Influence of the renal nerves on sodium excretion during progressive reductions in cardiac output

1995 ◽  
Vol 269 (3) ◽  
pp. R678-R690 ◽  
Author(s):  
T. E. Lohmeier ◽  
G. A. Reinhart ◽  
H. L. Mizelle ◽  
J. P. Montani ◽  
R. Hester ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Sodium Excretion ◽  
Pressure Control ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Renal Nerves ◽  
Sodium Retention

The purpose of this study was to elucidate the role of the renal nerves in promoting sodium retention during chronic reductions in cardiac output. In five dogs, the left kidney was denervated and the urinary bladder was surgically divided to allow separate 24-h urine collection from the innervated and denervated kidneys. Additionally, progressive reductions in cardiac output were achieved by employing an externally adjustable occluder around the pulmonary artery and by servo-controlling right atrial pressure (control = 0.9 +/- 0.2 mmHg) at 4.7 +/- 0.1, 7.5 +/- 0.1, and 9.8 +/- 0.2 mmHg for 3 days at each level. At the highest level of right atrial pressure, the 24-h values for mean arterial pressure (control = 97 +/- 3 mmHg) and cardiac output (control = 2,434 +/- 177 ml/min) were reduced approximately 25 and 55%, respectively; glomerular filtration rate fell by approximately 35% and renal plasma flow by approximately 65%. However, despite the sodium retention induced by these hemodynamic changes, there were no significant differences in renal hemodynamics or sodium excretion between the two kidneys during pulmonary artery constriction. In contrast, after release of the pulmonary artery occluder on day 9, sodium excretion increased more (approximately 28% during the initial 24 h) in innervated than in denervated kidneys. These results suggest that the renal nerves are relatively unimportant in promoting sodium retention in this model of low cardiac output but contribute significantly to the short-term elimination of sodium after partial restoration of cardiac output and mean arterial pressure.

What Goes Around Comes Around—Venous Return

2011 ◽  
pp. 48-54
Author(s):  
James R. Munis
Keyword(s):  
Cardiac Output ◽  
Steady State ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cardiovascular System ◽  
Venous Return ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Interconnected System ◽  
The Mean

By its nature, circulatory physiology is also susceptible to circular reasoning because every part of an interconnected system is affected by, and affects, every other part. If we're not careful, we end up saying things like ‘venous return equals cardiac output’ when, in the steady state, that is true by definition and nothing new is gained. If we grant that right atrial pressure (PRA) is the ‘downstream’ pressure for venous return, then it follows that PRA should be inversely related to venous return (and therefore, to cardiac output). If we simply apply Ohm's law to the cardiovascular system, we forget that the mean arterial pressure not only contributes to venous return but also is sustained by venous return. If venous return fails for any other reason (unrelated to arterial pressure), so too will mean arterial pressure eventually fail.

Hemodynamic studies in DOCA-salt hypertensive rats after opening of an arteriovenous fistula

1992 ◽  
Vol 262 (6) ◽  
pp. H1802-H1808 ◽  
Author(s):  
M. Huang ◽  
R. L. Hester ◽  
A. C. Guyton ◽  
R. A. Norman
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Hypertensive Rats

We determined the cardiovascular responses in normal and deoxycorticosterone acetate (DOCA)-salt hypertensive rats with reduced total peripheral resistance due to an arteriovenous (a-v) fistula. Animals were divided into four groups: control, fistula, DOCA-salt, and DOCA-salt fistula. The fistula was made by anastomosing the aorta and vena cava below the renal arteries. Four weeks after the creation of the fistula both DOCA-salt and DOCA-salt fistula animals received DOCA and salt for 6–8 wk. At the end of 10–12 wk we measured mean arterial pressure, cardiac output, tissue flows, and right atrial pressure. Flow measurements using radioactive microspheres were made in anesthetized animals. Cardiac index (CI) was 202% higher in the fistula group than in the control animals and 165% higher in the DOCA-salt fistula than in the DOCA-salt animals. There was no difference in cardiac output between the control and DOCA-salt animals. The increase in cardiac output was due to the fistula flow as evidenced by a significant increase in the number of microspheres in the lung. Mean arterial pressure was 115 +/- 4 mmHg (control) and 108 +/- 5 mmHg (fistula) in non-DOCA rats but increased in both DOCA groups, 159 +/- 3 mmHg (DOCA-salt) and 145 +/- 5 mmHg (DOCA-salt fistula). Right atrial pressure was increased above control in both fistula animals but was normal in DOCA-salt animals. Total peripheral resistance (TPR) was higher than control in DOCA-salt animals, but TPR in both the fistula and DOCA-salt fistula animals was lower than control.(ABSTRACT TRUNCATED AT 250 WORDS)

