Effects of baroreceptor denervation on endocrine and drinking responses to caval constriction in dogs

1990 ◽  
Vol 259 (3) ◽  
pp. R618-R626 ◽  
Author(s):  
E. W. Quillen ◽  
L. C. Keil ◽  
I. A. Reid
Keyword(s):  
Inferior Vena ◽  
Plasma Renin ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Plasma Norepinephrine ◽  
Inferior Vena Caval ◽  
Plasma Angiotensin ◽  
Access To Water ◽  
Plasma Arginine

Plasma arginine vasopressin (AVP), plasma renin activity (PRA), and water intake (H2OIN) are increased by thoracic inferior vena caval constriction (TIVCC). To assess the role of the cardiac and sinoaortic baroreceptors in these responses, 9 sham-, 10 cardiac-(CD), 6 sinoaortic-(SAD), and 4 combined cardiac and sinoaortic-(CD + SAD) denervated conscious dogs were studied. All animals were studied while normally hydrated 1) with no access to water (H2O-) and 2) while drinking was permitted (H2O+). TIVCC caused similar reductions (P less than 0.001) of mean arterial (-32 +/- 4 mmHg), left atrial pressure (-6.5 +/- 1.1 cmH2O), and right atrial pressure (-4.2 +/- 0.8 cmH2O) in all groups. After TIVCC in sham dogs with H2O-, AVP increased from 3.6 +/- 0.7 to 72.8 +/- 12.6 pg/ml (P less than 0.001). AVP was similar with SAD (57.1 +/- 6.9) but was reduced with CD (30.9 +/- 3.0) and CD + SAD (17.7 +/- 4.0). In all groups, PRA increased from 4.5 +/- 0.7 to 23.8 +/- 3.0 ng.ml-1 x 3 h-1 and plasma angiotensin II (ANG II) increased from 14.0 +/- 2.8 to 59.5 +/- 13.0 pg/ml (P less than 0.001). Plasma adrenocorticotropic hormone (ACTH) increased similarly in all groups (55 +/- 5 to 128 +/- 25 pg/ml). Plasma norepinephrine (NE) levels increased similarly in all groups (298 +/- 61 to 654 +/- 88 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Role of right heart receptors in the control of renin, vasopressin, and cortisol secretion in dogs

1992 ◽  
Vol 263 (5) ◽  
pp. R1071-R1077 ◽  
Author(s):  
D. H. Carr ◽  
D. B. Jennings ◽  
T. N. Thrasher ◽  
L. C. Keil ◽  
D. J. Ramsay
Keyword(s):  
Inferior Vena ◽  
Vena Cava ◽  
Plasma Renin ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Heart ◽  
Hormonal Responses ◽  
The Right ◽  
Maximal Reduction

We have reported that increased left heart pressure inhibits increases in plasma renin activity (PRA), arginine vasopressin (AVP), and cortisol during arterial hypotension. The goal of this study was to determine whether increases in right heart pressure also inhibited hormonal responses to hypotension. Seven dogs were chronically instrumented with inflatable cuffs around the ascending aorta (AA), the pulmonary artery (PA), and the thoracic inferior vena cava (IVC), as well as with catheters in both atria, the abdominal aorta, and vena cava. The IVC, the PA, and the AA cuffs were inflated on different days to cause step reductions in mean arterial pressure (MAP) of 5, 10, 20, and 30% below control MAP. Graded constriction of the AA caused large increases in left atrial pressure and plasma atrial natriuretic peptide (ANP), but had no effect on plasma AVP or cortisol and caused only a small increase in PRA at the maximal reduction of MAP. Constriction of the IVC reduced both atrial pressures and plasma ANP, but stimulated increases in PRA, AVP, and cortisol. Constriction of the PA increased right atrial pressure and plasma ANP and caused increases in plasma AVP and cortisol that were similar to responses during IVC constriction, but the PRA response was only half (P < 0.05). These results indicate that increasing pressure on the right side of the heart can attenuate the PRA response to hypotension, and suggest that the inhibition is mediated by the rise in plasma ANP.

