scholarly journals Is there diurnal variation of the vestibulosympathetic reflex: implications for orthostatic hypotension

2013 ◽  
Vol 305 (10) ◽  
pp. H1555-H1559
Author(s):  
Chester A. Ray ◽  
Charity L. Sauder ◽  
Stephanie A. Chin-Sang ◽  
Jonathan S. Cook
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Diurnal Variation ◽  
Orthostatic Hypotension ◽  
Arterial Blood Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Calf Blood Flow ◽  
Vestibulosympathetic Reflex

Incidences of adverse cardiac events and orthostatic hypotension are associated with diurnal variations. The primary purpose of the present study was to determine if the vestibulosympathetic reflex (VSR) follows a diurnal variation in humans. We hypothesized that the VSR would be attenuated at night based on the relation between melatonin and the VSR. Arterial blood pressure, heart rate, calf blood flow, and muscle sympathetic nerve activity (MSNA) were measured in nine healthy subjects (28 ± 1 yr, 5 men and 4 women) at rest and during head-down rotation. Each subject was tested during the day at 11:34 ± 13 and again at night 22:10 ± 5. MSNA was significantly decreased at night compared with day (8 ± 1 vs. 11 ± 2 bursts/min, respectively, P < 0.02). Heart rate and arterial blood pressure at rest were significantly increased at night compared with day (heart rate: 70 ± 4 vs. 66 ± 4 beats/min and mean arterial blood pressure: 91 ± 2 vs. 87 ± 1 mmHg, respectively). MSNA and hemodynamic responses to head-down rotation were not significantly altered at night compared with day (changes of 3 ± 1 bursts/min and 25 ± 6% for MSNA and calf blood flow, respectively). The data indicate that MSNA at rest decreases during the late evening hours and exhibits a diurnal variation, whereas the VSR does not. In summary, diurnal variation of orthostatic hypotension in humans does not appear to be associated with changes in the VSR and MSNA at rest.

Aging, opioid-receptor agonists and antagonists, and the vestibulosympathetic reflex in humans

2004 ◽  
Vol 96 (5) ◽  
pp. 1761-1766 ◽  
Author(s):  
Chester A. Ray ◽  
Kevin D. Monahan
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Opioid Receptor ◽  
Muscle Sympathetic Nerve Activity ◽  
Endogenous Opioids ◽  
Arterial Blood ◽  
Before And After ◽  
Vestibulosympathetic Reflex ◽  
Older Subjects

Animal studies indicate that opioids inhibit the firing rate of vestibular neurons, which are important in mediating the vestibulosympathetic reflex. Furthermore, this inhibition appears to be greater in more mature rats. In the present study, we tested the hypotheses that opioids inhibit the vestibulosympathetic reflex in humans and that endogenous opioids contribute to the age-related impairment of the vestibulosympathetic reflex. These hypotheses were tested by measuring muscle sympathetic nerve activity (MSNA), arterial blood pressure, and heart rate responses to otolith organ engagement during head-down rotation (HDR) in young (24 ± 2 yr old) and older (63 ± 2 yr) subjects before and after administration of either an opioid-receptor antagonist (16 mg naloxone in 9 young and 8 older subjects) or an opioid-receptor agonist (60 mg codeine in 7 young and 7 older subjects). Naloxone did not augment the reflex increase in MSNA during HDR in young (Δ7 ± 2 vs. Δ4 ± 2 bursts/min and Δ81 ± 23 vs. Δ60 ± 24% change in burst frequency and total MSNA before and after naloxone, respectively) or older subjects (Δ2 ± 2 vs. Δ1 ± 2 burst/min and Δ8 ± 7 vs. Δ8 ± 9% before and after naloxone). Similarly, codeine did not attenuate the increase in MSNA during HDR in young (Δ8 ± 1 vs. Δ7 ± 2 bursts/min and Δ53 ± 4 vs. Δ64 ± 16% before and after codeine) or older subjects (Δ6 ± 4 vs. Δ3 ± 3 bursts/min and Δ38 ± 21 vs. Δ33 ± 20%). Mean arterial blood pressure and heart rate responses to HDR were not altered by either naloxone or codeine. These data do not provide experimental support for the concept that opioids modulate the vestibulosympathetic reflex in humans. Moreover, endogenous opioids do not appear to contribute the age-associated impairment of the vestibulosympathetic reflex.