Increased cardiac output following occlusion of the descending thoracic aorta in dogs

1982 ◽  
Vol 243 (1) ◽  
pp. R152-R158 ◽  
Author(s):  
J. K. Stene ◽  
B. Burns ◽  
S. Permutt ◽  
P. Caldini ◽  
M. Shanoff
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Thoracic Aorta ◽  
Vascular System ◽  
Superior Vena ◽  
Vena Cava ◽  
Right Atrial ◽  
Mean Systemic Pressure ◽  
Extracorporeal Bypass

Occlusion of the thoracic aorta (AO) in dogs with a constant volume right ventricular extracorporeal bypass increased cardiac output (Q) by 43% and mean arterial pressure by 46%, while mean systemic pressure (MSP) was unchanged. We compared AO with occlusion of the brachiocephalic and left subclavian arteries (BSO) which decreased cardiac output by 5%, increased mean arterial pressure by 32%, and increased MSP by 11%. We feel these results confirm that AO elevates preload by transferring blood volume from the splanchnic veins to the vascular system drained by the superior vena cava. If the heart is competent to keep right arterial pressure at or near zero, this increase in preload will elevate Q above control levels. Comparing our data with results of other authors who have not controlled right atrial pressure, emphasizes the importance of a competent right ventricle in allowing venous return to determine Q.

The Effects of Increasing Plasma Concentrations of Dexmedetomidine in Humans

2000 ◽  
Vol 93 (2) ◽  
pp. 382-394 ◽  
Author(s):  
Thomas J. Ebert ◽  
Judith E. Hall ◽  
Jill A. Barney ◽  
Toni D. Uhrich ◽  
Maelynn D. Colinco
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Plasma Concentrations ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Central Venous ◽  
Pressor Test

Background This study determined the responses to increasing plasma concentrations of dexmedetomidine in humans. Methods Ten healthy men (20-27 yr) provided informed consent and were monitored (underwent electrocardiography, measured arterial, central venous [CVP] and pulmonary artery [PAP] pressures, cardiac output, oxygen saturation, end-tidal carbon dioxide [ETCO2], respiration, blood gas, and catecholamines). Hemodynamic measurements, blood sampling, and psychometric, cold pressor, and baroreflex tests were performed at rest and during sequential 40-min intravenous target infusions of dexmedetomidine (0.5, 0.8, 1.2, 2.0, 3.2, 5.0, and 8.0 ng/ml; baroreflex testing only at 0.5 and 0.8 ng/ml). Results The initial dose of dexmedetomidine decreased catecholamines 45-76% and eliminated the norepinephrine increase that was seen during the cold pressor test. Catecholamine suppression persisted in subsequent infusions. The first two doses of dexmedetomidine increased sedation 38 and 65%, and lowered mean arterial pressure by 13%, but did not change central venous pressure or pulmonary artery pressure. Subsequent higher doses increased sedation, all pressures, and calculated vascular resistance, and resulted in significant decreases in heart rate, cardiac output, and stroke volume. Recall and recognition decreased at a dose of more than 0.7 ng/ml. The pain rating and mean arterial pressure increase to cold pressor test progressively diminished as the dexmedetomidine dose increased. The baroreflex heart rate slowing as a result of phenylephrine challenge was potentiated at both doses of dexmedetomidine. Respiratory variables were minimally changed during infusions, whereas acid-base was unchanged. Conclusions Increasing concentrations of dexmedetomidine in humans resulted in progressive increases in sedation and analgesia, decreases in heart rate, cardiac output, and memory. A biphasic (low, then high) dose-response relation for mean arterial pressure, pulmonary arterial pressure, and vascular resistances, and an attenuation of the cold pressor response also were observed.

