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PubMed2004

Acute arterio-venous fistula occlusion decreases sympathetic activity and improves baroreflex control in kidney transplanted patients.

BACKGROUND: The acute bradycardia induced by the occlusion of an arteriovenous fistula (AVF), known as the Nicoladoni-Branham sign, is considerably larger than that which occurs during carotid sinus massage. This suggests increased arterial baroreflex sensitivity during acute AVF occlusion. Moreover, the influence of acute AVF occlusion on muscle sympathetic nerve traffic (MSNA, by microneurography) is unknown. We therefore assessed the effects of acute AVF occlusion on baroreflex sensitivity and on MSNA in patients with stable functional kidney grafts and patent AVF. METHODS: We measured blood pressure (BP), MSNA (n = 11), heart rate (HR), cardiac output (CO) and arterial baroreflex sensitivity (n = 18) at baseline and during acute, 30-s pneumatic AVF occlusions in 23 renal transplanted recipients. RESULTS: During the first 5 s of the AVF occlusion, mean BP increased from 98+/-4 to 112+/-4 mmHg (P<0.0001) while MSNA decreased to 28+/-5% of baseline values (P<0.0001) and HR decreased from 71+/-3 to 61+/-3 b.p.m. (P<0.0001). The largest increases in BP were accompanied by the most marked decreases in MSNA (r = -0.79, P = 0.003) and HR (r = -0.49; P = 0.01) during the first 5 s of the AVF occlusion. During AVF occlusion baseline CO of 6.9+/-0.3 decreased to 5.6+/-0.3 l/min (P<0.0001) while baroreflex sensitivity increased from 10+/-1 to 17+/-2 ms/mm Hg (P<0.001). CONCLUSIONS: Arterial baroreceptor activation and increased arterial baroreflex sensitivity decrease heart rate during AVF occlusion. In addition, our study is the first to demonstrate that arterial baroreflex activation decreases sympathetic nerve traffic during the Nicoladoni-Branham sign.

Arteriovenous Fistula↗
PubMed1994

Effect of beta-blockade on baroreflex sensitivity and cardiovascular autonomic function tests in patients with coronary artery disease.

We wished to assess the effects of beta-blockade on baroreflex sensitivity and standard tests of integrity of autonomic nervous function in patients with coronary artery disease, and to determine whether the effects of lipophilic (metoprolol) and hydrophilic (atenolol) beta-blockers differ. Beta-blocking drugs increase spontaneous heart rate variability in healthy subjects and in patients with coronary heart disease, but little is known about their effects on baroreflex sensitivity and heart-rate based tests of autonomic integrity. In a randomly allocated double-blind crossover study with three 2-week treatment periods, metoprolol CR 200 mg once a day, or atenolol 100 mg once a day, or placebo once a day, were administered to 18 male patients with stable coronary artery disease. Baroreflex sensitivity was determined from the natural baroreflex challenge of Valsalva strain. Heart rate reactions to standard stimuli were measured. No significant differences were found between the effects of atenolol and metoprolol. Beta-blockade did not significantly affect the baroreflex sensitivity, but it diminished the Valsalva ratio significantly (P < 0.001). The difference between maximum and minimum heart rate during hyperventilation was also significantly lower during beta-blockade. The heart rate response to standing up and the ratio of maximum to minimum heart rate during deep breathing were not influenced by beta-blockade. Discontinuation of beta-blockade seems to be unnecessary for reliable determination of baroreflex sensitivity in patients with coronary artery disease, when the natural pressure challenge of Valsalva strain is sued. Both hydrophilic and lipophilic bet-blockers interfere with certain diagnostic tests of autonomic nervous function.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1997

Sympathovagal effects of spinal anesthesia assessed by the spontaneous cardiac baroreflex.

