Influence of carotid sinus pressure on atrial receptors and renal blood flow

1982 ◽  
Vol 242 (2) ◽  
pp. H220-H226
Author(s):  
F. Karim ◽  
D. U. Mackay ◽  
C. T. Kappagoda
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Left Atrial ◽  
Renal Mass ◽  
Carotid Sinus ◽  
Systemic Arterial Pressure ◽  
Left Pulmonary Vein ◽  
Atrial Receptors ◽  
Sinus Pressure ◽  
Stimulation Of

Stimulation of the atrial receptors results in an increase in renal blood flow. The present investigation was undertaken to determine whether this response was modulated by the input from the baroceptors in the carotid sinus. The experiments were performed on dogs anesthetized with chloralose. The systemic arterial pressure was held constant. The carotid sinuses were perfused at 62 +/- 1.3, 95 +/- 2.7, and 145 +/- 8.3 mmHg. The atrial receptors were stimulated by distension of small balloons positioned at the left pulmonary vein-atrial junctions and the left atrial appendage. At a carotid sinus pressure of 62 +/- 1.3 mmHg, the blood flow increased from 182 +/- 8.5 to 199 +/- 8.9 ml . min-1 . 100 g-1 renal mass. At a carotid sinus pressure of 95 +/- 2.7 mmHg, the blood flow increased from 202 +/- 9.6 to 209 +/- 10.4 ml . min-1 . 100 g-1 renal mass. At a carotid sinus pressure of 145 +/- 8.3 mmHg, the blood flow increased from 237 +/- 13.0 to 239 +/- 12.5 ml . min-1 . 100 g-1 renal mass. The first two responses alone were statistically significant. The response at a carotid sinus pressure of 62 +/- 1.3 mmHg was abolished by cutting or cooling the cervical vagi to 8--10 degrees C. It is concluded that stimulation of the left atrial receptors produces a reflex increase in blood flow to the kidney, and this response is modulated by the input from the carotid sinus baroceptors.

Involvement of renal alpha- and beta-adrenoceptors in release of renin by carotid baroreflex

1979 ◽  
Vol 236 (4) ◽  
pp. H580-H585
Author(s):  
D. A. Powis ◽  
D. E. Donald
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Carotid Sinus ◽  
Systemic Arterial Pressure ◽  
Renin Release ◽  
Release Mechanism ◽  
Hemodynamic Changes ◽  
Alpha Adrenoceptor ◽  
Carotid Baroreflex

In anesthetized vagotomized dogs with renal arterial pressure constant, carotid sinus hypotension (BCO) caused a reflex rise in systemic arterial pressure, a fall in renal blood flow, and a similar increase in renin release from both kidneys. Unilateral alpha-adrenoceptor blockade with phenoxybenzamine resulted in an increase in basal renal blood flow, a depression of basal renin release, and an abolition of the responses to BCO in the treated kidney. The untreated kidney responsed to BCO as before. Nonblocked and alpha-blocked kidneys released similar amounts of renin when renal blood flow was mechanically reduced by aortic constriction. Administration of propranolol to the nonblocked kidney prevented the release of renin but not the hemodynamic changes resulting from BCO. The experiments demonstrated that under certain conditions carotid sinus hypotension produced alpha-adrenoceptor-mediated changes in the kidney sufficient to cause increased renin release. A step in the renin release mechanism subsequent to the alpha-adrenoceptor-mediated changes in sensitive to propranolol.

Effect of stimulating right atrial receptors on renal blood flow

1982 ◽  
Vol 60 (12) ◽  
pp. 1672-1679 ◽  
Author(s):  
F. Karim ◽  
S. Kaufman ◽  
C. T. Kappagoda
Keyword(s):  
Blood Flow ◽  
Renal Mass ◽  
Carotid Sinus ◽  
Superior Vena ◽  
Renal Perfusion ◽  
Right Atrial ◽  
Myelinated Fibres ◽  
Right Atrial Appendage ◽  
The Right ◽  
Atrial Receptors

This investigation was undertaken to determine the effect of stretching the superior vena caval – right atrial (SVC–RA) junction and the right atrial appendage on blood flow to the kidney (RBF) and to establish whether any changes observed were influenced by the input from the baroreceptors in the carotid sinus. The experiments were performed on seven dogs, anaesthetized with α-chloralose. The systemic arterial (i.e., renal perfusion) pressure was held constant. At a carotid sinus pressure (CSP) of 59.0 ± 1.2 mmHg (1 mmHg = 133.322 Pa), the RBF increased from 218 ± 16.1 to 231.7 ± 18.4 mL/min per 100 g renal mass (p < 0.025). At a CSP of 88.0 ± 3.5 mmHg, the RBF increased from 230.1 ± 19.2 to 237.1 ± 19.2 mL/min per 100 g renal mass (p < 0.05). At a CSP of 137 ± 3.7 mmHg there were no significant changes in RBF. These responses were abolished by cutting (four dogs) or cooling the vagi (one dog only). In a subsidiary investigation it was shown that stretching the SVC–RA junction activated receptors in the endocardial surface of the right atrium which discharged into myelinated fibres in the vagi, having an average conduction velocity of 8.1 m/s (range 3.8–15). It is concluded that stimulation of right atrial receptors increases the RBF and that this response is influenced by the input from the barorceptors in the carotid sinus.

