Reflexes from isolated carotid sinuses of intact and vagotomized conscious dogs

1980 ◽  
Vol 238 (6) ◽  
pp. H815-H822 ◽  
Author(s):  
R. B. Stephenson ◽  
D. E. Donald
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Response Curve ◽  
Vagal Afferents ◽  
Conscious Dogs ◽  
Stimulus Response ◽  
Carotid Baroreflex ◽  
Cervical Vagotomy ◽  
Curve Upward ◽  
Sinus Pressure

Exposure of the vascularly isolated carotid sinuses of 8 conscious dogs to static pressures between 50 and 240 mmHg caused significantly smaller increases [23 +/- 5(SE) mmHg] than decreases (37 +/- 4 mmHg) in arterial pressure frossure and heart rate and shifted the stimulus-response curve upward. Bilateral cervical vagotomy in conscious dogs caused sustained (3 h) increases in arterial pressure (40 +/- 5 mmHg), significantly larger than after atropinization (7 +/- 2 mmHg). In anesthetized, but not in conscious dogs, high sinus pressure reversed the hypertension caused by vagotomy. After vagotomy, low sinus pressure resulted in arterial pressures greater than 200 -mHg. In conscious dogs the carotid baroreflex can widely vary arterial pressure and heart rate despite buffering by extracarotid baroreceptors with vagal afferents, but cannot fully compensate for the acute loss of the latter. Extracarotid baroreceptors actively participate with carotid baroreceptors in the regulation of arterial pressure and better buffer carotid baroreflex-induced increases than decreases in arterial pressure.

Prostacyclin reduces "preload" in conscious dogs via a vagal reflex mechanism

1987 ◽  
Vol 253 (6) ◽  
pp. H1477-H1483
Author(s):  
D. M. Nganele ◽  
T. H. Hintze
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Left Ventricular ◽  
Vagal Afferents ◽  
Conscious Dogs ◽  
Reflex Mechanism ◽  
Capacitance Vessels ◽  
Preload Reduction ◽  
Cardiopulmonary Receptors ◽  
Electrical Pacing

The purpose of this study was to determine the effects of prostacyclin on left ventricular (LV) preload in conscious dogs. LV end-diastolic diameter (LV EDD) was used as an index of preload. Because prostacyclin reduces arterial pressure, data were sampled when mean arterial pressure, heart rate, and first derivative of LV pressure (dP/dt) had returned to control levels. There was no dose-response relationship in the preload reduction to prostacyclin, the threshold dose being 0.1 microgram/kg. Intravenous prostacyclin (2.0 micrograms/kg) reduced LV EDD 2.9 +/- 0.5% from 36 +/- 2.2 mm, (P less than 0.01). With heart rate held constant (146 +/- 2.5 beats/min) by electrical pacing, prostacyclin still reduced LV EDD by 4.0 +/- 1.0% from 32 +/- 2.5 mm (P less than 0.05). Intravenous administration of arachidonic acid (500 micrograms/kg) gave similar results. The magnitude of the preload response to prostacyclin was similar to that of nitroglycerin (25 micrograms/kg). Prazosin (1 mg/kg) or bilateral cervical vagal section completely abolished the preload response to prostacyclin but not to nitroglycerin. We, therefore, propose a mechanism where prostacyclin activates cardiopulmonary receptors with vagal afferents that results in a withdrawal of peripheral sympathetic tone to capacitance vessels to reduce preload, in contrast to nitroglycerin, whose mechanism of action is most probably a direct effect on capacitance vessels.