Left heart and arterial baroreceptors interact in control of plasma vasopressin, renin, and cortisol in awake dogs

1994 ◽  
Vol 266 (3) ◽  
pp. R879-R888 ◽  
Author(s):  
J. L. Andersen ◽  
L. J. Andersen ◽  
T. N. Thrasher ◽  
L. C. Keil ◽  
D. J. Ramsay
Keyword(s):  
Vena Cava ◽  
Plasma Renin ◽  
Significant Rise ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Arterial Hypotension ◽  
Left Heart ◽  
Arterial Baroreceptors ◽  
Plasma Arginine ◽  
Stimulation Of

Arterial hypotension induced by constriction of the ascending aorta (AA) causes increases in left atrial pressure (LAP) and plasma atrial natriuretic peptide (ANP), but no change in plasma arginine vasopressin (AVP), plasma renin activity (PRA), or cortisol. In the present study, we tested the hypothesis that the rise in left heart pressure during constriction of the AA suppressed the stimulation of AVP, renin, and cortisol secretion in response to arterial hypotension. Dogs were prepared with inflatable cuffs around the AA, the pulmonary artery (PA), and the thoracic inferior vena cava (IVC) and with catheters in the left and right atria and abdominal aorta. In one series of experiments, the AA was constricted to lower mean arterial pressure (MAP) 10 or 20% below control for 15 min. Then, either the PA or the IVC was constricted to bring LAP back to control levels but without altering the degree of arterial hypotension. Constriction of the AA alone led to significant increases in LAP and plasma ANP but no change in plasma AVP, cortisol, or PRA. Reducing LAP to control levels by constriction of either the PA or IVC led to significant and similar increases in plasma AVP, cortisol, and PRA. Plasma ANP fell significantly 10 min after LAP was normalized by constriction of the IVC but not when LAP was normalized by constriction of the PA, because PA constriction caused a significant rise in right atrial pressure that stimulated ANP secretion. The increases in plasma AVP and PRA after normalizing LAP by constriction of the PA were compared with the increases obtained during identical falls in MAP induced by constriction of the IVC alone, a maneuver that lowers LAP below control. The increases in plasma AVP in the two conditions were identical, indicating that the stimulation of left heart baroreceptors alone can account for the suppression of AVP secretion in response to unloading arterial baroreceptors. In contrast, there was a greater rise in PRA during hypotension caused by constriction of the IVC alone compared with the condition in which LAP was normalized but plasma ANP remained elevated. This suggests that increased left heart pressure inhibits renin secretion in response to arterial hypotension by reflex mechanisms and by increased plasma ANP concentration.

Arterial baroreceptors control plasma vasopressin responses to graded hypotension in conscious dogs

2000 ◽  
Vol 278 (2) ◽  
pp. R469-R475 ◽  
Author(s):  
Terry N. Thrasher ◽  
Hong-Gen Chen ◽  
Lanny C. Keil
Keyword(s):  
Inferior Vena ◽  
Control Period ◽  
Vena Cava ◽  
Plasma Renin ◽  
Conscious Dogs ◽  
Inferior Vena Caval ◽  
Arterial Baroreceptors ◽  
Treatment Conditions ◽  
The Individual

We studied the role of cardiac and arterial baroreceptors in the reflex control of arginine vasopressin (AVP) and renin secretion during graded hypotension in conscious dogs. The dogs were prepared with Silastic cuffs on the thoracic inferior vena cava and catheters in the pericardial space. Each experiment consisted of a control period followed by four periods of inferior vena caval constriction, during which mean arterial pressure (MAP) was reduced in increments of ∼10 mmHg. The hormonal responses were measured in five dogs under four treatment conditions: 1) intact, 2) acute cardiac denervation (CD) by intrapericardial infusion of procaine, 3) after sinoaortic denervation (SAD), and 4) during combined SAD+CD. The individual slopes relating MAP to plasma AVP and plasma renin activity (PRA) were used to compare the treatment effects using a 2 × 2 factorial analysis. There was a significant ( P < 0.01) effect of SAD on the slope relating plasma AVP to MAP but no effect of CD and no SAD × CD interaction. In contrast, the slope relating PRA and MAP was increased ( P < 0.05) by SAD but was not affected by CD. These results support the hypothesis that stimulation of AVP secretion in response to graded hypotension is primarily driven by unloading arterial baroreceptors in the dog.

