Vasopressin, renin, and cortisol responses to hemorrhage during acute blockade of cardiac nerves in conscious dogs

1993 ◽  
Vol 265 (1) ◽  
pp. R220-R229 ◽  
Author(s):  
C. P. O'Donnell ◽  
L. C. Keil ◽  
T. N. Thrasher

The effect of acute cardiac nerve blockade (CNB) on the increases in plasma renin activity (PRA), arginine vasopressin (AVP), and cortisol in response to a 30 ml/kg hemorrhage was determined in conscious dogs (n = 9). Procaine was infused into the pericardial space to produce acute reversible CNB, or saline was infused in the control hemorrhage. Blood was removed from the inferior vena cava at a rate of 1 ml.kg-1.min-1. In the control hemorrhage, plasma AVP increased from 1.8 +/- 0.3 to 219 +/- 66 pg/ml, PRA increased from 0.63 +/- 0.20 to 3.08 +/- 0.91 ng angiotensin I (ANG I).ml-1.3 h-1, and cortisol increased from 1.4 +/- 0.2 to 4.0 +/- 0.7 micrograms/dl. When the hemorrhage was repeated during acute CNB, plasma AVP increased from 2.8 +/- 1.6 to 185 +/- 59 pg/ml, PRA increased from 0.44 +/- 0.14 to 2.24 +/- 0.27 ng ANG I.ml-1.3 h-1, and cortisol increased from 1.9 +/- 0.3 to 5.4 +/- 0.6 micrograms/dl, and none of the increases differed significantly from the responses during the control hemorrhage. Left atrial pressure fell significantly after removal of 6 ml/kg of blood, but mean arterial pressure was maintained at control levels until blood loss reached 20 ml/kg during pericardial infusion of either saline or procaine. The declines in MAP at the 30 ml/kg level of hemorrhage in both treatments were similar. These results demonstrate that acutely blocking input from cardiac receptors does not reduce the increases in plasma AVP, cortisol, and PRA in response to a 30 ml/kg hemorrhage. The results of this study do not support the hypothesis that input from cardiac receptors is required for a normal AVP response to hemorrhage and suggest that other receptors, presumably arterial baroreceptors, can stimulate AVP and cortisol secretion in the absence of signals from the heart.

2000 ◽  
Vol 278 (2) ◽  
pp. R469-R475 ◽  
Author(s):  
Terry N. Thrasher ◽  
Hong-Gen Chen ◽  
Lanny C. Keil

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.


1995 ◽  
Vol 268 (4) ◽  
pp. R1069-R1077 ◽  
Author(s):  
L. J. Andersen ◽  
J. L. Andersen ◽  
T. N. Thrasher ◽  
L. C. Keil ◽  
D. J. Ramsay

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)


1994 ◽  
Vol 266 (3) ◽  
pp. R714-R721 ◽  
Author(s):  
C. P. O'Donnell ◽  
C. J. Thompson ◽  
L. C. Keil ◽  
T. N. Thrasher

Hypovolemia activates reflexes that stimulate secretion of renin and arginine vasopressin (AVP). A large body of evidence, obtained mainly in anesthetized preparations, supports the hypothesis that unloading cardiac receptors stimulates increases in plasma AVP and renin activity (PRA). We have observed significant increases in PRA before any change in either mean arterial pressure (MAP) or pulse pressure in conscious dogs undergoing continuous hemorrhage; however, plasma AVP did not change until there was a significant fall in MAP. These results are compatible with the hypothesis that cardiac receptors cause reflex stimulation of renin but not AVP secretion. The aim of the present study was to test the hypothesis that a decrease in atrial pressure alone is sufficient to stimulate an increase in plasma AVP and PRA. Graded thoracic inferior vena caval constriction (TIVCC) was used to reduce atrial pressure in four steps without altering MAP in conscious dogs. In a fifth step, TIVCC was increased to cause a fall in MAP. A reduction in left atrial pressure (LAP) of 4.2 +/- 0.9 mmHg was accompanied by a significant (P < 0.05) increase in PRA from a control value of 0.4 +/- 0.1 ng angiotensin I (ANG I).ml-1.3 h-1 to 1.1 +/- 0.2 ng ANG I.ml-1.3 h-1 but no change in plasma AVP (from 1.0 +/- 0.1 to 1.2 +/- 0.2 pg/ml) or MAP (from 85 +/- 5 mmHg to 86 +/- 4 mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)


1992 ◽  
Vol 263 (5) ◽  
pp. R1071-R1077 ◽  
Author(s):  
D. H. Carr ◽  
D. B. Jennings ◽  
T. N. Thrasher ◽  
L. C. Keil ◽  
D. J. Ramsay

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.


1988 ◽  
Vol 255 (5) ◽  
pp. H1084-H1090
Author(s):  
H. S. Geller ◽  
D. P. Nyhan ◽  
H. M. Goll ◽  
P. W. Clougherty ◽  
B. B. Chen ◽  
...  

Our objective was to investigate the integrated pulmonary vascular response of conscious dogs to combined inhibition of the autonomic nervous system, arginine vasopressin (V1) receptors (vasopressinergic V1), and converting enzyme to identify the overall influence of these three major neurohumoral mechanisms in vascular regulation of the pulmonary circulation. Multipoint pulmonary vascular pressure-cardiac index (P/Q) plots were generated by graded constriction of the thoracic inferior vena cava, which produced stepwise decreases in Q. When compared with the P/Q relationship measured in intact conscious dogs, combined neurohumoral block resulted in active, nonflow-dependent pulmonary vasodilation. A second objective was to assess the extent to which cyclooxygenase pathway inhibition modified both the intact P/Q relationship and the pulmonary vasodilator response to combined neurohumoral block. Cyclooxygenase inhibition alone (either indomethacin or sodium meclofenamate) resulted in active, nonflow-dependent pulmonary vasoconstriction. Moreover, the pulmonary vasodilation in response to combined neurohumoral block was entirely abolished following cyclooxygenase inhibition. Thus the integrated pulmonary vascular response of conscious dogs to combined neurohumoral block is active vasodilation. This response appears to be mediated by metabolites of the cyclooxygenase pathway.


1981 ◽  
Vol 61 (3) ◽  
pp. 345-347 ◽  
Author(s):  
J. F. Liard ◽  
O. Dériaz ◽  
M. Tschopp ◽  
J. Schoun

1. Seven conscious dogs received arginine-vasopressin infusions (100 and 1000 fmol min−1 kg−1) through catheters implanted in the left vertebral artery or the inferior vena cava while arterial pressure, cardiac output (electromagnetic flowmeter) and heart rate were measured. 2. Despite similar increases in plasma vasopressin concentrations, intravertebral administration induced a lesser increase in mean arterial pressure and a greater decrease in heart rate than the same infusion given intravenously. 3. These results suggest that vasopressin has an effect on structures of the central nervous system involved in cardiovascular control, possibly by affecting the baroreceptor reflex.


2007 ◽  
Vol 15 (2) ◽  
pp. e28-e29
Author(s):  
Gino Di Manici ◽  
Davide Di Lazzaro ◽  
Giuliana Bardelli ◽  
Francesco Grasselli ◽  
Uberto Da Col ◽  
...  

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