Reflex cardiovascular response to exercise is modulated by circulating vasopressin

1992 ◽  
Vol 263 (5) ◽  
pp. R1104-R1109 ◽  
Author(s):  
C. L. Stebbins
Keyword(s):  
Heart Rate ◽  
Receptor Antagonist ◽  
Cardiovascular Response ◽  
Regional Blood Flow ◽  
Plasma Concentrations ◽  
Cardiovascular Responses ◽  
Vascular Effect ◽  
Ganglionic Blockade ◽  
Hindlimb Muscles ◽  
Before And After

Peripheral vasopressin (AVP) can act centrally to sensitize the arterial baroreflex and/or peripherally to attenuate regional blood flow by a direct vascular effect. Because plasma concentrations of AVP increase during exercise, this study examined the possibility that AVP is capable of modulating the reflex cardiovascular response to static muscle contraction. Thus, in anesthetized cats, the pressor [mean arterial pressure (MAP)], myocardial contractile (dP/dt), and heart rate responses to 30-45 s of electrically induced static contraction of the hindlimb muscles were compared before and after intravenous injection of the V1 receptor antagonist d[CH2)5Tyr(Me)]-AVP (V1-x, n = 7), V1-x plus the V2 receptor antagonist [d(CH2)5,D-Phe2,Ile4,Arg8,Ala9]vasopressin (V2-x, n = 5), or the ganglionic blocker hexamethonium chloride (n = 5). In three additional cats, the contraction-induced cardiovascular response was monitored before and after injection of V1-x + V2-x and after hexamethonium. Subsequent to treatment with V1-x, the MAP and dP/dt responses to contraction were augmented by 18 +/- 5 and 22 +/- 10%, respectively (P < 0.05). After injection of V1-x + V2-x, the MAP and dP/dt responses were augmented to a similar extent (32 +/- 6 and 40 +/- 17%, respectively; P < 0.05). However, there was no difference in the magnitude of augmentation of these responses between the two conditions. The heart rate response was not altered by either treatment. Ganglionic blockade eliminated the cardiovascular responses to contraction. Last, when the pressor and contractile responses to contraction were initially augmented by administration of V1-x + V2-x, subsequent ganglionic blockade abolished the entire cardiovascular response.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Effect of Standardized Yelling on Subjective Perception and Autonomic Nervous System Activity in Motion Sickness

2021 ◽  
Vol 18 (23) ◽  
pp. 12854
Author(s):  
Min-Yu Tu ◽  
Hsin Chu ◽  
Chung-Yu Lai ◽  
Kwo-Tsao Chiang ◽  
Chi-Chan Huang ◽  
...  
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Motion Sickness ◽  
Cardiovascular Response ◽  
Low Frequency ◽  
Cardiovascular Responses ◽  
Subjective Perception ◽  
System Activity ◽  
Nervous System Activity ◽  
Before And After

This study investigated the effects of yelling intervention on symptoms and autonomic responses in motion sickness. Forty-two healthy participants were recruited, and they participated in Coriolis stimulation, a technique for inducing motion sickness. The experimental procedure comprised five 1-min rotating stimuli with 1-min rest after each stimulus. Then, the symptom severity was assessed using the Motion Sickness Symptom Rating (MSSR). The d2 Test of Attention scores and cardiovascular responses were recorded before and after Coriolis stimulation. The electrocardiogram results were documented to analyze heart rate variability (HRV). During Coriolis stimulus, the participants were required to yell 5–8 times in the experimental trial, and to keep quiet for each minute of rotation in the control trial. The yelling intervention significantly reduced the MSSR score (p < 0.001). Nevertheless, it did not significantly affect the d2 Test of Attention scores. Yelling while rotating did not significantly affect the heart rate nor blood pressure. However, it decreased the normalized low frequency of HRV (p = 0.036). Moreover, it improved motion sickness, but its effect on attention was not evident. Motion sickness could significantly affect cardiovascular responses and HRV. However, yelling did not affect cardiovascular response, and it reduced sympathetic nervous system activity.

scholarly journals Role of nitric oxide-containing factors in the ventilatory and cardiovascular responses elicited by hypoxic challenge in isoflurane-anesthetized rats

