Reflex Control of Blood Pressure and Heart Rate by Arterial Baroreceptors and by Cardiopulmonary Receptors in the Unanaesthetized Cat

1985 ◽  
Vol 3 (4) ◽  
pp. 327-335 ◽  
Author(s):  
Agustin J. Ramirez ◽  
Giovanni Bertinieri ◽  
Luca Belli ◽  
Anita Cavallazzi ◽  
Marco Di Rienzo ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Baroreceptors ◽  
Reflex Control ◽  
Cardiopulmonary Receptors

Reflex control of vasopressin during hemorrhage in hypertensive rabbits

1995 ◽  
Vol 269 (5) ◽  
pp. H1570-H1577
Author(s):  
C. A. Courneya ◽  
G. Weichert
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Arterial Pressure ◽  
Vascular Tone ◽  
Cardiac Denervation ◽  
Baroreceptor Function ◽  
Arterial Baroreceptors ◽  
Reflex Control

Hypertensive (HT) rabbits have impaired reflex control of heart rate and vascular tone, which is, at least in part, related to dysfunctional baroreceptors. We hypothesized that reflex control of vasopressin (AVP) would also be impaired in the HT rabbit. To test this, we compared hemorrhage-induced increases in AVP between conscious normotensive (NT) and HT rabbits. The hemorrhage-induced rise in AVP was found to be significantly (P < 0.05) attenuated in the HT rabbits. We tested a second hypothesis, that the observed impairment was related to arterial baroreceptor function, by hemorrhaging the same rabbits after reversible cardiac denervation. Under these conditions, only the arterial baroreceptors would be expected to contribute to reflex control of AVP. Impairment was still evident after cardiac denervation; that is, the hemorrhage-induced rise in AVP was significantly (P < 0.01) attenuated in the cardiac-denervated HT rabbits compared with NT rabbits. Thus impairment was, at least in part, related to arterial baroreceptors. Previously, we showed in NT rabbits that AVP only contributed to maintenance of arterial pressure (during hemorrhage), after the autonomic nervous system (ANS) had been blocked. Thus, in the present study, we compared the maintenance of arterial pressure during hemorrhage between NT and HT rabbits after ANS blockade. Blood pressure maintenance was significantly attenuated in the HT rabbits (P < 0.05). In addition, for a given fall in pressure, significantly less AVP (P < 0.05) was released in the ANS-blocked HT rabbits as compared with NT rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)

Characterization of baroreflex impairment in conscious dogs with pacing-induced heart failure

1993 ◽  
Vol 265 (5) ◽  
pp. R1132-R1140 ◽  
Author(s):  
N. B. Olivier ◽  
R. B. Stephenson
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Peripheral Resistance ◽  
Open Loop ◽  
Ventricular Pacing ◽  
Baroreflex Control ◽  
Rapid Ventricular Pacing ◽  
Reflex Control

Open-loop baroreflex responses were evaluated in eight conscious dogs before and during congestive heart failure to determine the effects of failure on baroreflex control of blood pressure, heart rate, cardiac output, and total peripheral resistance. Heart failure was induced by rapid ventricular pacing. Baroreflex function was determined by calculation of the range and gain of the open-loop stimulus-response relationships for the effect of carotid sinus pressure on blood pressure, heart rate, cardiac output, and total peripheral resistance. The range and gain of blood pressure responses were substantially reduced as early as 3 days after induction of heart failure (161 +/- 6 to 99 +/- 8 mmHg and -2.7 +/- 0.3 to -1.5 +/- 0.1, respectively) and remained depressed for the 21 days of heart failure. This depression in baroreflex control of blood pressure was associated with similar depressions in reflex range and gain for heart rate (125 +/- 9 to 78 +/- 11 beats/min and -2.05 +/- 0.2 to -1.16 +/- 0.2 beats/min, respectively) and cardiac output (1.74 +/- 0.2 to 0.46 +/- 0.2 l/min and -0.81 +/- 0.02 to -0.027 +/- 0.008 l/min, respectively). The group-averaged range and gain for reflex control of vascular resistance were not altered by heart failure. In three dogs, discontinuation of rapid ventricular pacing led to resolution of heart failure within 7 days and partial restoration of the range and gain of reflex control of blood pressure. We conclude that heart failure reversibly depresses baroreflex control of blood pressure principally through a concurrent reduction in reflex control of cardiac output, whereas reflex control of vascular resistance is not consistently affected.