Sympathetic vascular transduction is augmented in young normotensive blacks

2002 ◽  
Vol 92 (2) ◽  
pp. 651-656 ◽  
Author(s):  
Chester A. Ray ◽  
Kevin D. Monahan
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Forearm Blood Flow ◽  
Lower Body Negative Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Blacks And Whites

The purpose of the present study was to determine sympathetic vascular transduction in young normotensive black and white adults. We hypothesized that blacks would demonstrate augmented transduction of muscle sympathetic nerve activity (MSNA) into vascular resistance. To test this hypothesis, MSNA, forearm blood flow, heart rate, and arterial blood pressure were measured during lower body negative pressure (LBNP). At rest, no differences existed in arterial blood pressure, heart rate, forearm blood flow, and forearm vascular resistance (FVR). Likewise, LBNP elicited comparable responses of these variables for blacks and whites. Baseline MSNA did not differ between blacks and whites, but whites demonstrated greater increases during LBNP (28 ± 7 vs. 55 ± 18%, 81 ± 21 vs. 137 ± 42%, 174 ± 81 vs. 556 ± 98% for −5, −15, and −40 mmHg LBNP, respectively; P < 0.001). Consistent with smaller increases in MSNA but similar FVR responses during LBNP, blacks demonstrated greater sympathetic vascular transduction (%FVR/%MSNA) than whites (0.95 ± 0.07 vs. 0.82 ± 0.07 U; 0.82 ± 0.11 vs. 0.64 ± 0.09 U; 0.95 ± 0.37 vs. 0.35 ± 0.09 U; P < 0.01). In summary, young whites demonstrate greater increases in MSNA during baroreceptor unloading than age-matched normotensive blacks. However, more importantly, for a given increase in MSNA, blacks demonstrate greater forearm vasoconstriction than whites. This finding may contribute to augmented blood pressure reactivity in blacks.

Effects of l-arginine on systemic and renal haemodynamics in conscious dogs

1991 ◽  
Vol 81 (6) ◽  
pp. 727-732 ◽  
Author(s):  
Marohito Murakami ◽  
Hiromichi Suzuki ◽  
Atsuhiro Ichihara ◽  
Mareo Naitoh ◽  
Hidetomo Nakamoto ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Renal Haemodynamics ◽  
Conscious Dogs ◽  
Arginine Infusion ◽  
Arterial Blood

1. The effects of l-arginine on systemic and renal haemodynamics were investigated in conscious dogs. l-Arginine was administered intravenously at doses of 15 and 75 μmol min−1 kg−1 for 20 min. 2. Mean arterial blood pressure, heart rate and cardiac output were not changed significantly by l-arginine infusion. However, l-arginine infusion induced a significant elevation of renal blood flow from 50 ± 3 to 94 ± 12 ml/min (means ± sem, P < 0.01). 3. Simultaneous infusion of NG-monomethyl-l-arginine (0.5 μmol min−1 kg−1) significantly inhibited the increase in renal blood flow produced by l-arginine (15 μmol min−1 kg−1) without significant changes in mean arterial blood pressure or heart rate. 4. Pretreatment with atropine completely inhibited the l-arginine-induced increase in renal blood flow, whereas pretreatment with indomethacin attenuated it (63 ± 4 versus 82 ± 10 ml/min, P < 0.05). 5. A continuous infusion of l-arginine increased renal blood flow in the intact kidney (55 ± 3 versus 85 ± 9 ml/min, P < 0.05), but not in the contralateral denervated kidney (58 ± 3 versus 56 ± 4 ml/min, P > 0.05). 6. These results suggest that intravenously administered l-arginine produces an elevation of renal blood flow, which may be mediated by facilitation of endogenous acetylcholine-induced release of endothelium-derived relaxing factor and vasodilatory prostaglandins.

