatory mechanism to the impairment of the cardiopulmonary reflex following chronic myocardial infarction and thus contributing to sustain the arterial pressure and heart rate in low levels.

Animals↗
PubMed2006

Baroreflex responses in neuronal nitric oxide synthase knoukout mice (nNOS).

The present study sought to determine the influence of the neuronal isoform of nitric oxide synthase (nNOS) on the baroreflex gain (mean index: bpm/mm Hg) and on the respiratory response to baroreflex activation by using nNOS knockout (nNOS-/-) mice. Experiments were performed with nNOS+/+ wild type (WT; n=12) and nNOS-/- mice (n=11), both of the C57Bl6 strain, randomly assigned to the two groups. Carotid artery and external jugular vein were cannulated under halothane, and after recuperation, urethane was intravenously injected. Baroreflex gain was evaluated by intravenous injection of phenylephrine (PE: 15-18 microg/kg) and sodium nitroprusside (SNP: 46-50 microg/kg) in WT and nNOS-/- anesthetized mice. At baseline, nNOS-/- mice had a comparable heart rate (604.5+/-23.6 vs. 618.7+/-11.2 bpm) but higher mean arterial pressure (112.4+/-6.3 vs. 94.8+/-3.9 mm Hg, P<0.05) than WT mice. Heart rate reflex was significantly reduced (P<0.05) in nNOS-/- mice, tachycardic and bradycardic responses were -1.04+/-0.3 and -2.03+/-0.5 in nNOS-/- mice vs. -4+/-0.7 and -4.52+/-0.2 in WT mice, respectively. To characterize the effect of arterial pressure changes on respiratory output, PE was injected in a separate group of WT (n=7) and nNOS-/- (n=6) mice. Tidal diaphragm activity decreased in WT mice (P<0.05); however, diaphragm minute respiration and respiratory frequency were not different between the strains of mice. In nNOS-/- group, heart rate reflex by PE injection was significantly reduced (P<0.05). These findings suggest that the absence of nNOS activity leads to an elevation of the baseline blood pressure and also shows the importance of this enzyme on the transmission of baroreflex signals.

Analysis of Variance↗
PubMed2006

Central actions of angiotensin II on spontaneous baroreflex sensitivity in the trout Onc orhynchus mykiss.

The goal of the present study was to investigate the central action of native angiotensin II (ANG II) on the spontaneous baroreflex sensitivity (BRS) in unanesthetized trout. The animals were equipped with two subcutaneous electrocardiographic (ECG) electrodes, a dorsal aorta catheter and an intracerebroventricular (ICV) cannula which was inserted within the third ventricle of the brain. The ECG and the systolic blood pressure (SBP) signals were recorded during a pre-injection period of 5 min and during five post-injection periods of 5 min. All injections were made at the fifth minute of the test. The time-series were processed with a sequence technique in order to detect the sequences of three or more consecutive increases in the SBP pulse, or three or more decreases in the SBP pulse correlated respectively with one delay beat increase of the RR interval of the ECG signal or shortening of this interval. The slope of the average regression line between the SBP and the RR intervals for each type of sequence was taken as a measure of the spontaneous BRS. Compared with pre-injection values, the ICV injection of vehicle (0.5 microl) had no effect on heart rate (HR), SBP, the total number of positive or negative sequences or on the spontaneous BRS during the post-injection periods. By contrast, ANG II at doses of 5 and 50 pmol increased HR but only 50 pmol ANG II elevated SBP. For all doses, ANG II depressed the spontaneous BRS, but the peptide had no effect upon the number of each baroreflex sequences. Intra-arterial injections of atropine dramatically reduced the number of positive and negative baroreflex sequences and decreased the sensitivity of the few remaining sequences, suggesting that the autonomic control of the cardiac BRS was solely due to vagal parasympathetic control. In atropinized trout the ICV injection of 5 pmol ANG II had no effect upon HR, SBP and the baroreflex parameters. This study determines for the first time the spontaneous BRS in a non-mammalian species and demonstrates an inhibitory action of ICV injection of ANG II upon this variable through a probable control of the vagal parasympathetic activity.

Angiotensin II↗
PubMed1996

Arterial baroreflex sensitivity assessed from phase IV of the Valsalva maneuver.

