scholarly journals Impaired carotid baroreflex control of arterial blood pressure in multiple sclerosis

2016 ◽  
Vol 116 (1) ◽  
pp. 81-87 ◽  
Author(s):  
Mu Huang ◽  
Dustin R. Allen ◽  
David M. Keller ◽  
Paul J. Fadel ◽  
Elliot M. Frohman ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular Responses ◽  
Vascular Conductance ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
Carotid Baroreflex ◽  
Relapsing Remitting ◽  
Neck Pressure

Multiple sclerosis (MS), a progressive neurological disease, can lead to impairments in the autonomic control of cardiovascular function. We tested the hypothesis that individuals with relapsing-remitting MS ( n = 10; 7 females, 3 males; 13 ± 4 yr from diagnosis) exhibit impaired carotid baroreflex control of blood pressure and heart rate compared with sex, age, and body weight-matched healthy individuals (CON: n = 10; 7 females, 3 males). At rest, 5-s trials of neck pressure (NP; +40 Torr) and neck suction (NS; −60 Torr) were applied to simulate carotid hypotension and hypertension, respectively, while mean arterial pressure (MAP; finger photoplethysmography), heart rate (HR), cardiac output (CO; Modelflow), and total vascular conductance (TVC) were continuously measured. In response to NP, there was a blunted increase in peak MAP responses (MS: 5 ± 2 mmHg) in individuals with MS compared with healthy controls (CON: 9 ± 3 mmHg; P = 0.005), whereas peak HR responses were not different between groups. At the peak MAP response to NP, individuals with MS demonstrated an attenuated decrease in TVC (MS, −10 ± 4% baseline vs. CON, −15 ± 4% baseline, P = 0.012), whereas changes in CO were similar between groups. Following NS, all cardiovascular responses (i.e., nadir MAP and HR and percent changes in CO and TVC) were not different between MS and CON groups. These data suggest that individuals with MS have impaired carotid baroreflex control of blood pressure via a blunted vascular conductance response resulting in a diminished ability to increase MAP in response to a hypotensive challenge.

scholarly journals Sex differences in carotid baroreflex control of arterial blood pressure in humans: relative contribution of cardiac output and total vascular conductance

2011 ◽  
Vol 301 (6) ◽  
pp. H2454-H2465 ◽  
Author(s):  
Areum Kim ◽  
Shekhar H. Deo ◽  
Lauro C. Vianna ◽  
George M. Balanos ◽  
Doreen Hartwich ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sex Differences ◽  
Cardiac Output ◽  
Young Women ◽  
Vascular Conductance ◽  
Baroreflex Control ◽  
Relative Contribution ◽  
Arterial Blood ◽  
Carotid Baroreflex ◽  
Neck Pressure

It is presently unknown whether there are sex differences in the magnitude of blood pressure (BP) responses to baroreceptor perturbation or if the relative contribution of cardiac output (CO) and total vascular conductance (TVC) to baroreflex-mediated changes in BP differs in young women and men. Since sympathetic vasoconstrictor tone is attenuated in women, we hypothesized that carotid baroreflex-mediated BP responses would be attenuated in women by virtue of a blunted vascular response (i.e., an attenuated TVC response). BP, heart rate (HR), and stroke volume were continuously recorded during the application of 5-s pulses of neck pressure (NP; carotid hypotension) and neck suction (NS; carotid hypertension) ranging from +40 to −80 Torr in women ( n = 20, 21 ± 0.5 yr) and men ( n = 20, 21 ± 0.4 yr). CO and TVC were calculated on a beat-to-beat basis. Women demonstrated greater depressor responses to NS (e.g., −60 Torr, −17 ± 1%baseline in women vs. −11 ± 1%baseline in men, P < 0.05), which were driven by augmented decreases in HR that, in turn, contributed to larger reductions in CO (−60 Torr, −15 ± 2%baseline in women vs. −6 ± 2%baseline in men, P < 0.05). In contrast, pressor responses to NP were similar in women and men (e.g., +40 Torr, +14 ± 2%baseline in women vs. +10 ± 1%baseline in men, P > 0.05), with TVC being the primary mediating factor in both groups. Our findings indicate that sex differences in the baroreflex control of BP are evident during carotid hypertension but not carotid hypotension. Furthermore, in contrast to our hypothesis, young women exhibited greater BP responses to carotid hypertension by virtue of a greater cardiac responsiveness.