BACKGROUND: The changes in sympathovagal balance induced by spinal anesthesia remain controversial. The spontaneous baroreflex method allows the continuous assessment of the spontaneous engagement of the cardiac baroreflex, giving an index of sympathovagal balance. The purpose of this study was to follow the effects of spinal anesthesia on spontaneous baroreflex sensitivity. METHODS: Continuous electrocardiogram and noninvasive blood pressure were recorded in 24 patients scheduled for elective inguinal hernia repair and randomly assigned to three groups: (1) no volume loading, (2) volume loading of 15 ml/kg lactated Ringer's solution, and (3) continuous infusion of etilefrine (an ephedrine-like drug). Each patient was studied before, during, and after bupivacaine-induced spinal anesthesia (mean sensory block: T4). Spontaneous baroreflex sensitivity and parameters of time-domain analysis of heart rate variability were calculated from 30 min of recording of each period. RESULTS: No significant change in spontaneous baroreflex slope or parameters of time-domain analysis were observed after regional anesthesia in any group. However, three patients experienced episodes of bradycardia and hypotension in the absence of a high block; these three patients showed an increase in spontaneous baroreflex sensitivity and time-domain parameters. CONCLUSIONS: Using a noninvasive, continuous technique to estimate cardiac sympathovagal balance, no significant variation in autonomic balance induced by spinal anesthesia was observed. However, untoward episodes of bradycardia and hypotension occurred in three patients, who could not be prospectively identified by the parameters studied.

Adjuvants, Anesthesia↗
PubMed1999

Similar baroreflex bradycardic actions of atrial natriuretic peptide and B and C types of natriuretic peptides in conscious rats.

OBJECTIVE: We have previously shown that atrial natriuretic peptide (ANP) modulates cardiac barosensitive afferent pathways to enhance reflex bradycardia in rats. The present study examined whether B-type natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) also modulate heart rate reflex function. DESIGN: Baroreflex bradycardia was evoked by rapid (over 4-6 s) intravenous (i.v.) infusions of methoxamine (100 microg/kg; 'ramp' baroreflex technique) in the presence of infused i.v. natriuretic peptide and of vehicle (0.9% saline, 270 microl/h) in conscious adult Munich-Wistar rats. Initially a dose-response study to ANP (infused at 25, 50 and 100 pmol/kg per min i.v.) was performed in 10 rats to determine an appropriate dose for subsequent experiments with the other peptides. In a separate group of 11 animals, rat BNP-32 and rat CNP-22 were infused at 50 pmol/kg per min i.v. RESULTS: Reflex responses to ANP were dose-related, with a significant increase in baroreflex sensitivity of 50+/-15% at the 25 pmol dose, 102+/-10% at the 50 pmol dose and 117+/-11% at 100 pmol dose (all P<0.05). BNP and CNP (50 pmol/kg/min i.v.) substantially increased baroreflex bradycardia (by 115+/-17% and 62+/-15%, respectively; P<0.05) compared to vehicle infusion. CONCLUSIONS: Both BNP and CNP augmented baroreflex slowing of heart rate in response to rapid increases in blood pressure in rats. Whereas other reports have shown marked differences in cardiovascular responses between the natriuretic peptides, particularly with CNP, our findings demonstrate an important common action of ANP, BNP and CNP to facilitate vagal heart rate baroreflexes.

Animals↗
PubMed2000

The importance of high-frequency paced breathing in spectral baroreflex sensitivity assessment.

OBJECTIVE: Computation of the low-frequency (LF) blood pressure variability (BPV) to heart rate variability (HRV) transfer-index is a common method to assess baroreflex sensitivity (BRS), tacitly assuming that all LF-HRV is caused by baroreflex feedback of LF-BPV. However, respiration may also cause HRV by mechanisms not involving the baroreflex. Application of narrow-band (controlled) high-frequency breathing would keep such non-baroreflex-mediated HRV best out of the LF band. Spontaneous breathing, because of its broad-band character, might cause extra, non-baroreflex-mediated, HRV in the LF band, while paced LF breathing would even concentrate most non-baroreflex-mediated HRV in the LF band. Our study addresses the likely resulting BRS overestimation. DESIGN: We recorded HRV and BPV in 20 healthy young subjects in the sitting position. We varied the sympathovagal balance by gradual leg-lowering from horizontal till 60 degrees . At each angle the subjects performed controlled 0.10 Hz, spontaneous, and controlled 0.25 Hz respiration. RESULTS: Resting BRS values were 15.5(7.2), 13.1 (3.7), and 11.6(6.2) ms/mmHg, respectively. Both the 15/min and the free breathing values differed significantly, P< 0.01 and P= 0.04, from the 6/min breathing value. With lowered legs, the BRS values were 8.2(3.4), 8.3(2.9), and 8.3(3.4) ms/mmHg, respectively. CONCLUSION: Controlled 6/min breathing caused significant BRS overestimation under resting conditions. For the group, spontaneous respiration yielded acceptable BRS values, but individual BRS values deviated sometimes considerably. Conversely, with gravitational load, the respiratory pattern had only minor impact on BRS. Our results demonstrate that the risk of an overestimated BRS value is realistic as long as respiration is not controlled and of high-frequency.