To assess the feasibility of 2 noninvasive methods for arterial baroreflex sensitivity testing based on phase IV of the Valsalva maneuver, the performance of a simple arterial baroreflex sensitivity index compared with a slope method and reproducibility of repeated measurements of either parameter were evaluated in 36 subjects without structural heart disease. The study showed feasibility and reproducibility of both these methods for arterial baroreflex sensitivity assessment and demonstrated the importance of an appropriate rest period between repeated Valsalva maneuvers, giving a basis for prospective testing of noninvasive determination of arterial baroreflex sensitivity together with phenylephrine method in survivors of myocardial infarction.

Adolescent↗
PubMed1998

Nocturnal variation in human sympathetic baroreflex sensitivity.

To determine whether or not there are nocturnal variations in sympathetic baroreflex sensitivity (BRS), we measured spontaneous sympathetic BRSs in eight normal subjects (average 24.5 years old) between 2300 and 0700 h. Electrocardiogram, blood pressure, polysomnography, and muscle sympathetic nerve activity (MSA) using microneurography were recorded. We defined cardiac 'baroreflex sequences' as those that contain three or more adjacent pulses, with the systolic blood pressure and the subsequent pulse interval either continuously increased or decreased. A similar analysis was applied to sympathetic BRSs. We selected three or more adjacent pulses during which diastolic blood pressures continuously increased or decreased. Total activity in MSA was defined as burst per minute x burst amplitude and we calculated the regression coefficients between the diastolic blood pressure and the subsequent total activities in MSA. The regression coefficients were classified as either negative or positive ones. When they were less than zero, we termed them 'baroreflex sequences'. Cardiac and sympathetic BRSs were estimated from the average slope of the baroreflex sequences. Sympathetic BRS was significantly lower during sleep than while subjects were awake in the evening (P < 0.05), and it remained low after the subjects woke up in the morning (P < 0.05). Conversely, cardiac BRS had a tendency to increase during sleep in the night, but not statistically significant. This sympathetic BRS pattern may contribute to diurnal haemodynamic variables and may account, at least in part, for the connection between circadian rhythm and cardiovascular disease.

Adult↗
PubMed1998

Baroreflex control of muscle sympathetic nerve activity is attenuated in the elderly.

To determine whether the baroreflex control of sympathetic nerve activity is attenuated in the elderly, muscle sympathetic nerve activity (MSNA) from the tibial nerve was monitored using microneurography, and heart rate and blood pressure were recorded during the depressor (phase II) or pressor (phase IV) period to Valsalva's maneuver in 10 younger subjects and 7 aged subjects. The baroreflex slope for heart rate showed attenuation in the aged subjects during the pressor phase but not during the depressor phase, the baroreflex slope for MSNA was also attenuated in the aged subjects during the pressor and tended to be attenuated during the depressor phases. These data suggest impaired baroreflex function for both heart rate and sympathetic nerve activity in the elderly.

Adult↗
PubMed2000

Cardiopulmonary baroreflex stimulation and blood pressure-related hypoalgesia.

Results from both experimental animals and humans suggest that baroreflex stimulation may be involved in blood pressure-related hypoalgesia. However, most of this research, especially in the area of human experimentation, has focused on sinoaortic baroreceptors. Cardiopulmonary baroreflex stimulation may also be an important moderator of pain. Sixty-six healthy male undergraduates varying in risk for hypertension participated in an experimental protocol in which painful mechanical finger pressure was presented three times in a counterbalanced fashion. One pain stimulus was preceded by 6 min of supine rest, another by a period of rest interspersed with periodic Valsalva manoeuvres, and another by a period in which cardiopulmonary baroreceptors were stimulated by passive leg elevation. Significantly lower pain was reported by men with relatively elevated systolic blood pressure following leg elevation but not the other conditions. Cardiopulmonary baroreflex stimulation was documented by increased forearm blood flow and other data obtained via impedance cardiography. These results suggest that blood pressure related hypoalgesia may be at least partially related to cardiopulmonary baroreflex stimulation.

Adult↗
PubMed1998

The parabrachial nucleus mediates the decreased cardiac baroreflex sensitivity observed following short-term visceral afferent activation.