Effect of inspiration on inferior vena caval blood flow in dogs

1983 ◽  
Vol 55 (6) ◽  
pp. 1701-1708 ◽  
Author(s):  
T. C. Lloyd
Keyword(s):  
Inferior Vena ◽  
Vena Cava ◽  
Iliac Vein ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Hepatic Veins ◽  
Base Line ◽  
Inferior Vena Caval ◽  
Constant Rate ◽  
Inferior Vena Cava Flow

Inferior vena cava flow of anesthetized open-chest dogs was drained to a reservoir from a cannula above the diaphragm and returned to the atrium at constant rate. At selected base-line caval pressures, the caval flow and pressures in the abdomen (Pab), iliac vein (Piv), and downstream cavae (Pvc) were recorded during spontaneous breathing, cyclic phrenic nerve stimulation, and cyclic lowering of caval drain pressure. Each augmented flow unless Pab exceeded Pvc by at least ca. 5 cmH2O. In other dogs a cannulating flow probe was placed in the thoracic inferior cava and the chest was reclosed. Flow was augmented throughout most or all of spontaneous inspiration and was never depressed even though Pab exceeded right atrial pressure and Piv. I conclude that the collapse of hepatic veins and proximate cava does not occur at most normal pressures and a Starling resistor analog of abdominal veins based solely on abdominal and venous pressures is inappropriate. Both falling atrial pressure and rising Pab probably augment inspiratory abdominal venous return.

Right atrial pressure as measure of ventricular constraint in newborn lambs

2001 ◽  
Vol 280 (6) ◽  
pp. H2740-H2745
Author(s):  
Jean-Claude Fauchère ◽  
Adrian M. Walker ◽  
Elizabeth M. Skuza ◽  
Daniel A. Grant
Keyword(s):  
Inferior Vena ◽  
Filling Pressure ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Positive End Expiratory Pressure ◽  
Inferior Vena Caval ◽  
Sick Newborn ◽  
Pericardial Pressure ◽  
Strong Linear Relationship

Although the lungs and pericardium constrain the heart and limit cardiac output, no method exists to assess this constraint in sick newborns. We hypothesize that a useful estimate of ventricular constraint may be obtained by measuring right atrial pressure (PRA) in the newborn. To test this hypothesis, we measured PRA, thoracic inferior vena caval pressure (PIVC; saline-filled catheters), and ventricular constraint (pericardial pressure, PPER; liquid-containing balloon) in 4-wk-old (neonatal, n = 12) and 3-day-old (newborn, n = 6) anesthetized lambs. The measurements were made while LV filling pressure was altered (0–20 mmHg) and while positive end-expiratory pressure (PEEP) was maintained at 2.5 or 15 cmH2O. In all of the lambs, a strong linear relationship ( r) existed between PRA and PPER(PRA = 1.19 PPER + 0.0, r = 0.99) and between PIVC and PPER (PIVC = 1.24 PPER + 0.1, r = 0.99; PEEP of 2.5 cmH2O). Similar relationships were also observed with increased PEEP (PRA = 1.29 PPER−1.2, r = 0.98 and PIVC = 1.32 PPER−1.2, r = 0.97). Because PRA provides an accurate measure of ventricular constraint in the normal lamb, it may be a useful measure of ventricular constraint in the sick newborn.

Hemodynamic, gas exchange, and hormonal consequences of LBPP during PEEP ventilation

1987 ◽  
Vol 62 (1) ◽  
pp. 61-70 ◽  
Author(s):  
D. M. Payen ◽  
C. J. Brun-Buisson ◽  
P. A. Carli ◽  
Y. Huet ◽  
F. Leviel ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Control Level ◽  
Plasma Renin ◽  
Significant Rise ◽  
Right Atrial ◽  
Positive Pressure ◽  
Plasma Norepinephrine ◽  
Lower Body Positive Pressure ◽  
Plasma Arginine ◽  
Peep Ventilation

Hemodynamic, gas exchange, and hormonal response induced by application of a 25- to 40-mmHg lower body positive pressure (LBPP), during positive end-expiratory pressure (PEEP; 14 +/- 2.5 cmH2O) were studied in nine patients with acute respiratory failure. Compared with PEEP alone, LBPP increased cardiac index (CI) from 3.57 to 4.76 l X min-1 X m-2 (P less than 0.001) in relation to changes in right atrial pressure (RAP) (11 to 16 mmHg; P less than 0.01). Cardiopulmonary blood volume (CPBV) measured in five patients increased during LBPP from 546 +/- 126 to 664 +/- 150 ml (P less than 0.01), with a positive linear relationship between changes in RAP and CPBV (r = 0.88; P less than 0.001). Venous admixture (Qva/QT) decreased with PEEP from 24 to 16% (P less than 0.001) but did not change with LBPP despite the large increase in CI, leading to a marked O2 availability increase (P less than 0.001). Although PEEP induced a significant rise in plasma norepinephrine level (NE) (from 838 +/- 97 to 1008 +/- 139 pg/ml; P less than 0.05), NE was significantly decreased by LBPP to control level (from 1,008 +/- 139 to 794 +/- 124 pg/ml; P less than 0.003). Plasma epinephrine levels were not influenced by PEEP or LBPP. Changes of plasma renin activity (PRA) paralleled those of NE. No change in plasma arginine vasopressin (AVP) was recorded. We concluded that LBPP increases venous return and CPBV and counteracts hemodynamic effects of PEEP ventilation, without significant change in Qva/QT. Mechanical ventilation with PEEP stimulates sympathetic activity and PRA apparently by a reflex neuronal mechanism, at least partially inhibited by the loading of cardiopulmonary low-pressure reflex and high-pressure baroreflex. Finally, AVP does not appear to be involved in the acute cardiovascular adaptation to PEEP.