Adult↗
PubMed2002

Differential modulation of leptin-induced sympathoexcitation by baroreflex activation.

OBJECTIVE: Leptin induces increases in sympathetic nerve activity to various regions. This has implications for energy balance, thermogenesis and possibly cardiovascular regulation. The aim of the present study was to test the hypothesis that the increases in sympathetic nerve activity induced by leptin in different regions respond differentially to baroreflex activation. METHODS: A total of 24 anesthetized male Sprague-Dawley rats were assigned to either leptin (0.5 mg/kg body weight bolus i.v., followed by 0.5 mg/kg body weight i.v. during 3 h, n = 12) or vehicle (n = 12) treatment. Mean arterial pressure (MAP), heart rate (HR), interscapular brown adipose tissue sympathetic nerve activity (IBAT-SNA) and renal sympathetic nerve activity (RSNA) were recorded continuously. Before and 3 h after start of leptin or vehicle, baroreceptor activity was decreased by lowering MAP with nitroprusside and increased by raising MAP with phenylephrine. RESULTS: Compared with vehicle, leptin significantly increased IBAT-SNA (294 +/- 78%) and RSNA (211 +/- 28%), while not altering MAP (117 +/- 5 versus 118 +/- 4 mmHg). Baroreflex activation by phenylephrine completely suppressed the leptin-induced increase in RSNA. In contrast, the leptin-induced increase in IBAT-SNA could not be overridden by baroreflex activation. Compared with vehicle, leptin did not significantly alter the maximum gain of the RSNA-MAP (-3.8 +/- 0.7 versus -2.7 +/- 0.3% of maximum mmHg-1, NS) or the IBAT-SNA-MAP curves (-1.9 +/- 0.7 versus -1.4 +/- 0.3% of maximum mmHg-1, NS). CONCLUSIONS: Leptin-induced regional increases in sympathetic nerve activity respond non-uniformally to baroreflex activation. The increase in RSNA can be suppressed by baroreflex activation, suggesting that the leptin-induced increase in RSNA subserves circulatory functions. In contrast, the increase in IBAT-SNA with leptin is not prevented by baroreflex activation, suggesting the recruitment of sympathetic fibers that serve thermogenic or metabolic and not circulatory functions.

Adipose Tissue, Brown↗
PubMed2004

Sympathetic and baroreflex function in hypertensive or heart failure patients with ventricular arrhythmias.

OBJECTIVE: To determine whether in hypertension and in heart failure the occurrence of ventricular arrhythmias is associated with alterations in sympathetic drive and baroreflex function. DESIGN AND METHODS: We studied 28 untreated essential hypertensives (age, 53.0 +/- 1.1 years, mean +/- standard error of the mean), 15 without and 13 with monofocal premature ventricular contractions (PVCs) in Lown class I, and 30 heart failure patients (age, 53.8 +/- 1.3 years) in New York Health Association class II-III, 17 without and 13 with PVCs also in Lown class I. In each patient we measured, along with echocardiographic variables, the beat-to-beat mean blood pressure (Finapress), heart rate (HR) (EKG), muscle sympathetic nerve traffic (MSNA) (microneurography), venous plasma norepinephrine and renin activity (high-pressure liquid chromatography and radioimmunoassay, respectively). Measurements were performed at rest and during arterial baroreceptor stimulation and deactivation via stepwise intravenous infusion of phenylephrine and nitroprusside, respectively. RESULTS: The mean blood pressure, HR and MSNA were similar in hypertensive patients without and with PVCs. However, compared with non-arrhythmic patients, hypertensives with PVCs displayed a baroreflex-HR and baroreflex-MSNA modulation reduced by 27.7 +/- 4.2 and 17.9 +/- 2.8%, respectively (P < 0.05). Heart failure patients with PVCs showed haemodynamic and echocardiographic variables superimposable to those without PVCs. Compared with these patients, however, they exhibited a significant increase in MSNA values (75.8 +/- 3.0 versus 63.6 +/- 2.8 bs/100 hb, P < 0.05), coupled with a significant impairment in baroreflex-HR and baroreflex-MSNA control (-52.5 +/- 5.4 and -37.5 +/- 3.6%, P < 0.01). CONCLUSIONS: These data provide evidence that in both hypertension and heart failure, sympathetic and baroreflex mechanisms exert a pro-arrhythmogenic role. This role, however, appears to be more pronounced in heart failure than in hypertension, in which the impaired vagal function may exert a concomitant favouring effect.

