Reduction in arterial compliance alters carotid baroreflex  control of cardiac output in a model of hypertension

Baroreflex regulation of cardiac output is determined by the performance of the heart as well as the available blood flow returning to the heart (i.e., venous return). We hypothesized that a decrease in arterial compliance (Ca) would affect carotid baroreflex control of cardiac output by altering the slope of the venous return curve (VR curve). Baroreflex control of systemic arterial pressure (Pa), central venous pressure (Pv), heart rate, cardiac output (CO), and peripheral vascular resistance ( R) were determined during bilateral carotid occlusion (BCO) in spontaneously hypertensive (hypertensive, HT) and Sprague-Dawley (normotensive, NT) rats. Ca was determined from the rate of arterial pressure decay when CO was transiently stopped, and the VR curve was obtained during graded inflation of a vascular balloon positioned in the right atrium. The inverse slope of the VR curve was used as an index of the resistance to venous return (RVR). The baseline slope of the VR curve was −50.5 ± 3.3 vs. −35.5 ± 2.6 ml ⋅ kg−1 ⋅ min−1 ⋅ mmHg−1in NT vs. HT, respectively ( P < 0.05). Control values of Pa (96 ± 5 vs. 124 ± 8 mmHg) and R[0.43 ± 0.04 vs. 0.80 ± 0.07 peripheral resistance units (PRU)] were reduced in NT, whereas Ca (0.062 ± 0010 vs. 0.036 ± 0.003 ml ⋅ kg−1 ⋅ mmHg−1) was elevated in NT vs. HT, respectively ( P < 0.05). Analysis of the pressure dependence of Ca demonstrated that Ca was a nonlinear function of Pa, and the exponential decay constant for the Ca-Parelationship was reduced in HT (0.0055 ± 0.0012 vs. 0.0012 ± 0.0002 min, NT vs. HT, P < 0.05). Baroreflex activation by BCO significantly increased Pa(ΔPa, 20 ± 4 vs. 28 ± 3 mmHg) and R(Δ R, 0.16 ± 0.04 vs. 0.24 ± 0.06 PRU) in NT vs. HT, respectively. However, BCO significantly decreased CO in NT but not HT (ΔCO, −24 ± 5 vs. −4 ± 6 ml ⋅ kg−1 ⋅ min−1, P < 0.05). In NT, RVR was increased 39 ± 9% during BCO ( P < 0.05), whereas RVR increased 8 ± 3% in HT ( P = NS). From these findings, we conclude that the difference in baroreflex control of CO is mediated, in part, by the reduction in Ca, which minimized the baroreflex-evoked increase in RVR.

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Atrial natriuretic peptide increases resistance to venous return in rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1987.252.5.h894 ◽

1987 ◽

Vol 252 (5) ◽

pp. H894-H899 ◽

Cited By ~ 4

Author(s):

Y. W. Chien ◽

E. D. Frohlich ◽

N. C. Trippodo

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Arterial Pressure ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Total Peripheral Resistance ◽

Venous Return ◽

Venous Pressure ◽

Peripheral Resistance ◽

Atrial Natriuretic

To examine mechanisms by which administration of atrial natriuretic peptide (ANP) decreases venous return, we compared the hemodynamic effects of ANP (0.5 microgram X min-1 X kg-1), furosemide (FU, 10 micrograms X min-1 X kg-1), and hexamethonium (HEX, 0.5 mg X min-1 X kg-1) with those of vehicle (VE) in anesthetized rats. Compared with VE, ANP reduced mean arterial pressure (106 +/- 4 vs. 92 +/- 3 mmHg; P less than 0.05), central venous pressure (0.3 +/- 0.3 vs. -0.7 +/- 0.2 mmHg; P less than 0.01), and cardiac index (215 +/- 12 vs. 174 +/- 10 ml X min-1 X kg-1; P less than 0.05) and increased calculated resistance to venous return (32 +/- 3 vs. 42 +/- 2 mmHg X ml-1 X min X g; P less than 0.01). Mean circulatory filling pressure, distribution of blood flow between splanchnic organs and skeletal muscles, and total peripheral resistance remained unchanged. FU increased urine output similar to that of ANP, yet produced no hemodynamic changes, dissociating diuresis, and decreased cardiac output. HEX lowered arterial pressure through a reduction in total peripheral resistance without altering cardiac output or resistance to venous return. The results confirm previous findings that ANP decreases cardiac output through a reduction in venous return and suggest that this results partly from increased resistance to venous return and not from venodilation or redistribution of blood flow.

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Arterial compliance and its control by the baroreflex in hypertensive dogs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1993.265.2.h616 ◽

1993 ◽

Vol 265 (2) ◽

pp. H616-H620 ◽

Cited By ~ 5

Author(s):

M. J. Brunner ◽

G. G. Bishop ◽

K. Shigemi

Keyword(s):

Arterial Pressure ◽

Arterial Compliance ◽

Characteristic Curve ◽

Venous Pressure ◽

Experimental Hypertension ◽

Absolute Level ◽

Baroreflex Control ◽

Carotid Baroreflex ◽

The Right ◽

Different Levels

The effect of the carotid baroreflex on systemic arterial compliance was tested in normotensive and Goldblatt hypertensive dogs. After the development of experimental hypertension, dogs were acutely anesthetized with pentobarbital sodium and vagotomized. The carotid sinuses were then isolated and held at controlled carotid sinus pressures (CSP) of 50, 125, and 200 mmHg. The dogs were placed on constant flow, constant venous pressure, cardiopulmonary bypass. Arterial compliance was determined from the time constant of the exponential fall in arterial pressure, which occurred when the flow was stopped at three different levels of CSP. The reflex characteristic curve (mean arterial pressure vs. CSP) was shifted upward and to the right in the hypertensive group. Arterial compliance significantly decreased with decreasing CSP, but at any given level of CSP, arterial compliance was not different in the normotensive and hypertensive groups. A nonlinear analysis revealed that the arterial compliance-arterial pressure relationship was not altered by Goldblatt experimental hypertension. The results of this study indicate that the arterial compliance is primarily a function of the absolute level of arterial pressure. Baroreflex control of arterial compliance is important at lower levels of arterial pressure.

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Mechanism of decreased cardiac output during ANP infusion in conscious anephric dogs

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1992.262.1.r120 ◽

1992 ◽

Vol 262 (1) ◽

pp. R120-R125

Author(s):

H. L. Mizelle ◽

C. A. Gaillard ◽

R. D. Manning ