Elevated cardiac pressure inhibits renin release after arterial hypotension in conscious dogs

1984 ◽  
Vol 247 (6) ◽  
pp. R953-R959 ◽  
Author(s):  
M. E. Lee ◽  
T. N. Thrasher ◽  
D. J. Ramsay
Keyword(s):  
Left Atrial ◽  
Dose Range ◽  
Plasma Renin ◽  
Ascending Aorta ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Renin Release ◽  
Right Atrial ◽  
Apparent Paradox ◽  
Systemic Hypotension

The relative roles of cardiopulmonary, sinoaortic, and renal baroreceptors in the regulation of plasma renin activity (PRA) were evaluated in dogs with chronically implanted cuffs around the ascending aorta proximal to the brachiocephalic artery, the abdominal aorta just proximal to both renal arteries, or both. Inflation of either cuff was adjusted to cause a reduction of distal arterial pressure and hence renal perfusion pressure (RPP) of 0, 5, 10, 20, or 30% of control for 1 h. Reduction of RPP by inflation of the suprarenal cuff (n = 4) led to a significant (P less than 0.05) increase in PRA throughout the dose range examined. However, constriction of the ascending aorta (n = 7) to cause identical reductions in RPP failed to increase PRA. The apparent paradox in these results may be explained by differential effects of the two maneuvers on left atrial pressure. Left atrial pressure increased dose dependently during inflation of the ascending aortic cuff but did not change during inflation of the suprarenal cuff. To determine if elevated right atrial pressure (RAP) would inhibit renin release after systemic hypotension, another group of dogs (n = 4) was prepared with cuffs around the pulmonary artery. Inflation of the pulmonary cuff to cause similar systemic hypotension led to significant (P less than 0.05) increases in PRA and RAP. Therefore we conclude that powerful inhibitory signals, arising from the left heart, can inhibit renin release in response to systemic hypotension.

Cardiac receptors, vasopressin, and corticosteroid release during arterial hypotension in dogs

1986 ◽  
Vol 251 (3) ◽  
pp. R614-R620
Author(s):  
M. E. Lee ◽  
T. N. Thrasher ◽  
L. C. Keil ◽  
D. J. Ramsay
Keyword(s):  
Left Atrial ◽  
Ascending Aorta ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Right Atrial ◽  
Apparent Paradox ◽  
Systemic Hypotension ◽  
Plasma Vasopressin ◽  
Brachiocephalic Trunk ◽  
Pulmonary Arterial

The relative roles of cardiopulmonary and sinoaortic baroreceptors in the regulation of vasopressin and corticosteroid release were evaluated in conscious dogs. The dogs were prepared with inflatable cuffs around either the ascending aorta, proximal to the brachiocephalic trunk, or the pulmonary artery. Inflation of the cuffs was adjusted to cause a reduction of mean systemic arterial pressure (MAP) of 0, 5, 10, 20, or 30% of control for 1 h in separate experiments. In spite of the profound systemic hypotension caused by constriction of the ascending aorta, plasma vasopressin failed to increase and corticosteroids increased only in response to a 30% decrease in MAP. In contrast, a 5% reduction in MAP during pulmonary arterial constriction increased plasma vasopressin and corticosteroid concentrations significantly. The apparent paradox in these results is correlated with different effects of the two maneuvers on left atrial pressure. Left atrial pressure increased dose dependently during inflation of the ascending aortic cuff but decreased during inflation of the pulmonary arterial cuff. In contrast, graded inflation of the pulmonary arterial cuff caused dose-dependent increases in right atrial pressure, plasma vasopressin, and corticosteroids. Therefore, we conclude that powerful inhibitory signals, arising from the left heart, can inhibit vasopressin and hypotension release in response to systemic hypotension.