Adult↗
PubMed1994

Nitroprusside infusion improves arterial baroreflex control of heart rate in dogs with chronic congestive heart failure.

To determine if nitroprusside improves arterial baroreflex responsiveness in chronic congestive heart failure (CHF), we administered nitroprusside to 11 conscious dogs with pacing-induced CHF. Baroreflex sensitivity was determined by plotting the R-R interval against systolic aortic pressure after a bolus injection of phenylephrine (PE). At baseline, dogs with CHF had higher heart rate (HR), increased left atrial blood pressure (BP), and reduced left ventricular (LV) dP/dt as compared with 10 sham-operated normal animals. Baroreflex sensitivity index was significantly lower in CHF dogs, (8.3 +/- 1.3 ms/mm Hg) than normal dogs (25.1 +/- 1.2 ms/mm Hg, p < 0.001). Intravenous (i.v.) administration of nitroprusside (1 microgram/kg/min) to CHF dogs decreased left atrial BP (23 +/- 1-17 +/- 1 mm Hg) and HR (131 +/- 4-115 +/- 4 beats/min), but had no significant effect on either cardiac output (CO) or systolic aortic BP. This resulted in a 58% increase in baroreflex sensitivity index to 13.1 +/- 1.3 ms/mm Hg (p < 0.001); and the change correlated significantly with magnitude of decrease in left atrial BP (r = 0.884, p < 0.001) but not with the increase in R-R interval (r = 0.390, p > 0.10). In contrast, administration of nitroprusside sufficient to decrease left atrial BP (9.0 +/- 1.4-6.4 +/- 1.2 mm Hg) did not alter baroreflex sensitivity (26.4 +/- 3.4-26.4 +/- 3.9 ms/mm Hg) in 5 normal dogs. The results suggest that nitroprusside infusion increases arterial baroreflex sensitivity only in dogs with CHF and that this effect is probably functionally linked to the reductions of cardiac filling pressure.

Animals↗
PubMed2001

Arterial baroreflex deficit induced organ damage in sinoaortic denervated rats.

To verify the independent role of the arterial baroreceptor dysfunction involved in target-organ damage in hypertension, sinoaortic denervated (SAD) rats were used as a model of arterial baroreflex (ABR) deficit. SAD, isolated aortic-denervated (AD), and isolated sinus-denervated (SD) rats were instrumented to record blood pressure (BP), heart rate (HR), BP variability (BPV), HR variability (HRV), ABR function control of heart period (ABR-HP), and BP (ABR-BP). Vascular maximum contractile/relaxant function was determined and organ damage was estimated by observation of morphologic changes. Short-term (postoperative 1 week) SAD caused hypertension and tachycardia in rats. Eighteen weeks after operation, BP and HR values in SAD and SD rats were not different from those in sham-operated rats, but AD rats were hypertensive compared with control group. Although 24-h mean BP values of long-term SAD rats were not different from those of sham-operated rats, 24-h BPV of SAD rats was significantly higher than that of sham-operated rats. Arterial baroreflex function in short-term SAD rats was significantly less than in sham-operated rats, whereas in long-term SAD rats, ABR-HP and ABR-BP were higher than those in short-term SAD rats, but were still significantly lower than those in control groups. At postoperative 18 weeks, baroreflex function in SAD and AD rats was significantly less than function in SD and control groups. SBPmax after phenylephrine and DBPmin after nitroprusside were significantly higher in SAD, AD, and SD rats than in control rats. Baroreflex function was negatively correlated to DBPmin and SBPmax in all denervated rats (n = 44). Some morphologic changes were found 18 weeks after denervation in heart, kidney, and small artery in SAD, AD, and SD rats. Baroreflex function in all denervated rats was negatively related to 24-h BPV values. In contrast, 24-h BPV values in SAD, AD, and SD rats were positively related to organ-damage score. A negative correlation between ABR function and end-organ damage score was found. Arterial baroreflex deficit played an independent and important role in organ-damage in SAD rats with significantly elevated 24-h BPV.