Patterned cardiovascular responses to sleep and nonrespiratory arousals in a porcine model

1998 ◽  
Vol 85 (4) ◽  
pp. 1285-1291 ◽  
Author(s):  
Sandrine H. Launois ◽  
Joseph H. Abraham ◽  
J. Woodrow Weiss ◽  
Debra A. Kirby
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Eye Movement ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Mean Arterial Blood Pressure ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Arterial Blood

Patients with obstructive sleep apnea experience marked cardiovascular changes with apnea termination. Based on this observation, we hypothesized that sudden sleep disruption is accompanied by a specific, patterned hemodynamic response, similar to the cardiovascular defense reaction. To test this hypothesis, we recorded mean arterial blood pressure, heart rate, iliac blood flow and vascular resistance, and renal blood flow and vascular resistance in five pigs instrumented with chronic sleep electrodes. Cardiovascular parameters were recorded during quiet wakefulness, during non-rapid-eye-movement and rapid-eye-movement sleep, and during spontaneous and induced arousals. Iliac vasodilation (iliac vascular resistance decreased by −29.6 ± 4.1% of baseline) associated with renal vasoconstriction (renal vascular resistance increased by 10.3 ± 4.0%), tachycardia (heart rate increase: +23.8 ± 3.1%), and minimal changes in mean arterial blood pressure were the most common pattern of arousal response, but other hemodynamic patterns were observed. Similar findings were obtained in rapid-eye-movement sleep and for acoustic and tactile arousals. In conclusion, spontaneous and induced arousals from sleep may be associated with simultaneous visceral vasoconstriction and hindlimb vasodilation, but the response is variable.

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.

Nocturnal variations in peripheral blood flow, systemic blood pressure, and heart rate in humans

1991 ◽  
Vol 261 (4) ◽  
pp. H982-H988
Author(s):  
J. H. Sindrup ◽  
J. Kastrup ◽  
H. Christensen ◽  
B. Jorgensen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Flow Rate ◽  
Mean Arterial Blood Pressure ◽  
Blood Flow Rate ◽  
Tissue Blood Flow ◽  
Peripheral Blood Flow ◽  
Arterial Blood

Subcutaneous adipose tissue blood flow rate, together with systemic arterial blood pressure and heart rate under ambulatory conditions, was measured in the lower legs of 15 normal human subjects for 12-20 h. The 133Xe-washout technique, portable CdTe(Cl) detectors, and a portable data storage unit were used for measurement of blood flow rates. An automatic portable blood pressure recorder and processor unit was used for measurement of systolic blood pressure, diastolic blood pressure, and heart rate every 15 min. The change from upright to supine position at the beginning of the night period was associated with a 30-40% increase in blood flow rate and a highly significant decrease in mean arterial blood pressure and heart rate (P less than 0.001 for all). Approximately 100 min after the subjects went to sleep an additional blood flow rate increment (mean 56%) and a simultaneous significant decrease in mean arterial blood pressure (P less than 0.001) were observed. The duration of this hyperemic phase was 116 min. A highly significant reduction of the subcutaneous vascular resistance (50%) was demonstrated during the hyperemic blood flow rate phase compared with the surrounding phases (P less than 0.0001). The synchronism of the nocturnal subcutaneous hyperemia and the decrease in systemic mean arterial blood pressure point to a common, possibly central nervous or humoral, eliciting mechanism.