scholarly journals Carotid baroreflex control of arterial blood pressure at rest and during dynamic exercise in aging humans

2010 ◽  
Vol 299 (5) ◽  
pp. R1241-R1247 ◽  
Author(s):  
James P. Fisher ◽  
Areum Kim ◽  
Colin N. Young ◽  
Paul J. Fadel
Keyword(s):  
Blood Pressure ◽  
Response Curve ◽  
Dynamic Exercise ◽  
Baroreflex Control ◽  
Stimulus Response ◽  
Arterial Blood ◽  
Carotid Baroreflex ◽  
Older Subjects ◽  
Maximal Gain ◽  
Neck Pressure

The arterial baroreflex is fundamental for evoking and maintaining appropriate cardiovascular adjustments to exercise. We sought to investigate how aging influences carotid baroreflex regulation of blood pressure (BP) during dynamic exercise. BP and heart rate (HR) were continuously recorded at rest and during leg cycling performed at 50% HR reserve in 15 young (22 ± 1 yr) and 11 older (61 ± 2 yr) healthy subjects. Five-second pulses of neck pressure and neck suction from +40 to −80 Torr were applied to determine the full carotid baroreflex stimulus response curve and examine baroreflex resetting during exercise. Although the maximal gain of the modeled stimulus response curve was similar in both groups at rest and during exercise, in older subjects the operating point (OP) was located further away from the centering point (CP) and toward the reflex threshold, both at rest (OP minus CP; −10 ± 3 older vs. 0 ± 2 young mmHg, P < 0.05) and during exercise (OP minus CP; −10 ± 2 older vs. 1 ± 3 young mmHg, P < 0.05). In agreement, older subjects demonstrated a reduced BP response to neck pressure (simulated carotid hypotension) and a greater BP response to neck suction (simulated carotid hypertension). In addition, the magnitude of the upward and rightward resetting of the carotid baroreflex-BP stimulus response curve with exercise was ∼40% greater in older individuals. These data indicate that despite a maintained maximal gain, the ability of the carotid baroreflex to defend against a hypotensive challenge is reduced, whereas responses to hypertensive stimuli are greater with advanced age, both at rest and during exercise.

Carotid baroreflex control of leg vascular conductance at rest and during exercise

2003 ◽  
Vol 94 (2) ◽  
pp. 542-548 ◽  
Author(s):  
David M. Keller ◽  
Wendy L. Wasmund ◽  
D. Walter Wray ◽  
Shigehiko Ogoh ◽  
Paul J. Fadel ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Vascular Tone ◽  
Knee Extension ◽  
Vascular Conductance ◽  
Baroreflex Control ◽  
Carotid Baroreflex ◽  
Neck Pressure ◽  
Induced Changes ◽  
Knee Extension Exercise ◽  
Rest And Exercise

We sought to test the hypothesis that the carotid baroreflex (CBR) alters mean leg blood flow (LBF) and leg vascular conductance (LVC) at rest and during exercise. In seven men and one woman, 25 ± 2 (SE) yr of age, CBR control of LBF and LVC was determined at rest and during steady-state one-legged knee extension exercise at ∼65% peak O2 uptake. The application of 5-s pulses of +40 Torr neck pressure and −60 Torr neck suction significantly altered mean arterial pressure (MAP) and LVC both at rest and during exercise. CBR-mediated changes in MAP were similar between rest and exercise ( P > 0.05). However, CBR-mediated decreases in LVC (%change) to neck pressure were attenuated in the exercising leg (16.4 ± 1.6%) compared with rest (33 ± 2.1%) and the nonexercising leg (23.7 ± 1.9%) ( P < 0.01). These data suggest CBR control of blood pressure is partially mediated by changes in leg vascular tone both at rest and during exercise. Furthermore, despite alterations in CBR-induced changes in LVC during exercise, CBR control of blood pressure was well maintained.