2014 ◽  
Vol 116 (11) ◽  
pp. 1371-1381 ◽  
Author(s):  
James P. Mendoza ◽  
Rachael J. Passafaro ◽  
Santhosh M. Baby ◽  
Alex P. Young ◽  
James N. Bates ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Cardiovascular Responses ◽  
Vital Role ◽  
Initial Increase ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Anesthetized Rats ◽  
Before And After

Exposure to hypoxia elicits changes in mean arterial blood pressure (MAP), heart rate, and frequency of breathing (fr). The objective of this study was to determine the role of nitric oxide (NO) in the cardiovascular and ventilatory responses elicited by brief exposures to hypoxia in isoflurane-anesthetized rats. The rats were instrumented to record MAP, heart rate, and fr and then exposed to 90 s episodes of hypoxia (10% O2, 90% N2) before and after injection of vehicle, the NO synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME), or the inactive enantiomer d-NAME (both at 50 μmol/kg iv). Each episode of hypoxia elicited a decrease in MAP, bidirectional changes in heart rate (initial increase and then a decrease), and an increase in fr. These responses were similar before and after injection of vehicle or d-NAME. In contrast, the hypoxia-induced decreases in MAP were attenuated after administration of l-NAME. The initial increases in heart rate during hypoxia were amplified whereas the subsequent decreases in heart rate were attenuated in l-NAME-treated rats. Finally, the hypoxia-induced increases in fr were virtually identical before and after administration of l-NAME. These findings suggest that NO factors play a vital role in the expression of the cardiovascular but not the ventilatory responses elicited by brief episodes of hypoxia in isoflurane-anesthetized rats. Based on existing evidence that NO factors play a vital role in carotid body and central responses to hypoxia in conscious rats, our findings raise the novel possibility that isoflurane blunts this NO-dependent signaling.

Regional blood flow in conscious resting rats determined by microsphere distribution

1993 ◽  
Vol 74 (1) ◽  
pp. 203-210 ◽  
Author(s):  
I. Kuwahira ◽  
N. C. Gonzalez ◽  
N. Heisler ◽  
J. Piiper
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Regional Blood Flow ◽  
Sampling Technique ◽  
Organ Blood Flow ◽  
Sprague Dawley ◽  
Blood Flows ◽  
Hindlimb Muscles ◽  
Acclimation Period ◽  
The Difference

To determine organ blood flow in the resting state, a box was designed to keep conscious untrained rats minimally disturbed. Blood pressure, heart rate, and organ blood flow, determined by the microsphere distribution and reference sampling technique, were measured in 11 Sprague-Dawley rats. After an acclimation period, 15-microns-diameter microspheres labeled with 113Sn were infused into the ascending aorta, a reference blood sample was withdrawn from the caudal artery, and organ blood flows were computed according to standard procedures. The average values of heart rate (365 beats/min) and blood flow to the brain (45 ml.min-1.100 g-1) and hindlimb muscles (15 ml.min-1.100 g-1) were significantly lower than most values reported earlier, whereas splanchnic blood flow was significantly higher (106 ml.min-1.100 g-1). Blood flow to the soleus muscle, which is considered the most active for postural maintenance, was relatively high (99 ml.min-1.100 g-1). The combination of low skeletal muscle and high visceral blood flows observed in these experiments suggests a low sympathetic tone, which is consistent with the low level of circulating catecholamines also observed in this study. It is hypothesized that the difference between our present and previous results is a lower level of stress, attributable to a more complete acclimation to the experimental environment.