Role of renal sympathetic nerves in renin inhibition by elevated left atrial pressure

1989 ◽  
Vol 256 (2) ◽  
pp. R413-R420
Author(s):  
D. A. Scheuer ◽  
T. N. Thrasher ◽  
D. J. Ramsay
Keyword(s):  
Left Atrial ◽  
Neural Control ◽  
Sympathetic Nerves ◽  
Sympathetic Tone ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Renin Release ◽  
Aortic Constriction ◽  
Systemic Hypotension ◽  
Renal Sympathetic

We have reported that the renin response to systemic hypotension during a simultaneous increase in left atrial pressure (LAP) depends, in part, on intact renal nerves. Because efferent neural control of renin release is mediated by renal sympathetic nerves, we tested the hypothesis that withdrawal of renal sympathetic tone is an essential component of the inhibitory mechanism. In conscious dogs, the ascending aorta was partially constricted to produce a simultaneous decrease, of up to 30%, in renal perfusion pressure (RPP) and a rise in LAP. Sympathetic neural control of renin release was reversibly blocked with propranolol. Propranolol infusion did not affect the increases in LAP or atrial natriuretic factor (ANF) during ascending aortic constriction. There was no increase in renin (P greater than 0.1) during ascending aortic constriction, with or without propranolol infusion. Identical reductions in RPP during constriction of the abdominal aorta caused renin to rise (P less than 0.03). Therefore acute withdrawal of renal sympathetic tone is not necessary for the inhibition of the renin response to systemic hypotension by elevated LAP.

Reference sites not influenced by hydrostatic pressure for right and left atrial pressures

1964 ◽  
Vol 207 (2) ◽  
pp. 357-360 ◽  
Author(s):  
George G. Armstrong ◽  
John C. Hancock
Keyword(s):  
Hydrostatic Pressure ◽  
Reference Point ◽  
Left Atrial ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Right Atrial ◽  
Lateral Border ◽  
Zero Reference ◽  
The Right ◽  
Made In

Simultaneous recordings of left and right atrial pressures made in dogs being rotated into all positions in space allowed the location of rotational axes where right or left atrial pressure became independent of hydrostatic pressure. Utilization of these axes as zero reference levels made possible the measurement of right or left atrial pressure without the influence of hydrostatic factors. The right zero reference point lay 62.8% of the distance from the manubrium to the xiphoid, 61.2% of the posterior to anterior thoracic diameter, and 47.7% of the greatest transverse thoracic diameter as measured from the right lateral border. The left atrial zero reference point lay 62.1% of the manubrium to xiphoid distance, 57.2% of the posterior to anterior diameter of thorax, and 53.0% of the greatest transverse thoracic diameter as measured from the right lateral border. When referred to the anatomy of the dog, these points lay in the immediate vicinity of the right and left atrioventricular valves, respectively.

Effect of diaphragm contraction on canine heart and pericardium

1983 ◽  
Vol 54 (5) ◽  
pp. 1261-1268 ◽  
Author(s):  
T. C. Lloyd ◽  
J. A. Cooper
Keyword(s):  
Cardiac Output ◽  
Left Atrial ◽  
Servo Control ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Abdominal Pressure ◽  
Canine Heart ◽  
Pressure Changes

Pericardiophrenic attachments transmit diaphragm contraction to the pericardium. We investigated this in two ways. 1) We replaced the hearts of externally perfused dogs with a balloon from which we measured pressure changes. Diaphragm contraction increased pressure from 4.6 to 5.5 Torr, equivalent to an isobaric volume decrease of 1.5%, and decreased volumetric compliance by 3%. 2) We selectively servo controlled right atrial pressure, left atrial pressure, or cardiac output in open-chest dogs and monitored the effect of diaphragm contraction on cardiovascular and abdominal pressures, cardiac output, and the volume of blood added to or withdrawn from the circulation to achieve servo control. Diaphragm contraction decreased left atrial pressure 0.4 Torr when right atrial pressure was controlled and right atrial pressure increased 0.2 Torr while controlling left atrial pressure, but there were no significant changes in cardiac output. Atrial pressure did not change significantly when output was controlled. Servo control required removal of approximately 50 ml of blood, presumably reflecting a decreased splanchnic vascular capacity at the higher abdominal pressure. We conclude that the diaphragm may slightly tense the pericardium, but this has no important primary effect on the heart.