Cerebral blood flow and behavior during brain stimulation in the goat

1977 ◽  
Vol 232 (5) ◽  
pp. H495-H499
Author(s):  
M. Manrique ◽  
E. Alborch ◽  
J. M. Delgado
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Blood Pressure ◽  
Maxillary Artery ◽  
Internal Maxillary Artery ◽  
Arterial Blood ◽  
And Behavior ◽  
Stimulation Of

Cerebral blood flow, heart rate, arterial blood pressure, and behavior were studied in conscious goats during electrical stimulation of the diencephalon and mesencephalon. Stimulation of the subthalamic area produced a considerable increase in ipsilateral cerebral blood flow and heart rate, accompanied by either a small or a large increase in systemic arterial blood pressure. Cardiovascular effects were associated with changes in alertness. The increase in cerebral blood flow was partially abolished by previous administration of atropine directly into the internal maxillary artery. Stimulation of the mesencephalic reticular formation caused a marked increase in blood pressure with no change or with some decrease in cerebral blood flow. After administration of phentolamine into the internal maxillary artery, stimulation produced increase in cerebral blood flow. The behavioral response consisted of restlessness and attempted flight. These results suggest the existence of cholinergic vasodilator and adrenergic vasoconstrictor pathways to cerebral blood vessels that may be stimulated electrically.

Effect of intravenous infusion of adrenaline on the cardiovascular responses to distal body subatmospheric pressure in man

1988 ◽  
Vol 75 (4) ◽  
pp. 389-394 ◽  
Author(s):  
I. W. Fellows ◽  
I. A. MacDonald ◽  
T. Bennett ◽  
D. P. O'Donoghue
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Forearm Blood Flow ◽  
Cardiovascular Responses ◽  
Saline Infusion ◽  
Subatmospheric Pressure ◽  
Arterial Blood ◽  
Adrenaline Infusion

1. On two separate occasions, at least 1 week apart, seven young healthy male subjects received intravenous infusions of either adrenaline [0.27 nmol (50 ng) min−1 kg−1] or saline (154 mmol/l NaCl), plus ascorbic acid (5.68 mmol/l), over 30 min. 2. On each occasion, the subjects were exposed to distal body subatmospheric pressure (DBSP), 0 to 50 mmHg (0 to 6.65 kPa) in 10 mmHg (1.33 kPa) steps, before infusion, during the final 15 min of the infusion, and at 15 min and 30 min after the cessation of the infusion. 3. Venous adrenaline concentrations of 2.85 ±0.22 nmol/l were achieved during the adrenaline infusion, compared with 0.49 ± 0.07 nmol/l during the saline infusion (P < 0.001). At 15 min and at 30 min after cessation of the adrenaline infusion, venous adrenaline concentrations had fallen to levels similar to those achieved after the cessation of the saline infusion. 4. Heart rate rose significantly from 58 ±4 beats/min to 67 ±4 beats/min during the adrenaline infusion (P < 0.05), but there was no further significant change in response to 50 mmHg (6.65 kPa) DBSP. At 30 min after the cessation of the adrenaline infusion, heart rate rose from 60 ± 4 beats/min to 78 ± 7 beats/min in response to 50 mmHg DBSP. This increase was significantly greater than that observed before the adrenaline infusion [58 ± 4 beats/min to 69 ±7 beats/min during 50 mmHg (6.65 kPa) DBSP; P < 0.01]. 5. During the infusion of adrenaline, systolic arterial blood pressure rose and diastolic arterial blood pressure fell, but the blood pressure responses to DBSP were unaffected. 6. Forearm blood flow increased significantly during adrenaline infusion but there was no significant difference in the fall in forearm blood flow during DBSP compared with the values before infusion. At 15 min after the cessation of the adrenaline infusion, forearm vascular resistance rose proportionately more in response to DBSP than it had before the adrenaline infusion (P < 0.05). 7. These results are consistent with adrenaline-mediated facilitation of sympathetic neuronal release of noradrenaline in the heart and in the forearm vascular bed.

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