Previous investigations have provided evidence demonstrating that the extracellular release of glutamate into the parabrachial nucleus was significantly enhanced following visceral afferent activation. This period of enhanced glutamate release into the parabrachial nucleus corresponded to a time during which the pressor response to a bolus phenylephrine injection was significantly enhanced, and the reflex bradycardia was attenuated. This decrease in the sensitivity of the baroreflex is suggestive of an enhanced sympathetic tone as a result of the vagal stimulation. The present investigation was done to determine if the decreased baroreflex sensitivity observed following short-term vagal stimulation is mediated by an increase in sympathetic activity and was dependent on the parabrachial synapse. Male Sprague-Dawley rats were anaesthetized with sodium thiobutabarbitol and instrumented to monitor blood pressure and heart rate and for the placement of a stimulating electrode on the left cervical vagus nerve. Femoral arterial blood samples were taken before, during and after 2 h of vagal stimulation which were later assayed for plasma catecholamines. The results showed that plasma norepinephrine levels decreased during, and were significantly elevated immediately following termination of the vagal stimulation, indicative of an increase in sympathetic tone. To determine if the parabrachial nucleus is involved in mediating an enhanced sympathetic activity following vagal stimulation, a second group of animals underwent an identical surgical preparation, vagal stimulation and blood sampling protocol with the addition of bilateral microinjections of either the reversible anaesthetic, lidocaine, or saline into the parabrachial nucleus. The results showed that reversible blockade of the parabrachial nucleus prior to the onset of the vagal stimulation was effective in blocking both the elevation in plasma norepinephrine levels and the depressed baroreflex sensitivity previously observed following 2 h of vagal stimulation. These results suggest that the parabrachial nucleus mediated the sympathoexcitation and consequent depression in baroreflex sensitivity observed following visceral afferent activation.

Afferent Pathways↗
PubMed2001

Altered Mayer wave and baroreflex profiles in high spinal cord injury.

Spinal sympathetic neurons are distributed in cord segments from Th1 to L3. High spinal cord injury demonstrates severe orthostatic hypotension, but not lower cord injury. It remains to be clarified as to where is the critical spinal level disturbing neural cardiovascular regulations in response to orthostatic stress. To address this issue, beat-to-beat blood pressure (BP) (measured using a Finapres device) and RR interval (measured electrocardiographically) were recorded at rest and in a 60 degree head-up position in 26 patients with varying levels of spinal cord injury (C4 to Th12) and in 15 healthy (control) subjects. Sympathetic vascular tone was examined by the Mayer wave power spectrum of systolic blood pressure (SBP) variability. Baroreflex sensitivity was examined by transfer function analysis of SBP and RR interval variabilities. The Mayer wave power spectrum increased in response to postural shift in most patients injured at Th4 or below, whereas this parameter either remained unchanged or decreased in patients with higher-level injury. Baroreflex sensitivity tended to decrease with postural shift in patients injured at Th3 or below, whereas this parameter increased in all patients with higher-level injury. We divided spinal patients into high-level injury (Th3 or above, n = 14) and low-level injury (Th4 or below, n = 12) groups. Systolic blood pressure significantly fell (-10 +/- 4 mm Hg, P < .05) with postural shift in high-level injury group but did not change in low-level injury group or in control subjects. The low-level injury group and the control group demonstrated essentially similar autonomic nervous responses to postural shift, ie, a significant increase in Mayer wave power and an insignificant decrease in baroreflex sensitivity. On the contrary, the high-level injury group showed opposite responses, ie, an insignificant decrease in Mayer wave power and a significant increase in baroreflex sensitivity in response to postural shift. We conclude that spinal cord injury at Th3 or above eliminates normal neural cardiovascular responses to mild orthostatic stress in humans.

Adolescent↗
PubMed1997

Baroreflex control of muscle sympathetic nerve activity in mild hypertension.

