Alpha- and beta-adrenergic mechanisms in the control of vascular capacitance by the carotid sinus baroreflex system

1994 ◽  
Vol 267 (1) ◽  
pp. H201-H210 ◽  
Author(s):  
K. Shigemi ◽  
M. J. Brunner ◽  
A. A. Shoukas
Keyword(s):  
Adrenergic Receptor ◽  
Carotid Sinus ◽  
Venous Pressure ◽  
Systemic Circulation ◽  
Adrenergic System ◽  
Beta Adrenergic ◽  
Vascular Volume ◽  
Adrenergic Mechanisms ◽  
Vascular Capacitance ◽  
Carotid Sinus Baroreflex

We examined the active and passive contributions of the alpha- and beta-adrenergic receptor mechanisms to the changes in systemic vascular capacitance caused by the carotid sinus baroreflex system in anesthetized, vagotomized dogs. The carotid sinuses were isolated from the systemic circulation and perfused with controlled pressures. To determine the changes in vascular capacitance, a constant flow, constant venous pressure cardiopulmonary bypass was used. The changes in unstressed vascular volume were calculated when carotid sinus pressure was reduced from 200 to 50 mmHg without any adrenergic receptor antagonist, with either an alpha- (phentolamine) or a beta- (propranolol) antagonist and then with both. The reflex change in unstressed vascular volume in the systemic circulation (22.6 +/- 9.0 ml/kg without any antagonist) was reduced by 72% with phentolamine, by 35% with propranolol, and by 73% with both antagonists. Our results suggest that the alpha-adrenergic mechanisms contribute significantly to active changes in systemic venous capacity. In addition, the beta-adrenergic system has very little effect on active changes in venous vessels but does contribute to the overall capacity changes by dilating the hepatic outflow resistance when the carotid sinus baroreflex system is activated.

beta-Receptor influence on lung vasoconstrictor responses to hypoxia and humoral agents

1977 ◽  
Vol 43 (4) ◽  
pp. 612-616 ◽  
Author(s):  
R. J. Porcelli ◽  
A. T. Viau ◽  
N. E. Naftchi ◽  
E. H. Bergofsky
Keyword(s):  
Adrenergic Receptor ◽  
Adrenergic System ◽  
Hypercapnic Acidosis ◽  
Pulmonary Tissue ◽  
Beta Adrenergic ◽  
Vascular Responses ◽  
Adenosine Cyclic Monophosphate ◽  
Adrenergic Activity ◽  
Camp Levels

The role of the adrenergic receptor in mediating pulmonary vascular responses to gaseous and humoral agents was investigated by use of epinephrine injections in the perfused feline pulmonary circulation. Alteration of the balance between alpha- and beta-adrenergic activity was quantified by measurement of decreasing vasoconstrictor activity to epinephrine and rising lobar tissue 3′,5′-adenosine cyclic monophosphate (cAMP) levels. The increased beta-adrenergic activity thus generated was associated with marked reductions in the pulmonary vasoconstrictor responses to hypoxia, hypercapnic acidosis, and histamine, but not to serotonin. Repeated pulmonary vasodilations or increases in blood, but not pulmonary tissue, levels of cAMP induced by theophylline doses, which would not necessarily affect the beta-adrenergic activity, did not alter the pulmonary vasoconstrictor responses to hypoxia, hypercapnia, or histamine. These data support the significant role which the adrenergic system plays in mediating pulmonary vasoconstrictor responses to certain specific gaseous and humoral agents, and the specificity with which this mediation occurs serves to link hypoxia and histamine together so that the latter could serve as a mediator of the former.