Interaction of left atrial receptors and carotid sinus baroreceptors on heart rate in the dog

1985 ◽  
Vol 248 (5) ◽  
pp. H631-H636 ◽  
Author(s):  
K. K. Teo ◽  
G. C. Man ◽  
C. T. Kappagoda
Keyword(s):  
Heart Rate ◽  
Left Atrial ◽  
Carotid Sinus ◽  
Aortic Pressure ◽  
Response Curves ◽  
Stimulus Response ◽  
Alpha Chloralose ◽  
Atrial Receptors ◽  
Control State ◽  
Stimulation Of

This study was undertaken to determine the influence of 1) the left atrial receptors (LA) on the ability of the carotid sinus baroreceptors (CS) to regulate heart rate and 2) the CS on the reflex increase in heart rate mediated by the LA. The LA were stimulated by stretching the pulmonary vein-atrial junctions in dogs anesthetized with alpha-chloralose. Aortic pressure was controlled, and the pressure in the CS was regulated. Stimulus-response curves were obtained relating heart rate to pressures in the CS, in the control state, and during stimulation of LA (6 dogs). Factorial analysis revealed that LA exerted a significant influence on heart rate (P less than 0.01). Next the CS pressure was set at mid, low, and high levels and the LA stimulated. It was found that the effect on heart rate was greatest at the mid setting (+19.3 +/- 2.9 beats/min) and least at the low setting of the pressure in the CS (+0.9 +/- 0.5, 11 dogs). Sympathetic blockade attenuated significantly the response in the mid setting of the CS pressure and left intact the response at the high setting of the pressure in the CS. It is concluded that there is a significant interaction between these two reflexes.

Effect of baroreceptor reflex stimulation on blood flow to an atelectatic lung

1982 ◽  
Vol 52 (5) ◽  
pp. 1128-1132 ◽  
Author(s):  
W. B. Strawn ◽  
S. M. Hall ◽  
M. G. Levitzky
Keyword(s):  
Blood Flow ◽  
Carotid Sinus ◽  
Initial Period ◽  
Pulmonary Arteries ◽  
Baroreceptor Reflex ◽  
Physiological Salt Solution ◽  
Vascular Response ◽  
Left And Right ◽  
Reflex Stimulation ◽  
Stimulation Of

The effect of baroreceptor reflex stimulation by carotid sinus hypotension on the pulmonary vascular response to atelectasis was studied in eight dogs anesthetized with chloralose. Closed-chest dogs with electromagnetic flow probes previously implanted on their left (QL) and main (QT) pulmonary arteries had their left and right lungs ventilated separately. Their carotid sinuses were isolated bilaterally and perfused by a pulsatile pump with a physiological salt solution. After an initial period of bilateral 100% O2 ventilation with carotid sinus perfusion pressures (CSPP) set at each animal's initial mean arterial pressure (98 +/- 19 Torr), the left airway was occluded, QL/QT fell from 0.33 +/- 0.01 to 0.24 +/- 0.02 and PO2 fell from 323 +/- 35 Torr to 74 + 7 Torr. When CSPP was lowered to 21 +/- 3 Torr, there were no changes in QL/QT and PO2. These results suggest that stimulation of the baroreceptor reflex by carotid sinus hypotension does not interfere with the diversion of pulmonary blood flow away from a unilaterally atelectatic lung.

Aortic arch reflex control of total systemic vascular capacity

1987 ◽  
Vol 253 (3) ◽  
pp. H598-H603
Author(s):  
A. A. Shoukas ◽  
M. J. Brunner ◽  
A. S. Greene ◽  
C. L. MacAnespie
Keyword(s):  
Arterial Pressure ◽  
Aortic Arch ◽  
Carotid Sinus ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Reservoir Volume ◽  
Aortic Arch Pressure ◽  
Pressure Changes ◽  
Change In Mean ◽  
Sinus Pressure

