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PubMed2006

Endomorphin-2 in the medial NTS attenuates the responses to baroreflex activation.

We have previously reported that microinjections of endomorphin-2 (E-2; an endogenous mu-receptor agonist) into the medial subnucleus of the NTS (mNTS) elicit depressor and bradycardic responses via activation of ionotropic glutamate receptors located on secondary mNTS-neurons. Based on this report, it was hypothesized that activation of secondary mNTS neurons by E-2 may result in an exaggeration of baroreflex responses. In order to test this hypothesis, baroreflex responses were studied in adult, urethane-anesthetized, artificially ventilated, male Wistar rats before and after the microinjections of E-2 into the mNTS. Baroreceptors were stimulated by applying pressure increments (80-100 mm Hg) in the carotid sinus and by electrical stimulation (stimulus intensity: 0.5 V, frequencies 5, 10, and 25 pulses/s, pulse duration: 1 ms) of the aortic nerve for 30-s periods. Baroreceptor stimulation elicited depressor and bradycardic responses. Microinjections (100 nl) of E-2 (0.4 mmol/l) into the mNTS attenuated the baroreflex responses. Microinjections of naloxone (an opioid receptor antagonist) into the mNTS (0.5 mmol/l) did not alter baroreflex responses. Based on these results, it was concluded that activation of mu-opioid receptors in the mNTS attenuates baroreflex responses. Possible mechanisms for excitatory effects of E-2 in the mNTS resulting in depressor and bradycardic responses, on one hand, and inhibitory effects resulting in attenuation of baroreflex responses, on the other, are discussed.

Analgesics, Opioid↗
PubMed2005

Functional interaction between nucleus tractus solitarius NK1 and 5-HT3 receptors in the inhibition of baroreflex in rats.

OBJECTIVE: Previous data showed that in the nucleus tractus solitarius (NTS), 5-HT(3) receptors are critically involved in the inhibition of cardiac baroreceptor reflex response occurring during the defense reaction. Since stimulation of NTS NK(1) receptors has been found to inhibit the baroreflex bradycardia, we examined in this study whether this reflex response is inhibited during the defense reaction via an interaction between NK(1) and 5-HT(3) receptors. METHODS: For this purpose, we analyzed in urethane-anaesthetized rats the effects of intra-NTS GR205171, a selective NK(1) receptor antagonist, on the baroreflex bradycardia inhibition observed either during the defense reaction triggered by electrical stimulation of the dorsal periaqueductal grey matter (dPAG) or after NTS 5-HT(3) receptor activation. RESULTS: Intra-NTS GR205171, reversed, in dose-dependent manner, the inhibitory effect of dPAG stimulation on baroreflex bradycardia. This reversion was of 49% when both sinus carotid and aortic baroreceptors were stimulated by phenylephrine, and of 84% when aortic depressor nerve was stimulated. Similarly, intra-NTS GR205171 reversed partially or almost totally the inhibitory effect of local microinjections of phenylbiguanide, a 5-HT(3) receptor agonist, on baroreflex bradycardia induced either by phenylephrine administration or aortic nerve stimulation, respectively. CONCLUSION: These results strongly suggest that NK(1) receptors contribute downstream to the 5-HT(3) receptor-mediated inhibition of the aortic but not carotid cardiac baroreflex response occurring during the defense reaction, therefore implying that baroreceptor afferent inputs may be differentially modulated depending on their origin. This differentiation may be useful for a better understanding of baroreflex dysfunction in disease-induced conditions.

Animals↗
PubMed2005

Intraventricular injections of tachykinin NK3 receptor agonist reduce the gain of the baroreflex in unrestrained rats.