Splanchnic vascular capacitance and positive end-expiratory pressure in dogs

1991 ◽  
Vol 70 (2) ◽  
pp. 818-824 ◽  
Author(s):  
C. Risoe ◽  
C. Hall ◽  
O. A. Smiseth
Keyword(s):  
Blood Volume ◽  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Central Blood Volume ◽  
Positive End Expiratory Pressure ◽  
Splenic Volume ◽  
Vascular Volume ◽  
Vascular Capacitance ◽  
Anesthetized Dogs ◽  
Blood Volumes

We have investigated the effect of positive end-expiratory pressure ventilation (PEEP) on regional splanchnic vascular capacitance. In 12 anesthetized dogs hepatic and splenic blood volumes were assessed by sonomicrometry. Vascular pressure-diameter curves were defined by obstructing hepatic outflow. With 10 and 15 cmH2O PEEP portal venous pressure increased 3.1 +/- 0.3 and 5.1 +/- 0.4 mmHg (P less than 0.001) while hepatic venous pressure increased 4.9 +/- 0.4 and 7.3 +/- 0.4 mmHg (P less than 0.001), respectively. Hepatic blood volume increased (P less than 0.01) 3.8 +/- 0.9 and 6.3 +/- 1.4 ml/kg body wt while splenic volume decreased (P less than 0.01) 0.8 +/- 0.2 and 1.3 +/- 0.2 ml/kg body wt. The changes were similar with closed abdomen. The slope of the hepatic vascular pressure-diameter curves decreased with PEEP (P less than 0.01), possibly reflecting reduced vascular compliance. There was an increase (P less than 0.01) in unstressed hepatic vascular volume. The slope of the splenic pressure-diameter curves was unchanged, but there was a significant (P less than 0.05) decrease in unstressed diameter during PEEP. In conclusion, hepatic blood volume increased during PEEP. This was mainly a reflection of passive distension due to elevated venous pressures. The spleen expelled blood and thus prevented a further reduction in central blood volume.

Central and peripheral adrenergic modulation of carotid sinus-induced renin release

1982 ◽  
Vol 242 (3) ◽  
pp. R318-R325 ◽  
Author(s):  
H. D. Schultz ◽  
J. E. Zehr ◽  
A. Livnat
Keyword(s):  
Adrenergic Receptors ◽  
Carotid Sinus ◽  
Renin Release ◽  
Beta Adrenergic ◽  
Alpha Adrenergic Receptors ◽  
Systemic Pressure ◽  
Carotid Sinus Baroreflex ◽  
Adrenergic Blocker ◽  
Reflex Arc ◽  
Anesthetized Dogs

To study central and peripheral mechanisms that regulate the level of circulating renin during activation of the carotid sinus baroreflex, both carotid sinuses were isolated and perfused at constant flow in chloralase-anesthetized dogs. Sinus pressure was controlled by an adjustable reservoir while systemic pressure was stabilized using an external chamber. Arterial renin activity, measured by radioimmunoassay, was increased during sinus hypotension only if systemic pressure was held constant. The renin response was eliminated by either sinus or renal denervation. Administration of propranolol (iv) or phentolamine directly into the renal artery totally blocked the increase in renin during activation of the reflex. Perfusion of a beta-adrenergic blocker (propranolol) or an alpha-adrenergic blocker (phentolamine) through the third and fourth cerebroventricles had no effect on the increase in renin during sinus hypotension, whereas centrally administered clonidine, and alpha-agonist, blocked the response. We conclude that the sinus reflex arc affecting renin release involves not only activation of peripheral alpha- and beta-adrenergic receptors in the kidney but also inhibition of central alpha-adrenergic receptors. No evidence for central beta-involvement was found.