Blood pressure and heart rate responses to sudden changes of gravity during exercise

1996 ◽  
Vol 270 (6) ◽  
pp. H2132-H2142 ◽  
Author(s):  
D. Linnarsson ◽  
C. J. Sundberg ◽  
B. Tedner ◽  
Y. Haruna ◽  
J. M. Karemaker ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Parabolic Flight ◽  
Filter Function ◽  
Pass Filter ◽  
Low Pass Filter ◽  
Time Constants ◽  
Arterial Blood ◽  
Lower Amplitude ◽  
Cardiopulmonary Receptors

Heart rate (HR) and blood pressure responses to sudden changes of gravity during 80- to 100-W leg exercise were studied. One group was exposed to sudden changes between 1.0 and 0 g in the head-to-foot direction (Gz+), starting upright and with repeated 30-s tilts to the supine position. Another group was exposed to sudden Gz+ changes between 1.8 and 0 g in an aircraft performing parabolic flight. Arterial blood pressure at the level of the carotid (carotid distending pressure, CDP) showed a large transient increase by 27-47 mmHg when Gz+ was suddenly decreased and a similar drop when Gz+ was suddenly increased. HR displayed a reverse pattern with larger transients (-22 to -26 min-1) in response to Gz+ decreases and more sluggish changes of lower amplitude in the other direction. Central blood volume, as estimated from the inverse of transthoracic impedance (1/TTI), varied in concert with Gz+. A model is proposed in which HR responses are described as a function of CDP and 1/TTI after a time delay of 2.3-3.0 s and including a low-pass filter function with time constants of 0.34-0.35 s for decreasing HR and time constants of 2.9-4.6 s for increasing HR. The sensitivity of the carotid component was around -0.8 to -1.0 min-1 . mmHg-1 (4-7 ms/mmHg). The cardiopulmonary baroreceptor component was an additive input but was of modest relative importance during the initial HR responses. For steady-state HR responses, however, our model suggests that inputs from carotid and cardiopulmonary receptors are of equal importance.

Long-term treatment with supraphysiological doses of nandrolone decanoate reduces the sensitivity of Bezold–Jarisch reflex control of heart rate and blood pressure

2009 ◽  
Vol 59 (6) ◽  
pp. 379-384 ◽  
Author(s):  
Nazaré Souza Bissoli ◽  
Ana Raquel Santos Medeiros ◽  
Maria Carmen Silva Santos ◽  
Vera Cristina W. Busato ◽  
Robson Dettman Jarske ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Term Treatment ◽  
Nandrolone Decanoate ◽  
Long Term Treatment ◽  
Reflex Control

scholarly journals Modulation of cardiopulmonary depressor reflex in nucleus ambiguus by electroacupuncture: roles of opioids and γ-aminobutyric acid

2012 ◽  
Vol 302 (7) ◽  
pp. R833-R844 ◽  
Author(s):  
Stephanie C. Tjen-A-Looi ◽  
Peng Li ◽  
Min Li ◽  
John C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Low Frequency ◽  
Vagal Afferents ◽  
Nucleus Ambiguus ◽  
Aminobutyric Acid ◽  
Vagal Activity ◽  
Induced Hypotension ◽  
Cardiopulmonary Receptors ◽  
Depressor Reflex

Stimulation of cardiopulmonary receptors with phenylbiguanide (PBG) elicits depressor cardiovascular reflex responses, including decreases in blood pressure and heart rate mediated in part by the brain stem parasympathetic cardiac neurons in the nucleus ambiguus (NAmb). The present study examined NAmb neurotransmitter mechanisms underlying the influence of electroacupuncture (EA) on the PBG-induced hypotension and bradycardia. We hypothesized that somatic stimulation during EA modulates PBG responses through opioid and γ-aminobutyric acid (GABA) modulation in the NAmb. Anesthetized and ventilated cats were studied during repeated stimulation with PBG or cardiac vagal afferents while low-frequency EA (2 Hz) was applied at P5–6 acupoints overlying the median nerve for 30 min and NAmb neuronal activity, heart rate, and blood pressure were recorded. Microinjection of kainic acid into the NAmb attenuated the PBG-induced bradycardia from −60 ± 11 to −36 ± 11 beats/min. Likewise, EA reduced the PBG-induced depressor and bradycardia reflex by 52 and 61%, respectively. Cardiac vagal afferent evoked preganglionic cellular activity in the NAmb was reduced by EA for about 60 min. Blockade of opioid or GABAA receptors using naloxone and gabazine reversed the EA-related modulation of the evoked cardiac vagal activity by 73 and 53%, respectively. Similarly, naloxone and gabazine reversed EA modulation of the negative chronotropic responses from −11 ± 5 to −23 ± 6 and −13 ± 4 to −24 ± 3 beats/min, respectively. Thus EA at P5–6 decreases PBG evoked hypotension and bradycardia as well as the NAmb PBG-sensitive preganglionic cardiac vagal outflow through opioid and GABA neurotransmitter systems.