The tachykinin neuropeptides acting at NK3 receptors affect mean arterial pressure (MAP) through both neuroendocrine and neural mechanisms. NK3 receptors are found in brainstem nuclei that mediate the baroreflex, but the effects of NK3 receptor stimulation on baroreflex function are unknown. The present study tests the effects of intraventricular injections of senktide, a selective NK3 receptor agonist, on the sensitivity of the baroreflex in three stains of rats: Charles River Laboratory, Long-Evans, and Brattleboro rats, which lack the ability to synthesize vasopressin. Rats with lateral ventricle cannulas were administered injections of isotonic saline, 100 ng, or 200 ng senktide, and 5 min later arterial baroreceptor-heart rate (HR) function was examined by constructing full-range blood pressure-HR curves using alternating doses (5-20 microg kg min) of phenylephrine and nitroprusside to raise and decrease blood pressure approximately 50 mm Hg over a period of 1 min, respectively. Intraventricular injections of 200 ng senktide had no significant effect on baseline MAP, but significantly decreased the gain of the baroreflex in all three rat strains whereas the 100 ng dose had no effect on the baroreflex. These results show that NK3 receptor stimulation modulates the baroreflex that is independent of any action of vasopressin.

Animals↗
PubMed1998

Baroreflex-mediated bradycardia but not tachycardia is blunted peripherally by intravenous mu-opioid agonists.

OBJECTIVE: We sought to test the hypothesis that an intravenous dose of H-Tyr-D-Arg-Phe-Lys-NH2, a highly mu-receptor selective opioid peptide, suppresses baroreflex sensitivity through a peripheral mechanism. STUDY DESIGN: A transient change in mean arterial pressure was produced in chronically instrumented pregnant ewes by norepinephrine or sodium nitroprusside in the absence or in the presence of H-Tyr-D-Arg-Phe-Lys-NH2, a highly mu-selective opioid peptide. In some studies naloxone methiodide, a peripheral opioid antagonist, was infused starting 60 minutes before the administration of H-Tyr-D-Arg-Phe-Lys-NH2 and maintained for a total of 90 minutes. Linear plots were obtained when the changes in mean arterial pressure during the pressure rise were plotted against the changes in heart rate and the sensitivity of the baroreflex was derived as the slope of the linear regression line. RESULTS: We observed (1) lower baroreflex sensitivity after H-Tyr-D-Arg-Phe-Lys-NH2 administration with a hypertensive stimulus; (2) unchanged baroreflex sensitivity after H-Tyr-D-Arg-Phe-Lys-NH2 administration with a hypotensive stimulus; and (3) unchanged baroreflex sensitivity after H-Tyr-D-Arg-Phe-Lys-NH2 administration with a hypertensive stimulus in the presence of naloxone methiodide. CONCLUSION: H-Tyr-D-Arg-Phe-Lys-NH2 suppresses the hypertensive but not the hypotensive arm of the baroreflex through peripheral opioid receptors. These results suggest that mu-opioid receptors are present in the vagus nerves and that the activation of these opioid receptors inhibits reflex bradycardia in pregnant sheep.

Animals↗
PubMed1998

In vivo cardiovascular reactivity and baroreflex activity in diabetic rats.

OBJECTIVES: Abnormalities of the cardiovascular system, e.g. impaired vasoreactivity and changes in baroreflex control of heart rate, are known to occur in experimental diabetes. It is not clear whether these cardiovascular dysfunctions are direct consequences of cardiovascular deficits and/or have autonomic neuropathy as a cause. METHODS: To differentiate between cardiovascular deficits or neuronal impairment as a cause for these cardiovascular dysfunctions, we tested the effects of the ACTH4-9 analogue, Org 2766, a neurotrophic compound without cardiovascular effects, on arterial pressure, heart rate and baroreflex control of heart rate. At 15 weeks, rats were made diabetic by injection of streptozotocin, and from 0-6, 6-12 or 12-18 weeks thereafter 3 groups of rats were treated with Org 2766. These effects were evaluated during phenylephrine-induced increases, and sodium nitroprusside-induced decreases, in blood pressure, in rats that had been diabetic for various periods (2-42 weeks). RESULTS: Throughout, both depressor response and maximal vasodilator activity in response to sodium nitroprusside were significantly (P < 0.05) reduced as compared to those of the non-diabetic controls. The pressor response of the diabetic rats to phenylephrine was only significantly (P < 0.05) reduced at 4, 6 and 12 weeks, and at 18 weeks, the diabetic rats were either hypo- or normoresponsive; Org 2766 did not restore the disturbed pressor response. From weeks 4 to 42 both maximal decrease in heart rate and sensitivity of baroreflex-mediated bradycardia in the diabetic rats were significantly less (P < 0.05) than those in the non-diabetic controls. Org 2766 restored the diminished baroreflex-mediated bradycardia of diabetic rats to non-diabetic control levels at 6 weeks, had an ameliorating effect at 12 weeks and no effect at 18 weeks. CONCLUSIONS: Time-dependent decreases in baroreflex sensitivity in diabetic rats was demonstrated and a much less steep decline of baroreflex sensitivity occurred in non-diabetic control rats. The ACTH4-9 analogue, Org 2766, when given immediately upon the induction of diabetes seem to delay the development of autonomic neuropathy, which suggests that cardiovascular factors appear to be of minor importance.