The importance of the arterial baroreflex control of muscle sympathetic nerve activity (MSNA) has been investigated in physiological conditions and in cardiovascular dysfunctions. However, there is no consensus about the role played by the MSNA in hypertensive states, probably due to the diversity of the methods used to study the arterial baroreflex control of MSNA. In the present study we evaluated the reflex changes in MSNA by increasing and decreasing the mean arterial pressure (MAP) through 1 min intravenous infusion of phenylephrine (1 microgram/kg) and sodium nitroprusside (1 microgram/kg), respectively, in eight normotensive and eight mild hypertensive subjects. Both MAP and MSNA were significantly higher in hypertensive (117 +/- 2 mm Hg and 30 +/- 3 bursts/min) than in normotensive (96 +/- 4 mm Hg and 20 +/- 3 bursts/min) subjects. The reflex gain was calculated by the ratio percent of changes in MSNA/percent changes in MAP. The maximal reflex gain was statistically similar in normotensive and hypertensive groups during phenylephrine (5.1 +/- .4 v 4.3 +/- 0.4 bursts/mm Hg, respectively) and nitroprusside (10.7 +/- 2.3 v 8.1 +/- 1.3 bursts/mm Hg, respectively) infusion. The present data showing that arterial baroreflex control of MSNA is not depressed in hypertensive subjects indicate that the elevated basal MSNA and the mild hypertension in human beings is not a consequence of baroreflex control of MSNA dysfunction.

Adult↗
PubMed2002

Hypertension-related hypoalgesia, autonomic function and spontaneous baroreflex sensitivity.

OBJECTIVE: The mechanisms involved in the relationship between pain perception and hypertension are poorly understood. This study has sought to investigate whether the spontaneous baroreflex sensitivity and the autonomic nervous system balance are related to hypertension-associated hypoalgesia. METHODS: In the morning, 73 untreated male subjects (45 hypertensives, 28 normotensives) were submitted to a simultaneous recording of electrocardiographic and blood pressure signals in resting condition. The tracings were analysed off-line to evaluate the spectral components of the low frequency (LF) and high frequency (HF) powers (autoregressive algorithm; LF/HF ratio used in subsequent analysis as an index of sympathovagal balance), and the alphaLF (alphaLF), an index of baroreflex sensitivity. After the rest period, the subjects underwent dental pain perception evaluation (pulpar tester: test current increasing from 0 to 0.03 mA, expressed in relative Units) to determine the dental pain threshold and tolerance. Afterwards, a 24-h ambulatory blood pressure monitoring was performed. RESULTS: A significant relationship was observed between alphaLF and pain threshold (r = -0.34; p = 0.003). When a multivariate analysis was computed to control for age, 24-h systolic pressure and LF/HF ratio, alphaLF was a predictive independent factor associated with pain threshold (model p = 0.019; r = -0.31; p = 0.025). Moreover, the 24-h systolic pressure was independently associated with pain threshold (model p = 0.019; r = 0.30, p = 0.031). The relationship between alphaLF and relative tolerance was not statistically significant. When the association between the LF/HF ratio and pain sensitivity was assessed as a secondary endpoint, no significant relationship was observed. Since no significant interaction was found, the effect of alphaLF and LF/HF ratio on pain perception was assumed to be similar in normotensive and hypertensive subjects. CONCLUSIONS: The relationship found between unstimulated baroreflex sensitivity and pain threshold suggests a modulation of pain perception by baroreflex pathways in hypertension-associated hypoalgesia. In a baseline condition, the autonomic nervous system balance does not seem to influence pain sensitivity.

Adult↗
PubMed2003

The rostral ventrolateral medulla mediates sympathetic baroreflex responses to intraventricular angiotensin II in rabbits.

The present study examined the role of the rostral ventrolateral medulla (RVLM) in mediating the pressor and renal sympathetic baroreflex effects of intraventricularly administered angiotensin II (Ang II) in urethane anaesthetised rabbits. Microinjection of Ang II over a wide range of medullary sites showed that pressor responses were observed only in the RVLM. Ang II was particularly potent in producing a transient pressor response at this site with a half maximal dose of 9 fmol. The administration of the Ang II antagonist Sar(1)-Ile(8)-Ang II (10 pmol) bilaterally into the RVLM inhibited the pressor response to local and fourth ventricular Ang II, but not the pressor response to RVLM applied glutamate. To determine the contribution of the RVLM to the renal sympathetic baroreflex effects of Ang II, blood pressure-renal sympathetic nerve activity (RSNA) curves were constructed with intravenous infusion of phenylephrine or nitroprusside before and after Ang II, vehicle or glutamate infusions into the RVLM. Ang II infusion of 4 pmol/min into the RVLM increased blood pressure by 8+/-3 mm Hg and shifted the renal sympathetic baroreflex curve to the right. The maximum RSNA evoked by lowering blood pressure increased by 36+/-6%, similar to the effect seen with fourth ventricular Ang II and RVLM glutamate. These studies suggest that the major medullary pressor site of action of Ang II when injected into the hindbrain cerebro-spinal fluid of anaesthetized rabbits is the RVLM where it facilitates baroreflex control of RSNA.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed2006