Effect of loading right atrial and ventricular receptors on stimulated AVP, ACTH, and renin secretion in awake dogs

1995 ◽  
Vol 268 (4) ◽  
pp. R1069-R1077 ◽  
Author(s):  
L. J. Andersen ◽  
J. L. Andersen ◽  
T. N. Thrasher ◽  
L. C. Keil ◽  
D. J. Ramsay
Keyword(s):  
Mean Arterial Pressure ◽  
Left Atrial ◽  
Adrenocorticotropic Hormone ◽  
Inferior Vena ◽  
Vena Cava ◽  
Plasma Renin ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Heart ◽  
The Right

The goal of this study was to test the hypothesis that increasing or decreasing the load on baroreceptors in the right heart influenced the secretion of arginine vasopressin (AVP), adrenocorticotropic hormone (ACTH), and renin during a state of sustained arterial hypotension. The hypothesis was tested in chronically instrumented conscious dogs prepared with inflatable cuffs around the pulmonary artery (PA) and the thoracic inferior vena cava (IVC). In one protocol (n = 5), mean arterial pressure was reduced 10 or 20% below control by constriction of the PA, a maneuver that caused a fall in left atrial pressure (LAP) and an increase in right atrial pressure (RAP). Plasma AVP, ACTH, atrial natriuretic peptide (ANP), and plasma renin activity (PRA) all increased (P < 0.05) in response to constriction of the PA. Reducing RAP to control by constriction of the IVC during maintained constriction of the PA had no effect on MAP, LAP, plasma AVP, ACTH, or PRA, but plasma ANP fell significantly. In a separate protocol (n = 4), constriction of the IVC was used to reduce MAP 10 or 20% below control, and this led to significant decreases in both LAP and RAP and increases in plasma AVP, ACTH, and PRA. RAP was then increased above control by constriction of the PA without altering either MAP or LAP. Raising RAP from a level that was 6.3 +/- 1.3 mmHg below control to 3.5 +/- 1.0 mmHg above control had no effect on plasma AVP, ACTH, or PRA.(ABSTRACT TRUNCATED AT 250 WORDS)

Vasopressin and renin responses to hemorrhage in conscious, cardiac-denervated dogs

1983 ◽  
Vol 245 (3) ◽  
pp. H399-H405 ◽  
Author(s):  
B. C. Wang ◽  
W. D. Sundet ◽  
M. O. Hakumaki ◽  
K. L. Goetz
Keyword(s):  
Dominant Role ◽  
Plasma Renin ◽  
Aortic Pressure ◽  
Conscious Dogs ◽  
Right Atrial ◽  
Pulmonary Arterial ◽  
Left And Right ◽  
Plasma Arginine ◽  
Cardiac Receptors

We measured plasma arginine vasopressin (AVP) and plasma renin activity (PRA) during continuous hemorrhage in cardiac-denervated and sham-operated conscious dogs. Hemorrhage produced comparable decreases in aortic pressure, cardiac output, stroke volume, pulmonary arterial pressure, and left and right atrial pressures in each group of dogs. After 10 ml blood/kg body wt had been removed, AVP was increased in sham-operated dogs (P less than 0.05) but not in cardiac-denervated dogs. After 20 and 30 ml blood/kg body wt had been removed, AVP was increased in all dogs, but the response was markedly attenuated in cardiac-denervated dogs. Hemorrhage at 10 and 20 ml/kg caused comparable increases in PRA in each group of dogs. However, at 30 ml/kg hemorrhage the increase in PRA was significantly higher in cardiac-denervated dogs than in sham-operated dogs. Our results suggest that cardiac receptors play a dominant role in mediating the release of AVP during hemorrhage in conscious dogs. In contrast, we found no evidence for a dominant role of cardiac receptors in mediating renin secretion during hemorrhage.

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