Relating drug-induced changes in carotid artery mechanics to cardiovagal and sympathetic baroreflex control

2005 ◽  
Vol 83 (5) ◽  
pp. 439-446 ◽  
Author(s):  
Deborah D O'Leary ◽  
Craig D Steinback ◽  
Angela D Cechetto ◽  
Blaine T Foell ◽  
Jane C Topolovec ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Carotid Artery ◽  
Common Carotid Artery ◽  
Baroreflex Sensitivity ◽  
Muscle Sympathetic Nerve Activity ◽  
Pressure Change ◽  
Drug Induced ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
Induced Changes

Previous evidence indicates that sensitivity of the baroreflex cardiovagal and sympathetic arms is dissociated. In addition, pharmacologic assessment of baroreflex sensitivity (BRS) has revealed that cardiovagal, but not sympathetic, BRS is greater when blood pressure is increasing versus falling. The origin of this hysteresis is unknown. In this study, carotid artery distensibility and absolute distension (diameter) were assessed to test the hypothesis that vessel mechanics in barosensitive regions affect the BRS of cardiovagal, but not sympathetic, outflow. R-R interval (i.e. time between successive R waves), finger arterial blood pressure, muscle sympathetic nerve activity, and carotid artery dimensions (B-mode imaging) were measured during sequential infusions of sodium nitroprusside (SNP) and phenylephrine (PHE). Systolic and diastolic common carotid artery diameters and pulse pressure were recorded to calculate distensibility of this vessel under each drug condition. Cardiovagal BRS was greater when blood pressure was increasing versus decreasing (p < 0.01). Sympathetic BRS was not affected by direction of pressure change. Distensibility did not differ between SNP and PHE injections. However, compared with SNP, infusion of PHE resulted in larger absolute systolic and diastolic carotid diameters (p < 0.001). Therefore, cardiovagal reflex hysteresis was related to drug-induced changes in common carotid artery diameter but not distensibility. The lack of sympathetic hysteresis in this model suggests a relative insensitivity of this baroreflex component to carotid artery dimensions and provides a possible mechanism for the dissociation between cardiovagal and sympathetic BRS.Key words: Oxford method, baroreflex hysteresis, cardiovagal, MSNA, distensibility.

Spectral analysis of muscle sympathetic nerve activity in heat-stressed humans

2004 ◽  
Vol 286 (3) ◽  
pp. H1101-H1106 ◽  
Author(s):  
Jian Cui ◽  
Rong Zhang ◽  
Thad E. Wilson ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Systolic Blood Pressure ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Spectral Characteristics ◽  
Whole Body ◽  
Arterial Blood ◽  
Systolic Blood Pressure Variability ◽  
Induced Changes

Whole body heating increases muscle sympathetic nerve activity (MSNA); however, the effect of heat stress on spectral characteristics of MSNA is unknown. Such information may provide insight into mechanisms of heat stress-induced MSNA activation. The purpose of the present study was to test the hypothesis that heat stress-induced changes in systolic blood pressure variability parallel changes in MSNA variability. In 13 healthy subjects, MSNA, electrocardiogram, arterial blood pressure (via Finapres), and respiratory activity were recorded under both normothermic and heat stress conditions. Spectral characteristics of integrated MSNA, R-R interval, systolic blood pressure, and respiratory excursions were assessed in the low (LF; 0.03–0.15 Hz) and high (HF; 0.15–0.45 Hz) frequency components. Whole body heating significantly increased skin and core body temperature, MSNA burst rate, and heart rate, but not mean arterial blood pressure. Systolic blood pressure and R-R interval variability were significantly reduced in both the LF and HF ranges. Compared with normothermic conditions, heat stress significantly increased the HF component of MSNA, while the LF component of MSNA was not altered. Thus the LF-to-HF ratio of MSNA oscillatory components was significantly reduced. These data indicate that the spectral characteristics of MSNA are altered by whole body heating; however, heat stress-induced changes in MSNA do not parallel changes in systolic blood pressure variability. Moreover, the reduction in LF component of systolic blood pressure during heat stress is unlikely related to spectral changes in MSNA.