Cardiovascular function and norepinephrine-thermogenesis in cold-acclimatized rats

1963 ◽  
Vol 204 (5) ◽  
pp. 888-894 ◽  
Author(s):  
Eugene Evonuk ◽  
John P. Hannon
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Room Temperature ◽  
Metabolic Response ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Systemic Resistance

The cardiovascular and metabolic actions of norepinephrine (NE) and their inter-relationships were studied at normal room temperature in anesthetized, warm-acclimatized (W-A) (26 ± 1 C) and cold-acclimatized (C-A) (3 ± 1 C) rats. The cardiac output, heart rate, stroke volume, arterial pressure, right atrial pressure, and systemic resistance were measured prior to NE infusion; during NE infusion (2 µg/min) at the 25, 50, 75, and 100% levels of increased metabolism; and after infusion of NE had ceased. Norepinephrine caused a greater increase in the cardiac output, heart rate, stroke volume, and right atrial pressure in the C-A animals than it did in W-A animals. During the early metabolic response to NE (i.e., up to 25% increase in O2 consumption) there was a marked increase in the arterial pressure of both W-A and C-A rats, with the latter showing the greater maximum response. Beyond the 25% level of increased metabolism the arterial pressure and concomitantly the systemic resistance of the C-A animals declined sharply to the preinfusion levels where they remained throughout the course of infusion. In contrast to this, the arterial pressure and systemic resistance of the W-A animals remained high. It was concluded that norepinephrine-calorigenesis in the C-A rat is supported by a greater capacity to increase the cardiac output and an ability to preferentially reduce the systemic resistance to actively metabolizing areas (i.e., the viscera).

Vagally mediated regulation of renal function in conscious primates

1986 ◽  
Vol 250 (4) ◽  
pp. H546-H549
Author(s):  
S. F. Vatner ◽  
W. T. Manders ◽  
D. R. Knight
Keyword(s):  
Renal Function ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Rhesus Monkeys ◽  
Volume Expansion ◽  
Urine Flow ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Water Excretion

The effects of vagal denervation (VD) were examined on responses of Na+ and water excretion to acute volume expansion (18 ml/kg of 6% dextran in saline) in six conscious rhesus monkeys with chronic sinoaortic denervation (SAD). After SAD, volume expansion increased mean arterial pressure (from 95 +/- 6.6 to 119 +/- 7.5 mmHg), right atrial pressure (from 1.3 +/- 0.7 to 5.9 +/- 1.8 mmHg), urine flow (from 0.08 +/- 0.01 to 0.68 +/- 0.20 ml/min), and Na+ excretion (from 1.30 +/- 0.45 to 29.51 +/- 10.40 mueq/min). After VD, volume expansion increased mean arterial and right atrial pressures similarly, but induced significantly lower (P less than 0.05) increases in urine flow (from 0.05 +/- 0.01 to 0.19 +/- 0.03 ml/min) and Na+ excretion (from 0.87 +/- 0.27 to 11.50 +/- 6.13 mueq/min). Thus vagal mechanisms appear to play an important role in mediating excretion of Na+ and water in response to acute volume expansion in the conscious primate.

Effects of steps in cardiac output and arterial pressure in awake dogs with AV block

1989 ◽  
Vol 256 (2) ◽  
pp. H361-H367 ◽  
Author(s):  
D. S. O'Leary ◽  
A. M. Scher ◽  
J. E. Bassett
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Control Period ◽  
Peripheral Resistance ◽  
Pressure Control ◽  
Low Pressure ◽  
Atrial Rate ◽  
Initial Control ◽  
Pressure Control System

In awake dogs with atrioventricular block, we examined the responses in total peripheral resistance and atrial rate to square-wave changes in mean arterial pressure or cardiac output. We compared the responses 2-3 min after a step change with the responses 19-20 min after a step. With resetting of arterial pressure control, the compensatory responses should decrease as the baroreceptors reset to the prevailing pressure. With step changes in mean arterial pressure or cardiac output, the responses in both peripheral resistance and atrial rate increased from minutes 2-3 to minutes 19-20. The responses in peripheral resistance also increased in animals studied after bilateral vagal block. All of the above changes were significant in the majority of cases. In another experiment, the animals were "conditioned" by 20 min at imposed high or low pressure. When control was returned to the animal after conditioning at high pressure, arterial pressure was not significantly different (P greater than 0.05) from the initial control levels. When control was returned after conditioning at low pressure, arterial pressure was significantly greater (P less than 0.05) than during the initial control period. These results indicate an absence of resetting of the entire arterial pressure control system.