Adrenocorticotropic Hormone↗
PubMed2000

The relationships of resting baroreflex sensitivity, heart rate variability and measures of impulse control in children and adolescents.

The objectives of the present study were to assess: (1) the feasibility of using a non-invasive method to measure baroreflex sensitivity in children and adolescents; (2) the relationships of resting baroreflex sensitivity with resting levels of other cardiovascular variables; and (3) whether baroreflex sensitivity and heart rate variability, two indices of cardiac vagal control at rest, were related to measures of impulse control. Ninety-one Black and White children (ages 8-10) and adolescents (ages 15-17), both female and male, participated in the study. Baroreflex sensitivity, auscultatory blood pressure, EKG-derived heart rate, and the mean successive difference of interbeat intervals were collected during a 10-min rest period. Measures of impulse control came from the Interview for Antisocial Behavior. Baroreflex sensitivity was strongly positively correlated with mean successive difference and negatively correlated with heart rate for all participant groups; baroreflex sensitivity was negatively correlated with diastolic blood pressure, but only for children, males, and Blacks. Increased problems with impulse control was associated with decreased cardiac vagal control, but only in males. The usefulness of this technique as a measure of vagal activation is discussed.

Adolescent↗
PubMed1995

Treatment with enalapril fails to prevent impaired cardiopulmonary baroreflex control in dogs with left ventricular dysfunction.

That the cardiopulmonary baroreflex control of sympathetic nerve activity is impaired in dogs with left ventricular (LV) dysfunction has been shown previously. This study tested the hypothesis that treatment with the angiotensin-converting enzyme inhibitor enalapril prevents or delays the development of abnormalities of cardiopulmonary baroreflexes in dogs with LV dysfunction. Serial changes in LV volumes and neurohumoral profiles (plasma norepinephrine and renin activity) were assessed in conscious dogs with progressive LV dysfunction due to rapid ventricular pacing. Enalapril 5 mg orally twice daily was administered from days 4 to 12 of pacing. Cardiopulmonary baroreflexes were assessed in enalapril-treated paced dogs (n = 8) and untreated paced dogs (n = 8) by recording changes in renal nerve activity and pulmonary capillary wedge pressure during volume infusion in anesthetized sinoaortic denervated dogs on day 12 of rapid pacing. There was no difference in LV volume in the two groups. Neurohumoral factors were similar in both groups except for the expected high plasma renin activity in enalapril-treated dogs. Hemodynamic parameters also were comparable in the two groups. Cardiopulmonary baroreflex sensitivity for enalapril-treated dogs was not different from that of untreated paced dogs, and baroreflex gain in both groups was significantly lower than for the nonpaced control dogs (P < .05). Despite adequate converting enzyme blockade, treatment with enalapril failed to prevent the development of attenuated cardiopulmonary baroreflex control of sympathetic nerve activity in dogs with developing LV dysfunction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Prognostic value of baroreflex sensitivity assessed by phase IV of Valsalva manoeuvre in patients with mild-to-moderate heart failure.