Baroreflex control of muscle sympathetic nerve activity during skin surface cooling

2007 ◽  
Vol 103 (4) ◽  
pp. 1284-1289 ◽  
Author(s):  
Jian Cui ◽  
Sylvain Durand ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Skin Surface ◽  
Surface Cooling ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Arterial Blood

Skin surface cooling improves orthostatic tolerance through a yet to be identified mechanism. One possibility is that skin surface cooling increases the gain of baroreflex control of efferent responses contributing to the maintenance of blood pressure. To test this hypothesis, muscle sympathetic nerve activity (MSNA), arterial blood pressure, and heart rate were recorded in nine healthy subjects during both normothermic and skin surface cooling conditions, while baroreflex control of MSNA and heart rate were assessed during rapid pharmacologically induced changes in arterial blood pressure. Skin surface cooling decreased mean skin temperature (34.9 ± 0.2 to 29.8 ± 0.6°C; P < 0.001) and increased mean arterial blood pressure (85 ± 2 to 93 ± 3 mmHg; P < 0.001) without changing MSNA ( P = 0.47) or heart rate ( P = 0.21). The slope of the relationship between MSNA and diastolic blood pressure during skin surface cooling (−3.54 ± 0.29 units·beat−1·mmHg−1) was not significantly different from normothermic conditions (−2.94 ± 0.21 units·beat−1·mmHg−1; P = 0.19). The slope depicting baroreflex control of heart rate was also not altered by skin surface cooling. However, skin surface cooling shifted the “operating point” of both baroreflex curves to high arterial blood pressures (i.e., rightward shift). Resetting baroreflex curves to higher pressure might contribute to the elevations in orthostatic tolerance associated with skin surface cooling.

Baroreflex Control of Blood Pressure and Plasma Noradrenaline during Exericse in Essential Hypertension

1979 ◽  
Vol 57 (s5) ◽  
pp. 169s-171s ◽  
Author(s):  
P. Sleight ◽  
J. S. Floras ◽  
M. O. Hassan ◽  
J. V. Jones ◽  
B. A. Osikowska ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Baroreflex Sensitivity ◽  
Bicycle Ergometer ◽  
Plasma Noradrenaline ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
Ergometer Exercise ◽  
Resting Blood Pressure ◽  
Mean Pressure

1. Twelve subjects (mean age 46·3 ± 12·5 years) with mild to moderate hypertension were studied before, during and after bicycle ergometer exercise. 2. Baroreflex sensitivity was determined by the Oxford phenylephrine method; sensitivity at rest was inversely related to intra-arterial pressure and age. Age and resting arterial pressure were not related. 3. Exercise for 5 min at 50 W and 5 min at 75 W raised the mean arterial pressure from 116·4 ± 18·0 to 150·0 ± 25·4 mmHg, the heart rate from 73·2 to 126·7 beats/min and the plasma noradrenaline from 541 ± 142·7 to 1309·8 ± 543·5 pg/ml (P &lt; 0·001). 4. The increase in noradrenaline during exercise and the maximum mean pressure achieved were inversely related to resting baroreflex sensitivity (r = −0·68 and −0·77 respectively). Resting values of noradrenaline were not related to baroreflex sensitivity, age, or resting blood pressure. 5. It is possible that the rise in both plasma noradrenaline and arterial blood pressure produced by exercise is controlled by the baroreceptor reflexes; these are less effective in hypertensive subjects and thus the increases in noradrenaline and arterial pressure during exercise are greater in subjects with raised blood pressure.

scholarly journals Cyclooxygenase inhibition and baroreflex sensitivity in humans

2005 ◽  
Vol 288 (2) ◽  
pp. H737-H743 ◽  
Author(s):  
Kevin D. Monahan ◽  
Chester A. Ray
Keyword(s):  
Blood Pressure ◽  
Intravenous Infusion ◽  
Animal Studies ◽  
Baroreflex Sensitivity ◽  
Muscle Sympathetic Nerve Activity ◽  
Linear Portion ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Rate Limiting ◽  
Cardiac Period