Animals↗
PubMed2000

Differential baroreflex control of heart rate in sedentary and aerobically fit individuals.

PURPOSE: We compared arterial, aortic, and carotid-cardiac baroreflex sensitivity in eight average fit (maximal oxygen uptake, VO2max = 42.2+/-1.9 mL x kg(-1) x min(-1)) and eight high fit (VO2max = 61.9+/-2.2 mL x kg(-1) x min(-1)) healthy young adults. METHODS: Arterial and aortic (ABR) baroreflex functions were assessed utilizing hypo- and hyper-tensive challenges induced by graded bolus injections of sodium nitroprusside (SN) and phenylephrine (PE), respectively. Carotid baroreflex (CBR) sensitivity was determined using ramped 5-s pulses of both pressure and suction delivered to the carotid sinus via a neck chamber collar, independent of drug administration. RESULTS: During vasoactive drug injection, mean arterial pressure (MAP) was similarly altered in average fit (AF) and high fit (HF) groups. However, the heart rate (HR) response range of the arterial baroreflex was significantly attenuated (P < 0.05) in HF (31+/-4 beats x min(-1)) compared with AF individuals (46+/-4 beats x min(-1)). When sustained neck suction and pressure were applied to counteract altered carotid sinus pressure during SN and PE administration, isolating the ABR response, the response range remained diminished (P < 0.05) in the HF population (24+/-3 beats x min(-1)) compared with the AF group (41+/-4 beats x min(-1)). During CBR perturbation, the HF (14+/-1 beats-min(-1)) and AF (16+/-1 beats-min(-1)) response ranges were similar. The arterial baroreflex response range was significantly less than the simple sum of the CBR and ABR (HF, 38+/-3 beats x min(-1) and AF, 57+/-4 beats x min(-1)) in both fitness groups. CONCLUSIONS: These data confirm that reductions in arterial-cardiac reflex sensitivity are mediated by diminished ABR function. More importantly, these data suggest that the integrative relationship between the ABR and CBR contributing to arterial baroreflex control of HR is inhibitory in nature and not altered by exercise training.

Baroreflex↗
PubMed2005

Brainstem norepinephrine neurons mediate ethanol-evoked pressor response but not baroreflex dysfunction.

BACKGROUND: Ethanol elicits strain-dependent blood pressure and baroreflex sensitivity responses in spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) rats; the mechanisms underlying these divergent effects are not clear. The authors tested the hypothesis that differential neuronal actions of ethanol may account for these strain-dependent responses. To this end, the authors investigated the direct effects of ethanol on norepinephrine (NE)-containing neurons in the rostral ventrolateral medulla (RVLM), which modulate sympathetic neuronal activity, and on c-Jun-expressing neurons in the nucleus tractus solitarius (NTS), whose activity is inversely correlated with baroreflex sensitivity. METHODS: In a newly developed model system in conscious, freely moving rats, the effect of intra-RVLM or intra-NTS ethanol was investigated on neuronal NE at the microinjection site (in vivo electrochemistry), blood pressure, heart rate, spontaneous baroreflex sensitivity, and c-Jun expression in the NTS. RESULTS: Ethanol (1, 5, or 10 microg) microinjection into the RVLM elicited dose-dependent increases in RVLM NE and blood pressure in SHRs but not in WKY rats. Ethanol had no effect on the activity of the NE-containing neurons in the NTS of either strain. However, baroreflex dysfunction elicited by intra-NTS ethanol in conscious WKY rats was associated with enhanced expression of c-Jun in the NTS. CONCLUSIONS: (1) Ethanol activation of the NE-containing neurons in the RVLM of SHRs contributes to the centrally mediated pressor response, (2) the NE-containing neurons in the NTS are not involved in ethanol-induced baroreflex dysfunction, and (3) direct activation of the c-Jun-containing neurons in the NTS is implicated in baroreflex dysfunction elicited by ethanol in normotensive rats.