Sustained interruption of the aortic baroreflex by left cervical vagotomy in dogs

1984 ◽  
Vol 246 (3) ◽  
pp. H319-H323 ◽  
Author(s):  
S. C. Walgenbach
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Conscious Dogs ◽  
Conscious Dog ◽  
Bilateral Carotid ◽  
Cervical Vagotomy

Previous experiments demonstrated that acute left vagotomy interrupted 90% of the aortic baroreflex. The present study determined whether or not this interruption was sustained over a period of weeks. Bilateral carotid occlusions (BCO) were performed in conscious dogs before and for 3 wk after left vagotomy and immediately after subsequent right vagotomy. Prior to left vagotomy, BCO induced a rise in arterial pressure of 28 +/- 8 mmHg but no change in heart rate. After left vagotomy, BCO resulted in a rise in arterial pressure of 71 +/- 7 mmHg and a rise in heart rate of 43 +/- 6 beats/min. The BCO-induced elevations in arterial pressure and heart rate did not change significantly during the next 3 wk. Subsequent right vagotomy did not alter the rise in arterial pressure to BCO. These data indicate that left cervical vagotomy interrupts the aortic baroreflex for at least a 3-wk period and suggest that this procedure, when combined with reversible vascular isolation of the carotid sinuses, provides a method for studying cardiovascular adaptation to the acute loss of sinoaortic reflexes in the conscious dog.

Cardiorespiratory responses to chemical activation of right ventricular receptors

1987 ◽  
Vol 63 (2) ◽  
pp. 733-739 ◽  
Author(s):  
T. G. Waldrop ◽  
D. C. Mullins
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Chemical Activation ◽  
Left Ventricular ◽  
Vagal Afferents ◽  
Cardiorespiratory Function ◽  
Cervical Vagotomy ◽  
The Right

Previous reports have shown that activation of left ventricular receptors with sympathetic afferents elicits increases in respiratory output and arterial pressure. The purpose of the present study was to determine whether similar responses are produced by chemical activation of epicardial receptors in the right ventricle. Receptors were stimulated by applying either capsaicin (10 micrograms) or bradykinin (500 ng) to the epicardial surface of the right ventricle in anesthetized cats. Application of either chemical evoked an increase in respiratory output (phrenic nerve activity), a decrease in heart rate, and a nonsignificant increase in arterial pressure in intact cats. However, capsaicin and bradykinin produced significant increases in arterial pressure, heart rate, and respiratory output after bilateral cervical vagotomy. In contrast, a fall in both heart rate and arterial pressure with only small increases in respiratory output were evoked after bilateral removal of the stellate ganglia in cats with intact vagi. Only small responses to the chemical stimulation of right ventricular receptors persisted after combined vagotomy and stellate ganglionectomy. These findings suggest that 1) activation of epicardial receptors with sympathetic afferents originating in the right ventricle causes an increase in cardiorespiratory function, and 2) activation of right ventricular receptors with vagal afferents produces decreases in heart rate and arterial pressure.

scholarly journals Human carotid baroreflex during isometric lower arm contraction and ischemia

1998 ◽  
Vol 275 (3) ◽  
pp. H940-H945 ◽  
Author(s):  
Jonas Spaak ◽  
Patrik Sundblad ◽  
Dag Linnarsson
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Response Curve ◽  
Pressor Response ◽  
Response Curves ◽  
Muscle Ischemia ◽  
Carotid Baroreflex ◽  
Neck Chamber ◽  
Human Carotid

Our aim was to determine the roles of somatomotor activation and muscle ischemia for the tachycardia and hypertension of isometric arm contraction. Carotid-cardiac and carotid-mean arterial pressure (MAP) baroreflex response curves were determined in 10 men during rest, during isometric arm contraction at 30% of maximum, and during postcontraction ischemia. Carotid distending pressure (CDP) was changed by applying pressure and suction in a neck chamber. Pressures ranged from +40 to −80 mmHg and were applied repeatedly for 15 s during the three conditions. Maximum slopes and ranges of the response curves did not differ among conditions. The heart rate (HR) curve was shifted to a 14 ± 1.8 (mean ± SE) beats/min higher HR and a 9 ± 5.7 mmHg higher CDP during contraction and to a 14 ± 5.9 mmHg higher CDP during postcontraction ischemia with no change of HR compared with rest. The MAP curve was shifted to a 20 ± 2.8 mmHg higher MAP and to a 18 ± 5.4 mmHg higher CDP during contraction, and the same shifts were recorded during postcontraction ischemia. We conclude that neither somatomotor activation nor muscle ischemia changes the sensitivity of arterial baroreflexes. The upward shift of the MAP response curve, with no shift of the HR response curve during postexercise ischemia, supports the notion of parallel pathways for MAP and HR regulation in which HR responses are entirely caused by somatomotor activation and the pressor response is mainly caused by muscle ischemia.