Animal studies suggest that prostanoids (i.e., such as prostacyclin) may sensitize or impair baroreceptor and/or baroreflex responsiveness depending on the site of administration and/or inhibition. We tested the hypothesis that acute inhibition of cyclooxygenase (COX), the rate-limiting enzyme in prostanoid synthesis, impairs baroreflex regulation of cardiac period (R-R interval) and muscle sympathetic nerve activity (MSNA) in humans and augments pressor reactivity. Baroreflex sensitivity (BRS) was determined at baseline (preinfusion) and 60 min after (postinfusion) intravenous infusion of a COX antagonist (ketorolac; 45 mg) (24 ± 1 yr; n = 12) or saline (25 ± 1 yr; n = 12). BRS was assessed by using the modified Oxford technique (bolus intravenous infusion of nitroprusside followed by phenylephrine). BRS was quantified as the slope of the linear portion of the 1) R-R interval-systolic blood pressure relation (cardiovagal BRS) and 2) MSNA-diastolic blood pressure relation (sympathetic BRS) during pharmacological changes in arterial blood pressure. Ketorolac did not alter cardiovagal (19.4 ± 2.1 vs. 18.4 ± 2.4 ms/mmHg preinfusion and postinfusion, respectively) or sympathetic BRS (−2.9 ± 0.7 vs. −2.6 ± 0.4 arbitrary units·beat−1·mmHg−1) but significantly decreased a plasma biomarker of prostanoid generation (plasma thromboxane B2) by 53 ± 11%. Cardiovagal BRS (21.3 ± 3.8 vs. 21.2 ± 3.0 ms/mmHg), sympathetic BRS (−3.4 ± 0.3 vs. −3.2 ± 0.2 arbitrary units·beat−1·mmHg−1), and thromboxane B2 (change in −1 ± 12%) were unchanged in the control (saline infusion) group. Pressor responses to steady-state incremental (0.5, 1.0, and 1.5 μg·kg−1·min−1) infusion (5 min/dose) of phenylephrine were not altered by ketorolac ( n = 8). Collectively, these data indicate that acute pharmacological antagonism of the COX enzyme does not impair BRS (cardiovagal or sympathetic) or augment pressor reactivity in healthy young adults.

Fetal ACTH and blood pressure responses to thromboxane mimetic U-46619

1993 ◽  
Vol 265 (4) ◽  
pp. R858-R862 ◽  
Author(s):  
C. E. Wood ◽  
T. A. Cudd ◽  
C. Kane ◽  
K. Engelke
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Carotid Artery ◽  
Common Carotid Artery ◽  
Thromboxane A2 ◽  
Renin Secretion ◽  
Fetal Sheep ◽  
Arterial Blood ◽  
Carotid Arterial

This study was performed to test the hypothesis that thromboxane A2 stimulates increases in fetal adrenocorticotropic hormone (ACTH), vasopressin, or renin secretion and affects fetal cardiovascular function by an action on the fetal central nervous system. We infused a stable synthetic analogue of thromboxane A2, U-46619, into one common carotid artery or inferior vena cava or infused saline into one common carotid artery in chronically catheterized fetal sheep between 127 and 140 days gestation. We found that intracarotid but not intravenous infusions of U-46619 at a rate of 750 ng/min stimulated increases in fetal plasma ACTH concentration. Infusions of U-46619 at both sites increased fetal blood pressure; the infusion into the carotid arterial blood produced a more rapid increase in blood pressure and a significant decrease in central venous pressure. None of the infusions altered plasma vasopressin concentration or plasma renin activity, blood gases, hematocrit, or plasma cortisol concentration. We conclude that thromboxane A2 stimulates fetal ACTH, but not vasopressin or renin, secretion via an action within the area perfused by carotid arterial blood. Thromboxane A2 increases blood pressure via an action at the fetal central nervous system, as well as via a direct vasoconstrictor action in the systemic circulation.