Effect of sleep restriction on orthostatic cardiovascular control in humans

2000 ◽  
Vol 88 (3) ◽  
pp. 966-972 ◽  
Author(s):  
N. K. Muenter ◽  
D. E. Watenpaugh ◽  
W. L. Wasmund ◽  
S. L. Wasmund ◽  
S. A. Maxwell ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Lower Body Negative Pressure ◽  
Systolic Pressure ◽  
Cardiovascular Responses ◽  
Sleep Restriction ◽  
Orthostatic Tolerance ◽  
Arterial Baroreflex ◽  
Finger Arterial Pressure ◽  
Before And After

We hypothesized that sleep restriction (4 consecutive nights, 4 h sleep/night) attenuates orthostatic tolerance. The effect of sleep restriction on cardiovascular responses to simulated orthostasis, arterial baroreflex gain, and heart rate variability was evaluated in 10 healthy volunteers. Arterial baroreflex gain was determined from heart rate responses to nitroprusside-phenylephrine injections, and orthostatic tolerance was tested via lower body negative pressure (LBNP). A Finapres device measured finger arterial pressure. No difference in baroreflex function, heart rate variability, or LBNP tolerance was observed with sleep restriction ( P > 0.3). Systolic pressure was greater at −60 mmHg LBNP after sleep restriction than before sleep restriction (110 ± 6 and 124 ± 3 mmHg before and after sleep restriction, respectively, P = 0.038), whereas heart rate decreased (108 ± 8 and 99 ± 8 beats/min before and after sleep restriction, respectively, P = 0.028). These data demonstrate that sleep restriction produces subtle changes in cardiovascular responses to simulated orthostasis, but these changes do not compromise orthostatic tolerance.

Cardiovascular Responses to Submaximal Concentric and Eccentric Isokinetic Exercise in Older Adults

1999 ◽  
Vol 7 (1) ◽  
pp. 20-31 ◽  
Author(s):  
Elizabeth Thompson ◽  
Theo H. Versteegh ◽  
Tom J. Overend ◽  
Trevor B. Birmingham ◽  
Anthony A. Vandervoort
Keyword(s):  
Older Adults ◽  
Heart Rate ◽  
Perceived Exertion ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Knee Extension ◽  
Resistance Testing ◽  
Exercise Heart Rate ◽  
Arterial Blood ◽  
S Peak

Our purpose was to describe heart rate (HR), mean arterial blood pressure (MAP), and perceived exertion (RPE) responses to submaximal isokinetic concentric (CON) and eccentric (ECC) exercise at the same absolute torque output in older adults. Peak torques for ECC and CON knee extension were determined in healthy older males (n = 13) and females (n = 7). Subjects then performed separate, randomly ordered, 2-min bouts of CON and ECC exercise. Heart rate and MAP increased (p < .001) from resting values throughout both exercise bouts. CON exercise elicited a significantly greater cardiovascular response than ECC exercise after 60 s. Peak HR, MAP, and RPE after CON exercise were greater than after ECC exercise (p < .01). At the same absolute torque output, isokinetic CON knee extension exercise resulted in a significantly greater level of cardiovascular stress than ECC exercise. These results are relevant to resistance testing and exercise in older people.

Role of vasopressin in the cardiovascular response to hypoxia in the conscious rat

1986 ◽  
Vol 251 (6) ◽  
pp. H1316-H1323 ◽  
Author(s):  
B. R. Walker
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Hypoxic Exposure ◽  
Conscious Rat ◽  
Time Control ◽  
Hemodynamic Variables

Previous experiments have demonstrated that hypoxia stimulates the release of arginine vasopressin in conscious animals including the rat. The present study was designed to test whether AVP may exert a vasoconstrictor influence during hypoxia at varying levels of CO2. Systemic hemodynamics were assessed in conscious rats for 30 min under hypocapnic hypoxic, isocapnic hypoxic, hypercapnic hypoxic, and room air conditions. Progressive effects on heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR) were observed with varying CO2 under hypoxic conditions. Hypocapnic hypoxia [arterial PO2 (PaO2) = 32 Torr; arterial PCO2 (PaCO2) = 22 Torr] caused HR and CO to rise and TPR to fall. Isocapnic hypoxia (PaO2 = 36 Torr; PaCO2 = 35 Torr) was associated with no significant changes in HR and CO or TPR, whereas hypercapnic hypoxia (PaO2 = 35 Torr; PaCO2 = 51 Torr) caused HR and CO to fall and TPR to rise. Room air time control experiments were associated with no change in measured hemodynamic variables. To determine the possible role of circulating AVP on these cardiovascular responses, additional experiments were performed where the specific V1-vasopressinergic antagonist d(CH2)5Tyr(Me)AVP (10 micrograms/kg iv) was administered at the midpoint of hypoxic exposure. Antagonist administration had no effect on hypocapnic hypoxic animals or animals breathing room air; however, blood pressure and TPR were significantly reduced by d(CH2)5Tyr(Me)AVP in both isocapnic and hypercapnic hypoxic animals. The heart rate response to hypoxia at the various CO2 levels was unaffected; however, cardiac output and stroke volume were increased after V1-antagonism in the isocapnic and hypercapnic hypoxic animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of ventrolateral medullary AMPA-receptor antagonism on pressor response during muscle contraction