Ascending pathways mediating somatoautonomic reflexes in exercising dogs

1987 ◽  
Vol 62 (3) ◽  
pp. 1186-1191 ◽  
Author(s):  
J. W. Kozelka ◽  
G. W. Christy ◽  
R. D. Wurster
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Surgical Techniques ◽  
Arterial Occlusion ◽  
Cardiovascular Responses ◽  
Spinal Pathways ◽  
Arterial Blood ◽  
Bilateral Carotid ◽  
Dorsolateral Funiculus ◽  
Carotid Arterial

The ascending spinal pathways mediating somatocardiovascular reflexes during exercise were studied in unanesthetized dogs by placing lesions in the lumbar spinal cord. After training to run on a treadmill with hindlimbs only, 20 dogs were anesthetized and instrumented using sterile surgical techniques. To chronically record heart rate and arterial blood pressure, the aorta was cannulated via the omocervical artery. To test the intactness of descending spinal sympathetic pathways, reflex pressor responses to baroreceptor hypotension were produced by bilateral carotid arterial occlusion using pneumatic vessel occluders placed around the common carotid arteries. To generate transient ischemic exercise (120 s), a pneumatic occluder was placed around the left iliac artery. Eight to 10 days after instrumentation, blood pressure and heart rate were monitored at rest and during hindlimb running with and without simultaneous iliac arterial occlusion. The modest pressor response and tachycardia elicited by hindlimb exercise were markedly augmented by simultaneous hindlimb ischemia (i.e., iliac arterial occlusion). Lesion placement in the dorsolateral sulcus area and the dorsolateral funiculus at L2 significantly reduced the blood pressure and heart rate responses to simultaneous exercise occlusion. The cardiovascular responses to nonischemic exercise and bilateral carotid arterial occlusion were not altered by such spinal sections. It is concluded that in the dog the ascending spinal pathways mediating cardiovascular responses to ischemic exercise are located in the lateral funiculus, including the dorsolateral sulcus area and dorsolateral funiculus.

scholarly journals Cardiac and vasomotor components of the carotid baroreflex control of arterial blood pressure during isometric exercise in humans

2006 ◽  
Vol 572 (3) ◽  
pp. 869-880 ◽  
Author(s):  
James P. Fisher ◽  
Shigehiko Ogoh ◽  
Ellen A. Dawson ◽  
Paul J. Fadel ◽  
Niels H. Secher ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Isometric Exercise ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
Carotid Baroreflex ◽  
Exercise In Humans

Supine exercise restores arterial blood pressure and skin blood flow despite dehydration and hyperthermia

1999 ◽  
Vol 277 (2) ◽  
pp. H576-H583 ◽  
Author(s):  
José González-Alonso ◽  
Ricardo Mora-Rodríguez ◽  
Edward F. Coyle
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Blood Volume ◽  
Plasma Catecholamines ◽  
Central Blood Volume ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Cutaneous Vascular Conductance