Hypotension produced by vagal block in primates

1988 ◽  
Vol 254 (6) ◽  
pp. R857-R862
Author(s):  
K. G. Cornish ◽  
M. Barazanji ◽  
A. Ryberg ◽  
J. P. Gilmore
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Left Atrial ◽  
Volume Expansion ◽  
Water Immersion ◽  
Abdominal Cavity ◽  
Sympathetic Tone ◽  
Control Group ◽  
Blood Volume Expansion ◽  
Cardiopulmonary Receptors

In many species, the vagus has been reported to contain afferents that inhibit sympathetic tone. Vagal block (VB) increases blood pressure in both the intact and sinoaortic-denervated (SAD) dog. In the present study, VB was produced in intact and SAD monkeys by infiltrating the vagi with a local anesthetic. This was done in conjunction with blood volume expansion or head-out water immersion. The cardiovascular parameters monitored were heart rate (HR), blood pressure (BP), and left atrial pressure (LAP). VB decreased BP (-13 +/- 2.8 mmHg) in the control group and the SAD animals (-47 +/- 6.7 mmHg) without changing HR. Volume expansion decreased BP in the SAD animals (-6 +/- 3.4) but not in the intact monkeys (1.8 +/- 2.27), whereas HR did not change. Volume expansion after VB increased BP in both the SAD and the intact animals while producing a decrease in HR. Volume expansion caused LAP to increase in all groups (SAD 13.9 +/- 6.3; control VB 11.6 +/- 1.8, control 9.3 +/- 0.89, SAD VB 7.66 +/- 3.46). Immersion in the VB SAD animals increased BP to a greater extent than volume expansion. VB in the monkey must be removing input from peripheral receptors, which maintain sympathetic tone. Because immersion with VB increases BP more than volume expansion with VB, it is concluded that VB causes predominantly venous pooling. Because cardiopulmonary receptors generally inhibit sympathetic tone, it is concluded that those receptors responsible for the observed hypotension are located in the venous system, probably in the chest or the abdominal cavity.

Carotid arterial haemodynamics after mild degrees of lower-body negative pressure in man

1992 ◽  
Vol 83 (5) ◽  
pp. 535-540 ◽  
Author(s):  
P. J. Lacolley ◽  
B. M. Pannier ◽  
M. A. Slama ◽  
J. L. Cuche ◽  
A. P. G. Hoeks ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Weight Bearing ◽  
Normal Subjects ◽  
Lower Body ◽  
Head Up Tilt ◽  
Cardiopulmonary Receptors ◽  
Carotid Arterial

1. Pulsatile changes in the diameter of the common carotid artery were studied transcutaneously using an echo-tracking technique in 15 normal subjects: eight subjects before and during application of graded lower-body negative pressure from −5 to −15 mmHg, and seven subjects before and during weight-bearing head-up tilt at 30 and 60 degrees. 2. In concomitant studies of changes in forearm vascular resistance, it was seen that mild lower-body negative pressure produced deactivation of cardiopulmonary receptors without changes in systemic blood pressure or heart rate. 3. After lower-body negative pressure, a significant decrease in carotid arterial diastolic diameter [from 0.662 ± 0.028 to 0.624 ± 0.033 cm (lower-body negative pressure −10 mmHg) and 0.640 ± 0.030 cm lower-body negative pressure −15 mmHg), P<0.001 and <0.05] was observed. 4. After head-up tilt, carotid arterial diameter was also significantly decreased at 30 and 60 degrees, whereas a significant increase in heart rate occurred only at 60 degrees and mean blood pressure did not change. 5. The study provides evidence that the geometry of the arterial wall is substantially modified by noninvasive manoeuvres such as head-up tilting and lower-body negative pressure. The latter is assumed to selectively deactivate human cardiopulmonary receptors, but the present data suggest that local changes may also influence carotid baroreceptors.

Differences in Reflex Control of Arterial Pressure and Renin Release during Head-Up Tilting in the Cat

1978 ◽  
Vol 55 (s4) ◽  
pp. 179s-181s ◽  
Author(s):  
A. Stella ◽  
R. A. L. Dampney ◽  
R. Golin ◽  
A. Zanchetti
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Renin Release ◽  
Haemodynamic Response ◽  
First Episode ◽  
Haemodynamic Changes ◽  
Cervical Vagotomy ◽  
Reflex Control

1. Anaesthetized cats were subjected to two 10 min trials of head-up tilting spaced 30 min. Arterial pressure, heart rate, blood flow to an innervated kidney and to the contralateral denervated one, and renin release from both kidneys were measured. 2. The same haemodynamic changes and comparable increases in renin release from innervated kidneys occurred during both episodes of tilting when cats were subjected to sham cervical vagotomy between the two tilting trials. 3. Bilateral cervical vagotomy, performed after the first episode of head-up tilting, did not affect the haemodynamic response to the change in posture, but significantly and markedly reduced the increase in renin release from the innervated kidney. 4. After sino-aortic denervation a marked and sustained arterial hypotension occurred during tilting, and the postural increase in renin release from the innervated kidney was even greater. 5. In no condition, even during the marked fall in blood pressure in sino-aortic denervated cats, did head-up tilting increase renin release from the denervated kidney. 6. It is concluded that maintenance of arterial pressure during tilting is mainly due to sino-aortic reflexes, whereas vagal reflexes are mostly responsible for the postural increase in renin release.

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