Invariance of the resistance to venous return to carotid sinus baroreflex control

1996 ◽  
Vol 271 (3) ◽  
pp. H1022-H1030 ◽  
Author(s):  
T. Hatanaka ◽  
J. T. Potts ◽  
A. A. Shoukas
Keyword(s):  
Venous Return ◽  
Carotid Sinus ◽  
Arterial Compliance ◽  
Systemic Circulation ◽  
Major Site ◽  
Apparent Paradox ◽  
Baroreflex Control ◽  
Lumped Model ◽  
Carotid Sinus Baroreflex ◽  
Established Fact

Despite the well-established fact that the carotid sinus baroreflex system has profound control over the physical properties of the systemic circulation, the resistance to venous return (RVR) seems to be invariant of such control. We hypothesized that this apparent paradox may be explained from the baroreflex changes in systemic arterial compliance. In 12 pentobarbital-anesthetized mongrel dogs, RVR was measured at controlled carotid sinus pressures (CSP) of 50 and 200 mmHg with normal and artificially increased arterial compliance. Arterial compliance was determined from the arterial pressure decay when systemic blood flow was stopped with total vena caval occlusion. Changing CSP between 50 and 200 mmHg changed RVR significantly only under the condition of artificially increased arterial compliance. A four-parameter lumped model of the systemic circulation revealed that the baroreflex changes in arterial compliance and arterial resistance, which occurred in opposite directions, prevented a change in RVR when CSP was changed. The data also suggested that approximately 75% of RVR was attributed to large and conduit veins, the resistances along which were insensitive to baroreflex control. We concluded that the invariance of RVR results from a combination of 1) baroreflex change in the arterial compliance, 2) baroreflex insensitivity of the resistance along large and conduit veins, and 3) spatially distinct location between the major site of reflex change in capacitance and the major site of compliance.

Decreased beta-adrenergic receptor density in mononuclear leukocytes from thyroidectomized patients

1983 ◽  
Vol 103 (1) ◽  
pp. 40-45 ◽  
Author(s):  
G. Cognini ◽  
L. Piantanelli ◽  
E. Paolinelli ◽  
P. Orlandoni ◽  
A. Pellegrini ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Surgical Stress ◽  
Serum Levels ◽  
Mononuclear Leukocytes ◽  
Adrenergic System ◽  
Receptor Density ◽  
Beta Adrenergic Receptor ◽  
Peripheral Blood Mononuclear ◽  
Beta Adrenergic ◽  
Before And After

Abstract. Beta-adrenergic receptor characteristics were investigated in peripheral blood mononuclear leukocytes taken from patients before and after partial thyroidectomy. In order to discriminate the effect of surgical stress per se from that of thyroidectomy, the analysis was also performed on patients before and after cholecystectomy. Receptor characteristics were determined by using dihydroalprenolol as ligand in direct equilibrium binding experiments. The binding affinity showed no changes either when two different surgical treatments were compared or when the same patient was analysed before and after the operation. On the contrary, a significant decrease in receptor density was found in thyroidectomized patients when compared pre- and post-operatively. This fall in receptor number seems to be linked with thyroid function since no statistically significant changes were observed in cholecystectomized patients in relation to surgical operation. This view is further supported by data on T3 serum levels, which show a significant fall after thyroidectomy but no statistically significant modifications after cholecystectomy. It is concluded that betaadrenoceptor modulation plays an important role in the relationship between thyroid and beta-adrenergic system.

Effect of carotid sinus baroreceptor reflex on hepatic and splenic vascular capacitance in vagotomized dogs

1994 ◽  
Vol 266 (4) ◽  
pp. H1528-H1533 ◽  
Author(s):  
C. Risoe ◽  
W. Tan ◽  
O. A. Smiseth
Keyword(s):  
Volume Change ◽  
Carotid Sinus ◽  
Portal Pressure ◽  
Baroreceptor Reflex ◽  
Volume Changes ◽  
Splenic Volume ◽  
Vascular Volume ◽  
Vascular Compliance ◽  
Vascular Capacitance ◽  
Sinus Pressure