Mechanism of inhibition of renin secretion by increased left atrial pressure

1985 ◽  
Vol 248 (5) ◽  
pp. R641-R644
Author(s):  
M. E. Lee ◽  
T. N. Thrasher ◽  
D. J. Ramsay
Keyword(s):  
Left Atrial ◽  
Renal Perfusion ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Renin Release ◽  
Left Heart ◽  
Efferent Pathway ◽  
Mechanism Of Inhibition ◽  
Potent Inhibition ◽  
Aortic Cuff

Experiments were designed to elucidate the mechanism of the failure of systemic hypotension to stimulate renin release in the presence of elevated left heart pressure. We conducted a series of graded ascending aortic and suprarenal cuff inflations in dogs with bilateral renal denervation (n = 5). The renal perfusion pressure (RPP) was reduced by 10, 20, and 30% of control by inflation of either cuff. Comparison of the renin response with inflation of the ascending aortic to the suprarenal cuff revealed a clear increase in the threshold required to elicit a renin response to graded reduction of RPP after inflation of the ascending aortic cuff. These results may be explained by differential effects of the two maneuvers on left heart pressure. Left atrial pressure increased during inflation of the ascending aortic cuff but did not change during inflation of the suprarenal cuff. Since the kidneys were denervated, the shift in threshold must be caused by a humoral substance(s). In conclusion, our findings suggest that the efferent pathway of potent inhibition of renin release from the left heart is mediated, at least partially, by a humoral substance.

Cardiovascular effects of increasing airway pressure in the dog

1977 ◽  
Vol 232 (1) ◽  
pp. H35-H43 ◽  
Author(s):  
S. M. Scharf ◽  
P. Caldini ◽  
R. H. Ingram
Keyword(s):  
Lung Volume ◽  
Airway Pressure ◽  
Left Atrial ◽  
Venous Return ◽  
Pressure Rise ◽  
Cardiovascular Effects ◽  
Atrial Pressure ◽  
Pleural Pressure ◽  
Left Atrial Pressure ◽  
Right Atrial

In paralyzed anesthetized dogs the cardiovascular effects of increasing positive end-expiratory pressure (PEEP) were explored under two conditions: a) end-expiratory lung volume increasing, b) end-expiratory lung volume kept nearly constant by matching pleural pressure rise to end-expiratory airway pressure rise. Two series of experiments were done: I) xenous return was allowed to fall, II) venous return was kept constant by infusion of volume. Right atrial pressure, pulmonary arterial pressure, and left atrial pressure increased under all conditions when measured relative to atmospheric pressure, but increased relative to pleural pressure only under condition a. The rise in left atrial relative to pleural pressure may indicate a degree of left ventricular dysfunction associated with increasing end-expiratory lung volume. Furthermore, when end-expiratory lung volume increased, inequality of the rise in pulmonary artery wedge pressure exceeded the rise in left atrial pressure in series I. From plots of cardiac output as a function of right atrial pressure it was possible to conclude that the decrease in venous return is partially offset by an increase in mean circulatory pressure.

Action of Digitalis on the Nonfailing Heart of the Dog

1957 ◽  
Vol 192 (1) ◽  
pp. 114-120 ◽  
Author(s):  
Marion deV. Cotten ◽  
Phyllis E. Stopp
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Left Atrial ◽  
Venous Return ◽  
Contractile Force ◽  
Left Ventricular ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Right Atrial ◽  
Stroke Work

Ouabain induces a moderate increase in the contractility of the nonfailing heart of the dog with a complete circulatory system in doses which do not produce electrocardiographic signs of digitalis intoxication. The increased contractility was demonstrated both by the increase in ventricular contractile force and by the higher ventricular function curves obtained after administration of ouabain. The drug also increased systemic peripheral resistance and blood pressure, decreased systemic output, heart rate, left and right atrial pressures, and produced only small, variable changes in left ventricular stroke work. The reduction in systemic output and left atrial pressure and the absence of substantial changes in stroke work after ouabain appeared to be the result of a decrease in venous return to the heart. Evidence for this interpretation was obtained from experiments in which left atrial pressure was kept constant during the actions of ouabain by infusing 100–300 cc of whole blood. Under these conditions, ouabain brought about moderate increases in systemic output and left ventricular stroke work as well as in contractile force even though the changes in heart rate and blood pressure were comparable to those obtained in experiments in which left atrial pressure was uncontrolled. The data presented indicate that ouabain has two primary hemodynamic effects in the normal animal, namely, a direct cardiac stimulant action and a peripheral action resulting in a decreased venous return. The relationship of these findings to the mechanism of action of digitalis in congestive heart failure is discussed.

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)

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