BACKGROUND: In patients with heart failure, impairment of baroreflex function occurs early and contributes to sympathetic activation, however, at present its prognostic role has not been definitively established. AIMS: To evaluate the prognostic significance of baroceptor impairment in patients with different degrees of heart failure. METHODS: We enrolled 52 consecutive patients with heart failure, referred to our institution for functional evaluation. Twenty-eight suffered from ischemic cardiomyopathy and 26 from dilated cardiomyopathy. Thirteen patients were in NYHA class I, 20 in NYHA class II and 19 in class III. All patients underwent baroreflex assessment by phase IV Valsalva manoeuvre using Finapres finger monitoring of arterial blood pressure, echocardiography [with evaluation of left ventricular ejection fraction (LVEF), fractional shortening (LVFS), left ventricular end diastolic diameter (LVEDD) and mean pulmonary artery pressure] and functional evaluation by cardiopulmonary exercise test and 6-min walk corridor test within 2 days of hospital admission. RESULTS: Mean duration of follow-up was 26 months (range 6-35 months). At baseline, evaluation in 13 patients BRS was normal (>5 ms/mmHg), in 17 moderately impaired (1.5-5 ms/mmHg) and in 22 severely depressed (<1.5 ms/mmHg). Baroreflex function was relatively preserved in patients in NYHA class I (5.1+/-2.5) in comparison to patients in NYHA class II and III (2.1+/-2.3 and 2.08+/-1.9 ms/mmHg, respectively). Of the 52 patients who entered the study at the end of follow-up 15 died of cardiac cause and 5 underwent heart transplantation. Survival free from heart transplantation was 62% in patients with normal baroreflex function, 62% in patients with moderate impairment of baroreflex and 66% in patients with major derangement. NYHA class, LVEF, LVFS and LVEDD were significantly associated with event free survival while baroreflex function was not. CONCLUSIONS: Our results suggest that evaluation of BRS impairment by phase IV Valsalva manoeuvre has limited prognostic value in patients with heart failure.

Adult↗
PubMed2003

Whole body heating reduces the baroreflex response of sympathetic nerve activity during Valsalva straining.

The present experiment was carried out to examine the possible effects of whole body heating on the baroreflex control of muscle sympathetic nerve activity (MSNA) and heart rate (HR). Nine healthy male volunteers underwent the Valsalva maneuver during exposure to heat stress using a hot water-perfused suit. To exclude an effect from the unloading of the cardiopulmonary baroreceptors during hyperthermia, the central hypovolemia was counterbalanced by head-down tilt (HDT) at 8 degrees. The baroreflex slopes of MSNA and HR against mean arterial pressure were determined by regression analysis during the early phase II (falling blood pressure period) of the Valsalva maneuver. The core temperature increased from 36.9 +/- 0.1 degrees C at thermoneutral to 37.7 +/- 0.1 degrees C during heat exposure, whereas the left atrial diameter (LAD) decreased. Both the MSNA and HR increased (P < 0.05) during hyperthermia. The baroreflex slopes of MSNA and HR in the phase II decreased 30 +/- 8% (P < 0.05) and 24 +/- 9% (P < 0.05), respectively, during hyperthermia. The HDT increased LAD, but there was no change in HR, arterial pressure and the baroreflex slopes. These results suggest that hyperthermia reduces the baroreflex responses of MSNA and HR during a transient falling period of blood pressure. These reduced baroreflex responses may not be attributable to an unloading of the cardiopulmonary baroreceptors during heat stress.

Adult↗
PubMed2003

Antagonism of glutamatergic metabotropic receptors in the NTS of awake rats does not affect the gain of the baroreflex.

There is evidence suggesting that metabotropic receptors may play a role in the neurotransmission of the baroreflex in the nucleus tractus solitarius (NTS) of rats. In a recent study from our laboratory, we verified that microinjection of a metabotropic receptor agonist, trans-1-amino-1,3-cyclopentanediocarboxylic acid, into the NTS of awake and anesthetized rats produced baroreflex-like responses (hypotension and bradycardia). In the present study, we evaluated the possible role of L-glutamate metabotropic receptors of the NTS in the neuromodulation of the parasympathetic component of baroreflex activation in awake rats. Bilateral microinjection (50 nl) of a metabotropic receptor antagonist (alpha-methyl-4-carboxyphenylglycine, MCPG, 100 mM) into the rostral commissural NTS produced no change in the gain of the baroreflex bradycardia. In addition, microinjection of MCPG into the NTS produced no changes in baseline mean arterial pressure (MAP) or heart rate (HR), indicating that metabotropic receptors play no tonic role in the neurotransmission of the baroreflex. The dose of MCPG used to block the metabotropic receptors was effective in reducing the bradycardic and hypotensive responses to microinjection (50 nl) of trans-1-amino-1,3-cyclopentanediocarboxylic acid (5 mM) into the NTS. The data show that metabotropic glutamate receptors play no major role in the neuromodulation of the parasympathetic component of the baroreflex at the NTS level.

Animals↗
PubMed2003

Peripheral hyperosmolality reduces cardiac baroreflex sensitivity.

The effects of acute increases in peripheral osmolality on cardiac baroreflex sensitivity were tested in conscious, unrestrained rats by fitting values for arterial blood pressure and heart rate during acute pressor and depressor responses to a four-parameter, sigmoid logistic function curve. Cardiac baroreceptor reflex function curves were produced before and following 30 min intravenous (i.v.) infusion of 2.5 M NaCl, an equipressor concentration of phenylephrine, isotonic saline, or 2.5 M NaCl following central administration of an angiotensin-converting enzyme (ACE) inhibitor. Hypertonic saline infusion increased blood pressure, reduced heart rate and baroreflex sensitivity (gain and range), and shifted the baroreflex function curve to a higher operating blood pressure. These effects were prevented or attenuated by prior central administration of an ACE inhibitor. Isotonic volume expansion did not alter baroreflex responses. Finally, phenylephrine produced similar changes in blood pressure but did not alter cardiac baroreflex responses. These data demonstrate that acute increases in peripheral osmolality and/or sodium decrease cardiac baroreflex sensitivity through generation of central angiotensin II, independent of changes in extracellular fluid volume and blood pressure.

Animals↗
PubMed1999

Baroreflex control of heart rate is impaired in pre-eclampsia.

Autonomic nervous dysfunction, such as parasympathetic and sympathetic impairment, has been suggested as possible cause of pre-eclampsia, but the studies are not conclusive. Our purpose was to assess non-invasively if pre-eclampsia is associated with a decreased baroreflex function. Nine women with pre-eclampsia (PE), eight normotensive pregnant women, and seven healthy normotensive non-pregnant women were studied. Continuous finger blood pressure was recorded by a Portapres device in the left lateral recumbent position and active standing. Baroreflex gain was evaluated by cross-spectral analysis of systolic blood pressure and pulse interval. The result was that baroreflex gain at rest was lower in pre-eclamptic women both compared to non-pregnant and healthy pregnant subjects (P<0.05). Moreover, a decrease of the baroreflex sensitivity was present in all pregnant women in the orthostatic position (P<0.05). In conclusion pregnancy per se is associated with a decrease in the baroreflex control of the heart, whereas in pre-eclampsia, the baroreflex sensitivity is impaired further.

Adult↗
PubMed2006

Determinants of baroreflex function in juvenile end-stage renal disease.

Arterial baroreflex sensitivity (BRS) is markedly reduced in middle-aged patients with end-stage renal disease (ESRD), due to the combined effects of aging, arterial stiffening, and autonomic neuropathy. Much less is known about the effects of ESRD on arterial baroreflex in juvenile patients. Therefore, we investigated baroreflex function and its relation to carotid artery elasticity and heart rate variability in children and young adults with ESRD. We studied 42 subjects (9-30 years): 14 patients on maintenance hemodialysis (HD), 14 renal transplant recipients (RT), and 14 healthy control subjects (C). Baroreflex function was determined by pharmacological (BRS) and spontaneous (sequence and spectral indices) techniques. Carotid artery elasticity was characterized by stiffness index beta. Heart rate variability was assessed using time and frequency domain measures. Data are expressed as mean+/-s.d. BRS was markedly reduced in HD as compared to C (10.0+/-4.2 vs 25.7+/-5.9 ms/mm Hg); spontaneous indices were reduced to similar extent. Carotid artery stiffness was approximately 50% higher in HD than in C and was inversely related to BRS. Heart rate variability was also compromised in HD, and was directly related to spontaneous indices. No significant differences existed in any of these variables between RT and C. Decreased baroreflex function in juvenile HD is partly due to loss of carotid artery elasticity and partly due to impaired heart rate variability. Renal transplantation may partly prevent impairment or improve compromised baroreflex function in young patients with ESRD.

Adolescent↗
PubMed1995

Physiology and pathophysiology of heart rate and blood pressure variability in humans: is power spectral analysis largely an index of baroreflex gain?

1. It is often assumed that the power in the low- (around 0.10 Hz) and high-frequency (around 0.25 Hz) bands obtained by power spectral analysis of cardiovascular variables reflects sympathetic and vagal tone [corrected] respectively. An alternative model attributes the low-frequency band to a resonance in the control system that is produced by the inefficiently slow time constant of the reflex response to beat-to-beat changes in blood pressure effected by the sympathetic (with or without the parasympathetic) arm(s) of the baroreflex (De Boer model). 2. We have applied the De Boer model of circulatory variability to patients with varying baroreflex sensitivity to patients with varying baroreflex sensitivity and one normal subject, and have shown that the main differences in spectral power (for both low and high frequency) between and within subjects are caused by changes in the arterial baroreflex gain, particularly for vagal control of heart rate (R-R interval) and left ventricular stroke output. We have computed the power spectrum at rest and during neck suction (to stimulate carotid baroreceptors). We stimulated the baroreceptors at two frequencies (0.1 and 0.2 Hz), which were both distinct from the controlled respiration rate (0.25 Hz), in both normal subjects and heart failure patients with either sensitive or poor baroreflex control. 3. The data broadly confirm the De Boer model. The low-frequency (0.1 Hz) peak in either R-R or blood pressure variability) was spontaneously generated only if the baroreflex control of the autonomic outflow was relatively intact.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1998

Aldosterone blunts the baroreflex response in man.

1. Recent animal evidence suggests that aldosterone, like angiotensin II, may possess detrimental autonomic modulating properties. Aldosterone has been shown to impair the baroreflex response in animal models. This study is designed to test the hypothesis that aldosterone directly attenuates the baroreflex in vivo in man.2. Fourteen healthy male volunteers [mean age (S.D.) 25 (9) years] received intravenous d-aldosterone (12 pmol.min-1.kg-1) and 5% dextrose (vehicle) in a double-blind crossover fashion, co-infused with incremental doses of intravenous phenylephrine and sodium nitroprusside. Aldosterone had no significant effect on resting blood pressure, heart rate or baroreflex response to sodium nitroprusside. However, reflex responses to phenylephrine were impaired with aldosterone (P<0.01) while blood pressure responses were unaltered. Baroreflex sensitivity was significantly blunted in the aldosterone group [8.36+/-2.19 versus 10.12+/-2.27 ms/mmHg; P<0. 04].3. This study confirms previous observations from animal models that aldosterone impairs the baroreflex response. High aldosterone levels may contribute to the baroreflex dysfunction in cardiovascular diseases such as hypertension and heart failure.

Adult↗
PubMed2003

Effects of age on the cardiac and vascular limbs of the arterial baroreflex.