Animals↗
PubMed1994

Attenuation of arterial baroreflex control of renal sympathetic nerve activity during lidocaine infusion in alpha-chloralose-anesthetized dogs.

The purpose of this study was to identify the relationship between sensitivity of arterial baroreflex and plasma concentrations of lidocaine. Using twelve mongrel dogs anesthetized with alpha-chloralose, the left kidney was exposed retroperitoneally, and renal sympathetic nerve activity was recorded continuously. Lidocaine was infused in four different doses: 2 mg.kg BW-1 bolus + 100 micrograms.BW-1 x min; 3 mg.kg BW-1 bolus + 200 micrograms.kg BW-1 x min; 6 mg.kg BW-1 bolus + 400 micrograms.kg BW-1 x min; and 12 mg.kg BW-1 + 800 micrograms.kg BW-1 x min. Baroreflex depressor and pressor tests using sodium nitroprusside (5-10 micrograms.kg-1) and phenylephrine (2-4 micrograms.kg-1) were performed before and at 10 min after beginning lidocaine infusion. Plasma lidocaine concentrations determined by high performance liquid chromatography revealed that the steady-state levels were maintained during the baroreflex tests. Baroreflex sensitivity was preserved at plasma concentrations of lidocaine below 5 micrograms.ml-1. However, cardiac and sympathetic baroreflex sensitivity were significantly attenuated (P < 0.01) when plasma lidocaine concentrations were well above human convulsion levels (10 micrograms.ml-1). The results indicate that hemodynamic derangement observed in the lidocaine-induced central nervous system toxicity is, at least in part, due to the attenuated arterial baroreflex.

Animals↗
PubMed2004

Effects of nitrous oxide on baroreflex gain and heart rate variability.

BACKGROUND: Spontaneous baroreflex method allows continuous assessment of cardiovagal reflex function within resting blood pressure, but effects of nitrous oxide, per se, on the spontaneous baroreflex response remain unknown. This study was designed to determine the effects of nitrous oxide on spontaneous baroreflex gain and heart rate variability assessed by power spectral analysis in humans. METHODS: Electrocardiogram and non-invasive blood pressure were monitored in 12 healthy volunteers before and during a 15-min inhalation of 67% nitrous oxide in oxygen, while spontaneous respiration was maintained. Least-square regression analysis relating R-R interval and systolic blood pressure was performed to obtain spontaneous baroreflex gains. Heart rate variability was analyzed using fast Fourier transformation. RESULTS: Nitrous oxide did not significantly alter spontaneous baroreflex gains, which correlated well with high-frequency power (0.15-0.4 Hz) of heart rate variability before and during nitrous oxide inhalation. CONCLUSION: Our results indicate that (a) cardiovagal reflex response is not affected by nitrous oxide, per se, and (b) spontaneous baroreflex responses closely reflect beat-to-beat dynamic modulation of the cardiac cycle by the parasympathetic nervous system during inhalation of 67% nitrous oxide.

Adult↗
PubMed2006

Medial prefrontal cortex NMDA receptors and nitric oxide modulate the parasympathetic component of the baroreflex.