We determined whether the deleterious effects of dehydration and hyperthermia on cardiovascular function during upright exercise were attenuated by elevating central blood volume with supine exercise. Seven trained men [maximal oxygen consumption (V˙o 2 max) 4.7 ± 0.4 l/min (mean ± SE)] cycled for 30 min in the heat (35°C) in the upright and in the supine positions (V˙o 2 2.93 ± 0.27 l/min) while maintaining euhydration by fluid ingestion or while being dehydrated by 5% of body weight after 2 h of upright exercise. When subjects were euhydrated, esophageal temperature (Tes) was 37.8–38.0°C in both body postures. Dehydration caused equal hyperthermia during both upright and supine exercise (Tes = 38.7–38.8°C). During upright exercise, dehydration lowered stroke volume (SV), cardiac output, mean arterial pressure (MAP), and cutaneous vascular conductance and increased heart rate and plasma catecholamines [30 ± 6 ml, 3.0 ± 0.7 l/min, 6 ± 2 mmHg, 22 ± 8%, 14 ± 2 beats/min, and 50–96%, respectively; all P < 0.05]. In contrast, during supine exercise, dehydration did not cause significant alterations in MAP, cutaneous vascular conductance, or plasma catecholamines. Furthermore, supine versus upright exercise attenuated the increases in heart rate (7 ± 2 vs. 9 ± 1%) and the reductions in SV (13 ± 4 vs. 21 ± 3%) and cardiac output (8 ± 3 vs. 14 ± 3%) (all P< 0.05). These results suggest that the decline in cutaneous vascular conductance and the increase in plasma norepinephrine concentration, independent of hyperthermia, are associated with a reduction in central blood volume and a lower arterial blood pressure.

Interactions between brain acetylcholine and prostaglandins in control of vasopressin release

1991 ◽  
Vol 261 (2) ◽  
pp. R420-R426
Author(s):  
M. Inoue ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Stimulation Of

We have examined in conscious rats the interaction between centrally acting prostanoids and acetylcholine in the stimulation of vasopressin secretion. The intracerebroventricular (icv) administration of carbachol (25 ng) resulted in marked transient increases in the plasma vasopressin concentration and mean arterial blood pressure and a transient reduction in heart rate. Central cyclooxygenase blockade by pretreatment icv with either meclofenamate (100 micrograms) or indomethacin (100 micrograms) virtually completely blocked these responses. Prostaglandin (PG) D2 (20 micrograms icv) caused transient increases in the plasma vasopressin concentration (much smaller than after carbachol) and heart rate, whereas mean arterial blood pressure rose gradually during the 15-min course of the experiment. Pretreatment with the muscarinic antagonist atropine (10 micrograms icv) decreased the peak vasopressin response to icv PGD2 by approximately one-third but had no effect on the cardiovascular responses. We conclude that the stimulation of vasopressin release by centrally acting acetylcholine is dependent on increased prostanoid biosynthesis. On the other hand, stimulation of vasopressin release by icv PGD2 is partially dependent on activation of a cholinergic pathway.

Cardiovascular responses to severe hypercapnia of short duration

1964 ◽  
Vol 207 (3) ◽  
pp. 634-640 ◽  
Author(s):  
Emmett S. Manley ◽  
Clinton B. Nash ◽  
R. A. Woodbury
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Short Duration ◽  
Cardiovascular Responses ◽  
Myocardial Contraction ◽  
Contractile Force ◽  
Sympathetic Activation ◽  
Pentobarbital Anesthesia ◽  
Arterial Blood ◽  
Blood Ph

Dogs under pentobarbital anesthesia were employed in an investigation of the effect of abrupt, severe hypercapnia upon blood pressure, heart rate, and force of myocardial contraction. Electrocardiographic activity and arterial blood pH were also monitored. Hypercapnia was induced for 10-min periods with 15 and 30% CO2 in oxygen. The studies were undertaken in nontreated animals and animals treated with atropine, reserpine, chlorisondamine, P-286, or bilateral adrenalectomy. Severe hypercapnia was shown to be depressant to the cardiovascular parameters evaluated, but blood pressure and contractile force normally demonstrated compensation to this depression. Parasympathetic blockade with atropine did not reduce the depression observed in the nontreated dogs during hypercapnia. Results obtained with other pretreated animals indicate that compensation occurs primarily via sympathetic activation. Adrenal activation may assume importance in compensation to 30% CO2, but intact adrenals were not necessary for survival during hypercapnia. No arrhythmias (excluding bradycardia) were observed during or immediately following exposure to either concentration of CO2.

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