Central command blunts sensitivity of arterial baroreceptor-heart rate reflex at onset of voluntary static exercise

2006 ◽  
Vol 290 (1) ◽  
pp. H200-H208 ◽  
Author(s):  
Kanji Matsukawa ◽  
Hidehiko Komine ◽  
Tomoko Nakamoto ◽  
Jun Murata
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Response Curve ◽  
Central Command ◽  
Arterial Baroreflex ◽  
Static Exercise ◽  
Response Curves ◽  
Stimulus Response ◽  
Aortic Depressor Nerve ◽  
Blood Pressures

We have reported that baroreflex bradycardia by stimulation of the aortic depressor nerve is blunted at the onset of voluntary static exercise in conscious cats. Central command may contribute to the blunted bradycardia, because the most blunted bradycardia occurs immediately before exercise or when a forelimb is extended before force development. However, it remained unknown whether the blunted bradycardia is due to either reduced sensitivity of the baroreflex stimulus-response curve or resetting of the curve toward a higher blood pressure. To determine this, we examined the stimulus-response relationship between systolic (SAP) or mean arterial pressure (MAP) and heart rate (HR) at the onset of and during the later period of static exercise in seven cats ( n = 348 trials) by changing arterial pressure with infusion of nitroprusside and phenylephrine or norepinephrine. The slope of the MAP-HR curve decreased at the onset of exercise to 48% of the preexercise value (2.9 ± 0.4 beats·min−1·mmHg−1); the slope of the SAP-HR curve decreased to 59%. The threshold blood pressures of the stimulus-response curves, at which HR started to fall due to arterial baroreflex, were not affected. In contrast, the slopes of the stimulus-response curves during the later period of exercise returned near the preexercise levels, whereas the threshold blood pressures elevated 6–8 mmHg. The maximal plateau level of HR was not different before and during static exercise, denying an upward shift of the baroreflex stimulus-response curves. Thus central command is likely to attenuate sensitivity of the cardiac component of arterial baroreflex at the onset of voluntary static exercise without shifting the stimulus-response curve.

Effect of vasopressin and phenylephrine on arterial pressure and heart rate in conscious dogs

1986 ◽  
Vol 251 (2) ◽  
pp. H253-H260
Author(s):  
J. L. Robinson
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Response Curve ◽  
Baroreflex Sensitivity ◽  
Conscious Dogs ◽  
Baroreflex Control ◽  
Pressure Stimulus ◽  
Before And After ◽  
Autonomic Receptors ◽  
The Difference

The effect of arginine vasopressin (AVP) and phenylephrine (PE) infusions on mean arterial pressure (MAP) and heart rate (HR) were compared in conscious dogs with all autonomic receptors intact (I), during muscarinic blockade (MB) and during ganglionic blockade (GB). After either MB or GB, the dose-MAP response curve for AVP and PE was shifted to the left of the I response curve; a greater shift was observed with AVP than with PE. The MAP threshold after GB for AVP and PE occurred at 10 and 50% of the threshold dose observed during the I response, respectively. Not only did the MAP threshold occur at a lower dose after MB and GB, but also the slope of the response curve was steeper than that of the I response. Comparing the amount of drug necessary to increase MAP 25 mmHg above control for PE and AVP before and after GB, the intact PE response required 4.3 +/- 1.0 (P less than 0.01) times more drug than during GB versus the intact AVP required 16.8 +/- 2.8 (P less than 0.01) times more drug than during GB. The baroreflex control of HR when all receptors were intact was 3.4 +/- 0.4 (P = 0.001) times more sensitive during AVP compared with PE; no differences were observed after MB. There were no significant changes in HR to AVP or PE after GB, thus indicating a lack of a direct effect of these agents on the HR. Our results show that MB and GB equally potentiate the pressor effects of AVP and PE, and the augmentation was much greater for AVP than for PE. The difference in the potentiation of these two vasoconstrictors is consistent with the finding that the baroreflex sensitivity during AVP was enhanced compared with PE. We have postulated that, in the resting conscious dog, AVP increases the sensitivity of the baroreflex primarily by producing a greater level of parasympathetic tone to the heart in response to a given pressure stimulus.