The ventral portion of the medial prefrontal cortex (vMPFC) is involved in the modulation of the parasympathetic component of the baroreflex. In the present study, we verified the effect of blockade of vMPFC glutamatergic receptors and nitric oxide synthases (NOS) on the parasympathetic component of baroreflex in awake rats. Bilateral microinjection of the non-selective ionotropic glutamate antagonist kynurenic acid (KYN) into the vMPFC caused a shift of the threshold of reflex bradycardia toward higher pressures in response to increases in mean arterial pressure (MAP) caused by intravenous infusion of phenylephrine, thus indicating a tonic facilitatory influence action of vMPFC glutamate receptors on the parasympathetic component of the baroreflex. The effect of blockade of vMPFC-NMDA receptors by AP7 was similar to that observed after KYN, suggesting mediation via NMDA receptors. Pretreatment with the NOS inhibitor L-NAME or the specific neural NOS (nNOS) N(omega)-propyl-l-arginine microinjected in the vMPFC caused a shift of the reflex threshold toward higher pressures that was similar to that observed after blockade of NMDA receptors, thus indicating participation of the NO/NMDA-receptor pathway in the vMPFC modulation of the parasympathetic component of the baroreflex. In conclusion, our data indicate that glutamatergic neurotransmission in the vMPFC has a tonic facilitatory influence on the parasympathetic component of the baroreflex. Because local treatment with either the nNOS inhibitor N(omega)-propyl-l-arginine or the specific NMDA antagonist AP7 had similar effects on the baroreflex, it is also suggested that this modulation involves an NMDA-NO interaction within the vMPFC.

2-Amino-5-phosphonovalerate↗
PubMed2001

Adenoviral vector demonstrates that angiotensin II-induced depression of the cardiac baroreflex is mediated by endothelial nitric oxide synthase in the nucleus tractus solitarii of the rat.

Angiotensin II (ANGII) acting on ANGII type 1 (AT1) receptors in the solitary tract nucleus (NTS) depresses the baroreflex. Since ANGII stimulates the release of nitric oxide (NO), we tested whether the ANGII-mediated depression of the baroreflex in the NTS depended on NO release. In a working heart-brainstem preparation (WHBP) of rat NTS microinjection of either ANGII (500 fmol) or a NO donor (diethylamine nonoate, 500 pmol) both depressed baroreflex gain by -56 and -67 %, respectively (P < 0.01). In contrast, whilst ANGII potentiated the peripheral chemoreflex, the NO donor was without effect. NTS microinjection of non-selective NO synthase (NOS) inhibitors (L-NAME; 50 pmol) or (L-NMMA; 200 pmol) prevented the ANGII-induced baroreflex attenuation (P > 0.1). In contrast, a neurone-specific NOS inhibitor, TRIM (50 pmol), was without effect. Using an adenoviral vector, a dominant negative mutant of endothelial NOS (TeNOS) was expressed bilaterally in the NTS. Expression of TeNOS affected neither baseline cardiovascular parameters nor baroreflex sensitivity. However, ANGII microinjected into the transfected region failed to affect the baroreflex.Immunostaining revealed that eNOS-positive neurones were more numerous than those labelled for AT1 receptors. Neurones double labelled for both AT1 receptors and eNOS comprised 23 +/- 5.4 % of the eNOS-positive cells and 57 +/- 9.2 % of the AT1 receptor-positive cells. Endothelial cells were also double labelled for eNOS and AT1 receptors. We suggest that ANGII activates eNOS located in either neurones and/or endothelial cells to release NO, which acts selectively to depress the baroreflex.

Adenoviridae↗
PubMed1995

Effect of posture on baroreflex sensitivity in healthy subjects.

In this study we investigated whether body position has significant effects on baroreflex sensitivity in healthy subjects. Baroreflex sensitivity was calculated from pressure overshoot after the release of a Valsalva strain in the supine and sitting positions in 10 subjects. At rest, no difference was found in supine and sitting mean R-R intervals (837 +/- 82 and 858 +/- 86 ms, respectively), whereas systolic and diastolic blood pressures were lower in the supine position (111.3 +/- 24.6 vs. 141.2 +/- 12.6 mmHg, P < 0.01 and 54.8 +/- 14.7 vs. 75.6 +/- 13.4 mmHg, P < 0.001, respectively). Baroreflex sensitivity in the supine (9.0 +/- 4.1 ms x mmHg-1) and sitting positions (8.8 +/- 4.9 ms x mmHg-1) did not differ significantly from each other. The correlation between supine and sitting baroreflex sensitivity was 0.96 (P < 0.001) and in 9 out of 10 subjects the discrepancy between supine and sitting baroreflex sensitivity was < 2.0 ms x mmHg-1. We conclude that baroreflex sensitivity measured in the supine and sitting positions do not differ significantly from each other.