Spontaneous baroreflex cardiac sensitivity in end-stage liver disease: effect of liver transplantation.

BACKGROUND AND OBJECTIVE: End-stage liver disease is associated with an imbalance in the autonomic nervous system. The purpose of this study was to estimate the effect of liver transplantation on this imbalance. METHOD: The study involved 10 patients undergoing liver transplantation and 9 patients without liver impairment undergoing liver surgery. The spontaneous baroreflex sensitivity was measured before and 1 month after surgery for the liver surgery group; before and 1, 3, 6, 12 and 18 months after orthotopic liver transplantation. RESULTS: The spontaneous baroreflex slope of patients with end-stage liver disease was decreased before liver transplantation compared to the liver surgery group (3.9 +/- 2.5 ms mmHg(-1) vs. 9.9 +/- 5.0 ms mmHg(-1), P = 0.002). The mean slope was significantly increased at 12 and 18 months compared to the pre-transplantation value (3.9 +/- 2.5 ms mmHg(-1) vs. 8.1 +/- 6.6 ms mmHg(-1) and 7.4 +/- 4.8 ms mmHg(-1), respectively; P = 0.042). Nevertheless, further analysis of individual data showed that only four patients exhibited a marked increase in their baroreflex slope 12 months after the liver transplantation whereas it remained decreased in the six others. CONCLUSIONS: These results confirm that the baroreflex sensitivity is depressed in end-stage liver disease in line with an autonomic nervous system imbalance. The liver transplantation reverses this disturbance only in some patients.

Analysis of Variance↗
PubMed1999

Impaired baroreflex function and arterial compliance in primary aldosteronism.

The purpose of this study was to evaluate if changes in vascular properties were related to baroreflex function in patients with primary aldosteronism. Twenty-three patients with primary aldosteronism, 22 essential hypertensive patients and 16 normal controls were studied. Continuous finger blood pressure (BP) was recorded by Portapres device during supine rest and active stand up. Compliance was estimated from the time constant of pressure decay during diastole. Baroreflex sensitivity was calculated by autoregressive cross-spectral analysis of systolic BP and interbeat interval. The result was that baroreflex gain and compliance were lower in primary aldosteronism patients in the supine position (P = 0.002 and P < 0.05 respectively). Aldosterone plasma levels (R2 = 0.31, P = 0.01), age, systolic and diastolic BP, high and low frequency components of diastolic BP variability were independently related to compliance in primary aldosteronism. In conclusion primary aldosteronism is associated with an impaired baroreflex function related in part to a reduced arterial compliance. Despite a reduction of BP values and aldosterone levels, surgical or pharmacological treatment did not significantly change compliance values.

Adult↗
PubMed1994

Sympathetic restraint of baroreflex control of heart period in normotensive and hypertensive subjects.