BACKGROUND: Healthy ageing has several effects on the autonomic control of the circulation. Several studies have shown that baroreflex-mediated vagal control of the heart deteriorates with age, but so far there is little information regarding the effect of ageing on sympathetically mediated baroreflex responses. The aim of this study was to assess the effects of ageing on baroreflex control of the heart and blood vessels. MATERIALS AND METHODS: In 40 healthy volunteers, aged 20-87 years, we applied oscillatory neck suction at 0.1 Hz to assess the sympathetic modulation of the heart and blood vessels and at 0.2 Hz to assess the effect of parasympathetic stimulation on the heart. Breathing was maintained at 0.25 Hz. Blood pressure, electrocardiographic RR intervals and respiration were recorded continuously. Spectral analysis was used to evaluate the magnitude of the low-frequency (0.03-0.14 Hz) and high-frequency (0.15-0.50 Hz) oscillations in the RR interval and blood pressure. Responses to neck suction were assessed as the change in power of the RR interval and blood pressure fluctuations at the stimulation frequency from baseline values. RESULTS: Resting low- and high-frequency powers of the RR interval decreased significantly with age (P < 0.01). However, the low-frequency power of systolic blood pressure did not correlate with age. Spontaneous baroreflex sensitivity (alpha-index) showed a significant inverse correlation with age (r = -0.46, P < 0.05). Responses of the RR interval and systolic blood pressure to 0.1 Hz neck suction stimulation were not related to age, however, the RR interval response to 0.2 Hz neck suction declined significantly with age (r = -0.61, P < 0.01). CONCLUSIONS: These results confirm an age-related decrease in cardiovagal baroreflex responses. However, sympathetically mediated baroreflex control of the blood vessels is preserved with age.

Adult↗
PubMed2002

Impaired baroreflex function during pregnancy is associated with stiffening of the carotid artery.

OBJECTIVE: The baroreflex sensitivity and the distensibility of the carotid artery were measured during normotensive pregnancy to test the hypothesis that changes in baroreflex sensitivity are related to carotid artery stiffening. DESIGN: Data were obtained from pregnant subjects during each trimester (T1, T2, T3; n = 23) and postpartum (n = 11). End-diastolic diameter and pulsatile distension of the carotid artery were measured with an ultrasound wall-tracking system, and the distensibility coefficient was calculated. Spontaneous fluctuations in cardiac interval and systolic pressure were used to determine baroreflex sensitivity. RESULTS: Both distensibility coefficient and baroreflex sensitivity were reduced from T1 to T3 (5.1 +/- 1.6 vs. 3.7 +/- 0.9 10(-3)/mmHg and 10.1 +/- 2.9 vs. 5.7 +/- 1.8 ms/mmHg, respectively). Baroreflex sensitivity and carotid distensibility coefficient were linearly related in each subject (r = 0.62 +/- 0.12). Augmentation index and return time changes indicated a global increase in arterial distensibility. CONCLUSIONS: Stiffening of the carotid artery significantly contributes to the impairment of baroreflex sensitivity during pregnancy, and represents a region specific change as global arterial distensibility was found to increase during pregnancy.

Adult↗
PubMed1999

Arterial baroreflex function in humans anaesthetized with sevoflurane.

Volatile anaesthetic agents attenuate arterial baroreflex function, while noxious stimuli may modify baroreflex-induced circulatory responses during anaesthesia. We have examined baroreflex control of heart rate during the entire course of sevoflurane anaesthesia in adult patients undergoing surgical procedures. Baroreflex sensitivity was assessed in nine healthy patients undergoing general anaesthesia with sevoflurane. After an 8-10-h fast and no premedication, measurements of R-R intervals were made at conscious baseline (awake), during 2% end-tidal sevoflurane and 67% nitrous oxide before incision (anaesthesia), during surgery at 2% end-tidal sevoflurane and 67% nitrous oxide (surgery) and 20 min after extubation (recovery). Baroreflex responses were triggered by bolus i.v. injections of phenylephrine 50-100 micrograms and nitroprusside 100-200 micrograms to increase and decrease systolic arterial pressure by 20-30 mm Hg, respectively. Baroreflex sensitivities to both pressor and depressor tests were significantly depressed during anaesthesia, surgery and the recovery periods compared with awake values. Pressor test sensitivity during recovery increased significantly from that during surgery (mean 6.16 (SD 2.95) vs 4.42 (3.19) ms mm Hg-1; P < 0.05), but was still significantly less than the awake value (22.50 (17.02) ms mm Hg-1). No improvement in the depressor test sensitivity was seen during the recovery period.

Adult↗