Adult↗
PubMed2005

Nocturnal hemodialysis increases arterial baroreflex sensitivity and compliance and normalizes blood pressure of hypertensive patients with end-stage renal disease.

BACKGROUND: Impaired neural control of heart rate, elevated arterial stiffness, and hypertension place patients with end-stage renal disease (ESRD) at increased risk of cardiovascular mortality. Nocturnal hemodialysis (6 x 8 hours/week), a more intense program than conventional hemodialysis (3 x 4 hours/week), lowers blood pressure and restores brachial dilator responses to hyperemia and nitrates. METHODS: We hypothesized that nocturnal hemodialysis would increase arterial baroreflex sensitivity for heart rate of hypertensive ESRD patients by an afferent vascular mechanism. Ten consecutive hypertensive ESRD patients (age 42 +/- 4) (mean +/- SEM) receiving conventional hemodialysis were studied before and 2 months after conversion to nocturnal hemodialysis. Regression slopes relating RR interval responses to rises or falls in systolic blood pressure were averaged to derive spontaneous baroreflex sensitivity for heart rate for each patient, and the stroke volume/pulse pressure ratio was used to estimate total arterial compliance. RESULTS: Dialysis dose (Kt/V per session) increased from 1.2 +/- 0.05 to 2.1 +/- 0.1 (P < 0.05). Despite withdrawal of antihypertensive medications (from 2.9 to 0.1 drugs/patient), nocturnal hemodialysis lowered systolic blood pressure (from 143 +/- 4 to 120 +/- 6 mm Hg) (P= 0.001). Both baroreflex sensitivity (from 4.76 +/- 1.1 msec/mm Hg to 6.91 +/- 1.1 msec/mm Hg) (P= 0.04) and total arterial compliance (from 0.98 +/- 0.13 mL/mm Hg to 1.43 +/- 0.2 mL/mm Hg) (P= 0.02) were higher following conversion to nocturnal hemodialysis. Increases in baroreflex sensitivity correlated with increases in stroke volume/pulse pressure (r= 0.845, P= 0.002). CONCLUSION: These findings are consistent with the concept that nocturnal hemodialysis increases baroreflex sensitivity via greater afferent baroreceptor responsiveness to pulsatile pressure. A more favorable risk profile, due to enhanced baroreflex regulation of the circulation and vascular compliance, may translate into lower cardiovascular event rates in ESRD patients receiving nocturnal hemodialysis.

Adult↗
PubMed1994

Coupling between variations in strength and baroreflex latency of sympathetic discharges in human muscle nerves.

1. Pulse-synchronous multiunit muscle nerve sympathetic activity was recorded simultaneously from two nerves together with ECG in eleven healthy subjects; seven recordings were made from the two peroneal nerves during prolonged expiratory apnoeas and four from a radial and a peroneal nerve during lower body negative pressure of 10-40 mmHg. The neural records were displayed in mean voltage neurograms (time constant 0.1 s) and for each mean voltage burst the following measures were taken and related to each other: amplitude, duration, rise time, decay time and baroreflex latency (from the appropriate R-wave of the ECG to the peak of the burst). 2. Average baroreflex latencies were 1.3 s in the peroneal nerves and 0.9 s in the radial nerve. There were significant positive correlations between both the amplitudes and the baroreflex latencies of corresponding bursts in peroneal-peroneal recordings and in radial-peroneal recordings. 3. In all nerves baroreflex latency shortened significantly when burst amplitude increased. The correlation between burst amplitude and baroreflex latency was weaker in the radial than in the peroneal nerve. The average variation of baroreflex latency in peroneal-peroneal recordings was 0.20 +/- 0.02 s in both legs, and in radial-peroneal recordings the variation was 0.09 +/- 0.01 s in the radial nerve and 0.12 +/- 0.02 s in the peroneal nerve. 4. When peroneal burst amplitudes increased, burst duration increased. This was due to increases of both the rise time and the decay time of the burst, the latter being the greater.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