Hemodynamic responses to acute volume expansion in Dahl salt-sensitive rats

1991 ◽  
Vol 260 (1) ◽  
pp. R32-R38
Author(s):  
R. S. Reddy ◽  
C. Baylis ◽  
T. A. Kotchen
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Volume Expansion ◽  
Peripheral Resistance ◽  
Extracellular Fluid ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Hemodynamic Responses ◽  
Cardiopulmonary Baroreflex

The purpose of this study is to evaluate hemodynamic responses to acute volume expansion in chronically instrumented, conscious Dahl salt-sensitive (Dahl-S) and Dahl salt-resistant (Dahl-R) rats that have been maintained on either 0.45% NaCl, 1% NaCl, or 7% NaCl (5 days) intakes. Total peripheral resistance (TPR), but not arterial pressure, was increased by 5 days of 7% NaCl in Dahl-S (P less than 0.05) but not in Dahl-R. In Dahl-S, but not in Dahl-R, right atrial pressure increased with increasing dietary NaCl (P less than 0.05). On the 0.45% NaCl intake, atrial pressure did not differ in the two strains, whereas on both the 1 and 7% NaCl diets atrial pressure was higher in Dahl-S than in Dahl-R (P less than 0.05). In response to acute extracellular fluid volume expansion, arterial pressure did not change, and cardiac output increased in Dahl-S and in Dahl-R. On the 0.45% NaCl intake, TPR decreased (P less than 0.01) similarly in response to volume expansion in both strains; however, on the 1% NaCl intake TPR decreased in Dahl-R (P less than 0.05) but not in Dahl-S. In contrast, in animals fed 7% NaCl for 5 days, TPR decreased acutely in Dahl-S (P less than 0.01) but not in Dahl-R. These observations suggest that cardiopulmonary baroreflex activity is impaired in Dahl-S on a 1% NaCl intake, possibly as a consequence of elevated right atrial pressure. This alteration of the cardiopulmonary baroreflex may contribute to increased TPR in Dahl-S on a high-NaCl intake.

Systemic hemodynamic effects of leukotrienes C4 and D4 in the rat

1983 ◽  
Vol 244 (4) ◽  
pp. H628-H633 ◽  
Author(s):  
M. A. Pfeffer ◽  
J. M. Pfeffer ◽  
R. A. Lewis ◽  
E. Braunwald ◽  
E. J. Corey ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Right Atrial ◽  
Moderate Pressure ◽  
Hemodynamic Effects ◽  
Systemic Hemodynamic ◽  
Leukotriene D4

Although local administration of the sulfidopeptide leukotrienes into cutaneous and coronary vascular beds indicates that these naturally occurring metabolites of arachidonic acid are vasoconstrictors, their systemic administration has produced both pressor and depressor responses. The systemic hemodynamic effects of intravenous leukotriene C4 (LTC4) and leukotriene D4 (LTD4) were assessed in ether-anesthetized rats and compared with the effects produced by equimolar doses (2 X 10(-10) to 4 X 10(-8) mol/kg) of norepinephrine and angiotensin. Mean arterial pressure, right atrial pressure, and cardiac output (electromagnetic flowmetry) were recorded during bolus administrations of these vasoactive compounds. LTC4 and LTD4 had similar hemodynamic effects that were characterized by moderate pressure elevations produced by dose-dependent increases in total peripheral resistance, since cardiac output declined. Although the peak mean arterial pressure levels produced by LTC4 and LTD4 (135 +/- 7 and 129 +/- 5 mmHg, respectively) were less than those by norepinephrine (157 +/- 3 mmHg) and angiotensin (174 +/- 5 mmHg), the peak total peripheral resistance values of LTC4 and LTD4 (2.23 +/- 0.32 and 1.86 +/- 0.17 mmHg X ml-1 X min-1, respectively) were between those of the well-known vasopressors, norepinephrine (1.50 +/- 0.09) and angiotensin (2.72 +/- 0.41). The pressor response to LTC4 and LTD4 was less marked than that to norepinephrine and to angiotensin because of the concomitant reduction in cardiac output. These results indicate that LTC4 and LTD4 are systemic vasoconstrictors with potencies similar to those of norepinephrine and angiotensin.

Sign in / Sign up

Export Citation Format

Share Document