Mechanisms of how baroreflex activation changes splanchnic vascular volumes were studied in eight vagotomized dogs, anesthetized by chloralose/urethan. Hepatic and splenic vascular volume changes were determined from organ dimensions by sonomicrometry. Pulsatile carotid sinus pressure (CSP) in isolated and separately perfused carotid sinuses was changed among 200, 120, and 40 mmHg. Lowering CSP from 120 to 40 mmHg significantly decreased both hepatic and splenic vascular volume (at similar portal pressure) by 1.9 +/- 0.5 and 1.8 +/- 0.6 ml/kg body wt, respectively. Increasing CSP from 120 to 200 mmHg tended to increase regional vascular volumes (P = NS). The combined volume change of liver and spleen between CSP 40 and 200 mmHg was 4.2 +/- 0.6 ml/kg body wt (P < 0.001). Pressure-volume (dimension) curves at high, low, and baseline CSP were determined to separate active and passive mechanisms of vascular volume changes. Changes in CSP did not change regional vascular compliance. Low CSP significantly decreased unstressed liver and unstressed splenic volume by 3.3 +/- 0.9 and 1.9 +/- 0.5 ml/kg body wt, respectively. These results indicate that liver and spleen both contribute to blood volume mobilization by vasoconstriction during low CSP and that the carotid sinus baroreceptor reflex modulates hepatic and splenic vascular capacitance by changing unstressed volume rather than by changing vascular compliance.

Effect of endurance training on beta-adrenergic system in three different skeletal muscles

1993 ◽  
Vol 74 (4) ◽  
pp. 1641-1646 ◽  
Author(s):  
G. Plourde ◽  
S. Rousseau-Migneron ◽  
A. Nadeau
Keyword(s):  
Adenylate Cyclase ◽  
Adrenergic Receptor ◽  
Skeletal Muscles ◽  
Vastus Lateralis ◽  
Treadmill Running ◽  
Adrenergic System ◽  
Vastus Lateralis Muscle ◽  
Receptor Density ◽  
Beta Adrenergic ◽  
Lateralis Muscle

The beta-adrenergic receptor density (Bmax) and adenylate cyclase (AC) activity in the soleus muscle and deep red and white superficial portions of the vastus lateralis muscle were evaluated in a group of rats submitted to a progressive 10-wk treadmill running program (n = 19) and compared with a group of rats kept sedentary (n = 17) during the same period of time.(ABSTRACT TRUNCATED AT 250 WORDS)

Increased pulmonary vascular capacitance with β-adrenergic receptor stimulation: an experimental study of the effect of isoproterenol on the pulmonary vascular volume–pressure relationship

1988 ◽  
Vol 66 (1) ◽  
pp. 85-89 ◽  
Author(s):  
O. A. Smiseth ◽  
N. W. Scott-Douglas ◽  
D. Manyari ◽  
I. Kingma ◽  
E. R. Smith ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Diastolic Pressure ◽  
Blood Pool ◽  
Left Ventricular ◽  
Cardiac Volume ◽  
Receptor Stimulation ◽  
Vascular Volume ◽  
Vascular Capacitance ◽  
Blood Pool Scintigraphy ◽  
Β Receptor

The present study is an investigation of the effect of β-adrenergic receptor stimulation by isoproterenol on pulmonary vascular capacitance. The experiments were done in six intact-chest, anaesthetized dogs in which pulmonary and cardiac blood volumes were assessed by blood pool scintigraphy. Isoproterenol (0.150 μg∙kg−1∙min−1) significantly (p < 0.005) lowered pulmonary capillary wedge pressure (PPCW) and pulmonary artery pressure (PPA) but did not significantly change pulmonary blood volume (PBV). Left ventricular end-diastolic pressure and total cardiac volume both significantly (p < 0.005) decreased. Pulmonary vascular volume – pressure (V–P) relationships before and during isoproterenol were described by means of blood transfusions and hemorrhage. In individual dogs the PBV–PPCW and the PBV–(PPCW + PPA)/2 relationships were significantly shifted upward by isoproterenol (p < 0.05 or less); slope changes were variable. Pooled data from all dogs also showed a significant (p < 0.001) upward shift in the pulmonary vascular V–P relationship regardless of which measure of distending pressure was used. These results suggest that β-receptor stimulation by isoproterenol increases pulmonary vascular capacitance by increasing the unstressed volume.

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