The ability of the aortic arch baroreceptors to change vascular capacity was measured and, in the same animal, compared with carotid sinus reflex changes in capacity. Seven dogs were anesthetized with pentobarbital sodium and perfused with constant flow. Changes in external reservoir volume reflected reciprocal changes in total systemic vascular capacity and changes in arterial pressure parallel changes in total peripheral resistance. The aortic arch and carotid sinus baroreceptor areas were isolated, and the pressures were controlled separately. With carotid sinus pressure held constant at 125 mmHg, aortic arch pressure was increased and decreased between 225 and 50 mmHg, and the changes in reservoir volume and systemic arterial pressure were measured. Results from increasing and decreasing aortic arch or carotid sinus pressure were not significantly different and were averaged. The mean change in reservoir volume was 1.9 +/- 0.2 ml/kg and the change in mean arterial pressure was 18.7 +/- 3.7 mmHg. The changes in reservoir volume and arterial pressure caused by the aortic arch reflex were not influenced by the level of carotid sinus pressure. Carotid sinus pressure changes between 200 and 50 mmHg at a constant aortic arch pressure caused reservoir volume and arterial pressure to change by 7.2 +/- 0.9 ml/kg and 45.1 +/- 4.1 mmHg, respectively. The level of aortic arch pressure did not modify these responses.

Renal actions of atrial natriuretic peptide on the postischemic kidney

1988 ◽  
Vol 66 (5) ◽  
pp. 601-607 ◽  
Author(s):  
Satoshi Akabane ◽  
Masahito Imanishi ◽  
Yohkazu Matsushima ◽  
Minoru Kawamura ◽  
Morio Kuramochi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Renal Artery ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Natriuretic Peptide ◽  
Filtration Rate ◽  
Systemic Arterial Pressure

The objective of this study was to evaluate the renal actions of atrial natriuretic peptide (ANP) in the unilateral postischemic kidney of anesthetized dogs with a severe reduction in glomerular filtration rate. The dose of atrial natriuretic peptide (50 ng∙kg−1∙min−1) we gave did not alter the mean systemic arterial pressure, renal blood flow, and glomerular filtration rate in the normal kidney, as determined in foregoing studies. ANP was infused into the intrarenal artery continuously for 60 min after the release from 45 min of complete renal artery occlusion. In the vehicle-infused group, the glomerular filtration rate fell dramatically (6% of control), the renal blood flow decreased (60% of control), and the mean systemic arterial pressure tended to increase (136% of control). The urine flow rate and urinary excretion of sodium decreased significantly (25 and 25%, respectively) at 30 min after reflow in the postischemic period. Continuous renal artery infusion of ANP resulted in a marked increase in urine flow rate (246% of control) and the urinary excretion of sodium (286% of control). The administration of ANP led to an improvement in renal blood flow (99% of control) and glomerular filtration rate (40% of control), and attenuated the rise in mean systemic arterial pressure (109% of control), compared with findings in the vehicle-infused group. Plasma renin activity and prostaglandin E2 concentration in the renal venous blood were elevated after the release from complete renal artery occlusion in both groups. These results indicate that the vascular effects of ANP on the postischemic kidney were enhanced and that the peptide maintained the natriuretic effect.

"Summation" of the increase in heart rate from stimulation of atrial receptors

1980 ◽  
Vol 58 (6) ◽  
pp. 666-672
Author(s):  
P. V. Greenwood ◽  
C. T. Kappagoda
Keyword(s):  
Heart Rate ◽  
Left Atrial ◽  
Superior Vena ◽  
Right Atrial ◽  
Propranolol Hydrochloride ◽  
Superior Vena Caval ◽  
The Right ◽  
Atrial Receptors ◽  
Stimulation Of ◽  
Wire Cage

In dogs anaesthetized with chloralose, application of stimuli which are likely to activate left atrial (L.A.) and right atrial (R.A.) receptors (complex unencapsulated endings) has been shown to result in an increase in heart rate. The present investigation was undertaken to determine whether the response elicited by the application of one stimulus (i.e., to the left atrium) could be enhanced by the application of a second stimulus (i.e., to the right atrium) in the same animal.The L.A. receptors were stimulated by distending a small balloon at the right upper pulmonary vein-L.A. junction and the R.A. receptors by "expanding" a spherical wire cage positioned at the superior vena caval (S.V.C.)-R.A. junction. Pressures in the S.V.C., R.A., L.A., and femoral artery were measured and the electrocardiogram monitored.In eight dogs stimulation of L.A. receptors resulted in an increase in heart rate (H.R.) of 18.5 beats/min (SEM 6.0; N = 23). In the same animals stimulation of R.A. receptors resulted in an increase in H.R. of 14.6 beats/min (SEM 2.0; N = 25). Application of both stimuli simultaneously resulted in an increase of 32.2 beats/min (SEM 8.0; N = 13). In four dogs propranolol hydrochloride (0.5 mg/kg) markedly diminished the response. In three dogs the response was abolished by bretylium tosylate (10 mg/kg).It is concluded that the increase in H.R. resulting from the application of these two stimuli could be "summated" and these findings support the proposition that the receptors in the two atria act as a functional entity.

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