1997 ◽  
Vol 272 (6) ◽  
pp. H2774-H2781 ◽  
Author(s):  
T. Kobayashi ◽  
D. Caringi ◽  
D. J. Mokler ◽  
A. Ally
Keyword(s):  
Heart Rate ◽  
Muscle Contraction ◽  
Ampa Receptors ◽  
Tibial Nerve ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Ventrolateral Medulla ◽  
Contrast Administration ◽  
Tibial Nerve Stimulation ◽  
Before And After

Effects of administering 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) at a concentration that preferentially blocks alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors into rostral ventrolateral medulla (rVLM) or caudal ventrolateral medulla (cVLM) on cardiovascular responses elicited during static muscle contraction were investigated using anesthetized rats. Two microdialysis probes were inserted bilaterally into either the rVLM or the cVLM using stereotaxic guides. A tibial nerve stimulation-evoked static muscle contraction for 30 s increased mean arterial pressure (MAP) and heart rate (HR) by 27 +/- 3 mmHg and 28 +/- 4 beats/min, respectively. Microdialysis of CNQX into the rVLM for 30 min attenuated the contraction-evoked increases in MAP and HR (10 +/- 2 mmHg and 12 +/- 2 beats/min). Developed tensions were similar during the contractions before and after microdialyzing CNQX. In contrast, administration of CNQX into the cVLM potentiated the muscle contraction-evoked cardiovascular responses (MAP, 25 +/- 4 vs. 39 +/- 6 mmHg; HR, 27 +/- 3 vs. 42 +/- 3 beats/min), with no change in developed tensions. Results demonstrate that AMPA receptors within the rVLM and the cVLM appear to play opposite modulatory roles in the central integration of cardiovascular responses elicited during static muscle contraction.

scholarly journals Cardiovascular Responses to the Induction of Mild Hypothermia in the Presence of Epidural Anesthesia

2001 ◽  
Vol 94 (4) ◽  
pp. 678-682 ◽  
Author(s):  
Masahiro Yoshida ◽  
Keizo Shibata ◽  
Hironori Itoh ◽  
Ken Yamamoto
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Ejection Fraction ◽  
General Anesthesia ◽  
Epidural Anesthesia ◽  
Mild Hypothermia ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Plasma Catecholamine ◽  
Plasma Catecholamine Concentrations

Background The combining of epidural anesthesia with general anesthesia impairs central and peripheral thermoregulatory control and therefore is often accompanied by unintended intraoperative hypothermia. However, little is known about the cardiovascular response to hypothermia during combined epidural and general anesthesia. The authors assessed the effects of hypothermia during such combined anesthesia. Methods The authors randomly assigned 30 mongrel dogs anesthetized with isoflurane (1.0%) to three groups of 10: control, receiving general anesthesia alone; thoracic injection, additionally receiving thoracic epidural anesthesia; and lumbar injection, additionally receiving thoracolumbar epidural anesthesia. Core temperature was lowered from 38.5 degrees C to approximately 34 degrees C (mild hypothermia) using a femoral arteriovenous shunt in an external cool water bath. During hypothermia, the authors measured heart rate, cardiac output, and plasma catecholamine concentrations in each group. Ejection fraction was also measured using echocardiography. Results Compared with measurements during baseline conditions (general anesthesia alone with no epidural injection and no hypothermia) in the control, thoracic, and lumbar injection groups, the injections followed by hypothermia produced 17, 32, and 41% decreases in heart rate; 22, 32, and 47% reductions in cardiac output; 66, 85, and 92% decreases in the epinephrine concentrations; and 27, 44, and 85% decreases in the norepinephrine concentrations. In contrast, ejection fraction did not change in any group. Conclusion Mild hypothermia during combined epidural anesthesia and general anesthesia markedly reduced cardiac output in dogs, mainly by decreasing heart rate.