Phenylephrine-induced elevations in arterial blood pressure are attenuated in heat-stressed humans

2002 ◽  
Vol 283 (5) ◽  
pp. R1221-R1226 ◽  
Author(s):  
Jian Cui ◽  
Thad E. Wilson ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Arterial Blood Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Peripheral Resistance ◽  
Whole Body ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
The Relationship

To test the hypothesis that phenylephrine-induced elevations in blood pressure are attenuated in heat-stressed humans, blood pressure was elevated via steady-state infusion of three doses of phenylephrine HCl in 10 healthy subjects in both normothermic and heat stress conditions. Whole body heating significantly increased sublingual temperature by ∼0.5°C, muscle sympathetic nerve activity (MSNA), heart rate, and cardiac output and decreased total peripheral vascular resistance (TPR; all P < 0.005) but did not change mean arterial blood pressure (MAP; P > 0.05). At the highest dose of phenylephrine, the increase in MAP and TPR from predrug baselines was significantly attenuated during the heat stress [ΔMAP 8.4 ± 1.2 mmHg; ΔTPR 0.96 ± 0.85 peripheral resistance units (PRU)] compared with normothermia (ΔMAP 15.4 ± 1.4 mmHg, ΔTPR 7.13 ± 1.18 PRU; all P < 0.001). The sensitivity of baroreflex control of MSNA and heart rate, expressed as the slope of the relationship between MSNA and diastolic blood pressure, as well as the slope of the relationship between heart rate and systolic blood pressure, respectively, was similar between thermal conditions (each P > 0.05). These data suggest that phenylephrine-induced elevations in MAP are attenuated in heat-stressed humans without affecting baroreflex control of MSNA or heart rate.

Change in spontaneous baroreflex control of pulse interval during heat stress in humans

2003 ◽  
Vol 95 (5) ◽  
pp. 1789-1798 ◽  
Author(s):  
Kichang Lee ◽  
Dwayne N. Jackson ◽  
Douglas L. Cordero ◽  
Takeshi Nishiyasu ◽  
Jochen K. Peters ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Stroke Volume ◽  
Linear Relationship ◽  
Baroreflex Sensitivity ◽  
Pulse Interval ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
Transfer Function Analysis ◽  
Spontaneous Baroreflex

Spontaneous baroreflex control of pulse interval (PI) was assessed in healthy volunteers under thermoneutral and heat stress conditions. Subjects rested in the supine position with their lower legs in a water bath at 34°C. Heat stress was imposed by increasing the bath temperature to 44°C. Arterial blood pressure (Finapres), PI (ECG), esophageal and skin temperature, and stroke volume were continuously collected during each 5-min experimental stage. Spontaneous baroreflex function was evaluated by multiple techniques, including 1) the mean slope of the linear relationship between PI and systolic blood pressure (SBP) with three or more simultaneous increasing or decreasing sequences, 2) the linear relationship between changes in PI and SBP (ΔPI/ΔSBP) derived by using the first differential equation, 3) the linear relationship between changes in PI and SBP with simultaneously increasing or decreasing sequences (+ΔPI/+ΔSBP or -ΔPI/-ΔSBP), and 4) transfer function analysis. Heat stress increased esophageal temperature by 0.6 ± 0.1°C, decreased PI from 1,007 ± 43 to 776 ± 37 ms and stroke volume by 16 ± 5 ml/beat. Heat stress reduced baroreflex sensitivity but increased the incidence of baroreflex slopes from 5.2 ± 0.8 to 8.6 ± 0.9 sequences per 100 heartbeats. Baroreflex sensitivity was significantly correlated with PI or vagal power ( r2 = 0.45, r2 = 0.71, respectively; P < 0.05). However, the attenuation in baroreflex sensitivity during heat stress appeared related to a shift in autonomic balance (shift in resting PI) rather than heat stress per se.

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