Comparison of carotid baroreflex control of plasma AVP concentration in conscious and anesthetized dogs

1991 ◽  
Vol 261 (4) ◽  
pp. R950-R956 ◽  
Author(s):  
K. E. Wehberg ◽  
G. J. Gala ◽  
M. J. Brunner
Keyword(s):  
Heart Rate ◽  
Carotid Sinus ◽  
Normal Component ◽  
Vagal Afferents ◽  
Baroreflex Control ◽  
Carotid Baroreflex ◽  
Carotid Sinus Baroreflex ◽  
Anesthetized Dogs ◽  
Plasma Arginine ◽  
Sinus Pressure

We compared carotid sinus baroreflex control of endogenous plasma arginine vasopressin (AVP) in chronically prepared conscious and acutely prepared anesthetized dogs. The carotid sinuses of both conscious and pentobarbital-anesthetized dogs were isolated bilaterally and perfused at constant pressures. Carotid sinus pressure (CSP) was changed between 200 and 50 mmHg in 25-mmHg steps in intact conscious and anesthetized dogs. Similar runs were repeated after vagotomy. Mean arterial pressure (MAP) and heart rate (HR) were monitored. At each interval of CSP, blood was withdrawn for AVP analysis by radioimmunoassay. MAP responses to changes in CSP were not different in the four experimental groups. Both anesthesia and vagotomy increased the HR responses to changes in CSP. With vagi intact, AVP increased at high CSP in conscious but not in anesthetized dogs. After vagotomy, low CSP led to an increase in plasma AVP that did not differ between conscious and anesthetized dogs. The results suggest that the release of AVP is modulated by the action of the carotid baroreflex as a normal component of an integrated efferent response. The response is similar in conscious and pentobarbital-anesthetized dogs and is normally buffered by reflexes with vagal afferents.

scholarly journals Identifying the role of group III/IV muscle afferents in the carotid baroreflex control of mean arterial pressure and heart rate during exercise

2018 ◽  
Vol 596 (8) ◽  
pp. 1373-1384 ◽  
Author(s):  
Thomas J. Hureau ◽  
Joshua C. Weavil ◽  
Taylor S. Thurston ◽  
Ryan M. Broxterman ◽  
Ashley D. Nelson ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Muscle Afferents ◽  
Baroreflex Control ◽  
Group Iii ◽  
Carotid Baroreflex

Compensation to exsanguination hypotension in healthy conscious dogs

1963 ◽  
Vol 205 (5) ◽  
pp. 1000-1004 ◽  
Author(s):  
Robert F. Rushmer ◽  
Nolan Watson ◽  
Donald Harding ◽  
Donald Baker
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Human Subjects ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure ◽  
Conscious Dogs ◽  
Series Of Experiments ◽  
The Mean ◽  
The Right

In some earlier studies on exsanguination hypotension in conscious dogs, reduction in systemic arterial pressure to shock levels was accompanied by a transient tachycardia during the removal of blood, but the heart rate returned to level, at or near control values during extended periods with the mean arterial pressure between 40 and 60 mm Hg. This observation stimulated a series of experiments on five healthy conscious dogs in which transient hypotension was induced by withdrawing blood from the region of the right atrium to determine which mechanisms were dominant in the compensatory reaction. A surprising degree of variability in response was encountered, such that tachycardia was the main response on some occasions, increased peripheral resistance on others, and in still others, several mechanisms appeared to play a role. Similar variability in the response to exsanguination have been reported in human subjects. These observations suggest that the baroceptor reflexes are not simple servo controls and their role in everyday cardiovascular responses should be re-examined.

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