The Effects of Cardioselective and Non-Selective β-Adrenoceptor Blockade on the Hypokalaemic and Cardiovascular Responses to Adrenomedullary Hormones in Man

1983 ◽  
Vol 65 (2) ◽  
pp. 143-147 ◽  
Author(s):  
A. D. Struthers ◽  
J. L. Reid ◽  
R. Whitesmith ◽  
J. C. Rodger
Keyword(s):  
Heart Rate ◽  
Serum Potassium ◽  
Qt Interval ◽  
Diastolic Pressure ◽  
Plasma Concentrations ◽  
Systolic Pressure ◽  
Cardiovascular Responses ◽  
Potassium Influx ◽  
Adrenomedullary Hormones ◽  
Stimulation Of

1. Adrenaline was infused intravenously in nine normal volunteers to plasma concentrations similar to those found after myocardial infarction. This study was undertaken on three occasions after 5 days' treatment with placebo or the β-adrenoceptor antagonists, atenolol or timolol. 2. Adrenaline increased the systolic pressure by 11 mmHg, decreased the diastolic pressure by 14 mmHg, and increased the heart rate by 7 beats/min. These changes were prevented by atenolol. However, after timolol the diastolic pressure rose (+19 mmHg) and heart rate fell (− 8 beats/min). 3. Adrenaline caused the corrected QT interval (QTc) to lengthen (0.36 ± 0.02 s to 0.41 ± 0.06 s). No significant changes were found in the QTc when subjects were pretreated with atenolol or timolol. 4. The serum potassium fell from 4.06 to 3.22 mmol/l after adrenaline. Serum potassium fell to a lesser extent to 3.67 mmol/l after atenolol and actually increased to 4.25 mmol/l after timolol. Adrenaline-mediated hypokalaemia appears to result from the stimulation of a β2-adrenoceptor linked to membrane Na+/K+-ATPase causing potassium influx.

scholarly journals Perturbations of Adjuvant Chemotherapy on Cardiovascular Responses and Exercise Tolerance in Patients with Early-Stage Breast Cancer

Biology ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 910
Author(s):  
Hsin-Fu Lin ◽  
Ching-Ying Tseng ◽  
Toby Mündel ◽  
Yi-Yuan Lin ◽  
Chung-Chi Lin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Heart Rate ◽  
Exercise Tolerance ◽  
Early Stage ◽  
Heart Rate Recovery ◽  
Cardiovascular Responses ◽  
Early Stage Breast Cancer ◽  
Exercise Heart Rate ◽  
Post Exercise ◽  
Before And After

Background: Adjuvant chemotherapies are commonly used for treating early-stage breast cancer. However, whether chemotherapeutic regimens affect exercise tolerance and cardiovascular responses remains unclear. Therefore, we investigated the effects of receiving CAF and AC-T on exercise tolerance and cardiovascular responses in patients with early-stage breast cancer. Methods: Thirty-four patients with breast cancer (age: 44 ± 1 years; stage I-II) received either CAF (n = 15) or AC-T (n = 19), depending on clinical decisions. Their step-exercise tolerance and cardiovascular responses were assessed before and after chemotherapy. Results: After chemotherapy, there were no differences in baseline measurements between patients receiving CAF or AC-T. The increases in resting heart rate (RHR) of those receiving AC-T was significantly greater than that of those receiving CAF. CAF and AC-T did not result in increased pulse wave velocity (PWV), yet the subendocardial viability ratio (SEVR) in patients receiving AC-T was significantly lower than the baseline. Greater change in post-exercise heart rate recovery (recovery HR) after chemotherapy was observed in those who had received AC-T; the Recovery HR in AC-T patients was significantly higher during post-exercise period than that in CAF patients. Conclusions: AC-T chemotherapy increases RHR and impairs exercise tolerance after chemotherapy more than CAF. Moreover, AC-T also lowers myocardial perfusion more than CAF after chemotherapy.

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