1. We assessed the effects of changing levels of sympathetic drive on the gain of baroreflex control of the sino-atrial node, in normotensive and hypertensive subjects. 2. Autoregressive spectral and cross-spectral analysis of R-R interval and systolic arterial pressure (non-invasive Finapres method) variabilities providing an estimate of baroreflex gain through the frequency domain index alpha were performed on data from 63 normotensive and 78 mild hypertensive subjects. Subjects were studied at rest and during active orthostatism, which induces sympathetic predominance. Seven control subjects and 14 hypertensive subjects were also studied after chronic atenolol treatment, to attenuate beta-adrenoceptor-mediated responses. 3. In both normotensive and hypertensive subjects, the index alpha was reduced by active standing and increased by chronic beta-adrenoceptor blockade. Furthermore, at rest, the index alpha was correlated with R-R variance and appeared significantly reduced with age. The age-related negative correlation of the index alpha was no longer evident during the standing-induced increase in sympathetic drive, in both normotensive and hypertensive subjects. 4. The index alpha, a non-invasive frequency domain estimate of the overall gain of baroreflex control of the sino-atrial node, which appears to be reduced in essential hypertension, is negatively modulated by physiological increases in sympathetic drive, and augmented by pharmacological blockade of beta-adrenoceptors. 5. In essential hypertension the enhanced sympathetic drive present already at rest, and the simultaneous reduction of the gain of baroreflex mechanisms, are the expression of a complex alteration in neural cardiovascular control.

Adult↗
PubMed1995

A new non-invasive statistical method to assess the spontaneous cardiac baroreflex in humans.

1. A new method was developed to evaluate cardiac baroreflex sensitivity. The association of a high systolic blood pressure with a low heart rate or the converse is considered to be under the influence of cardiac baroreflex activity. This method is based on the determination of the statistical dependence between systolic blood pressure and heart rate values obtained non-invasively by a Finapres device. Our computerized analysis selects the associations with the highest statistical dependence. A 'Z-coefficient' quantifies the strength of the statistical dependence. The slope of the linear regression, computed on these selected associations, is used to estimate baroreflex sensitivity. 2. The present study was carried out in 11 healthy resting male subjects. The results obtained by the 'Z-coefficient' method were compared with those obtained by cross-spectrum analysis, which has already been validated in humans. Furthermore, the reproducibility of both methods was checked after 1 week. 3. The results obtained by the two methods were significantly correlated (r = 0.78 for the first and r = 0.76 for the second experiment, P < 0.01). When repeated after 1 week, the average results were not significantly different. Considering individual results, test-retest correlation coefficients were higher with the Z-analysis (r = 0.79, P < 0.01) than with the cross-spectrum analysis (r = 0.61, P < 0.05). 4. In conclusion, as the Z-method gives results similar to but more reproducible than the cross-spectrum method, it might be a powerful and reliable tool to assess baroreflex sensitivity in humans.

Adult↗
PubMed2003

Central angiotensin modulation of baroreflex control of renal sympathetic nerve activity in the rat: influence of dietary sodium.

AIM: Administration of angiotensin II (angII) into the cerebral ventricles or specific brain sites impairs arterial baroreflex regulation of renal sympathetic nerve activity (SNA). Further insight into this effect was derived from: (a) using specific non-peptide angII receptor antagonists to assess the role of endogenous angII acting on angII receptor subtypes, (b) microinjection of angII receptor antagonists into brain sites behind an intact blood-brain barrier to assess the role of endogenous angII of brain origin and (c) alterations in dietary sodium intake, a known physiological regulator of activity of the renin-angiotensin system (RAS), to assess the ability to physiologically regulate the activity of the brain RAS. METHODS: In rats in balance on low, normal or dietary sodium intake, losartan or candesartan was injected into the lateral cerebral ventricle or the rostral ventrolateral medulla (RVLM) and the effects on basal renal SNA and the arterial baroreflex sigmoidal relationship between renal SNA and arterial pressure were determined. RESULTS: With both routes of administration, the effects were proportional to the activity of the RAS as indexed by plasma renin activity (PRA). The magnitude of both the decrease in basal renal SNA and the parallel resetting of arterial baroreflex regulation of renal SNA to a lower arterial pressure was greatest in low-sodium rats with highest PRA and least in high-sodium rats with lowest PRA. Disinhibition of the paraventricular nucleus (PVN) by injection of bicuculline causes pressor, tachycardic and renal sympathoexcitatory responses mediated via an angiotensinergic projection from PVN to RVLM. In comparison with responses in normal sodium rats, these responses were greatly diminished in high-sodium rats and greatly enhanced in low-sodium rats. CONCLUSION: Physiological changes in the activity of the RAS produced by alterations in dietary sodium intake regulate the contribution of endogenous angII of brain origin in the modulation of arterial baroreflex regulation of renal SNA.

Angiotensin II↗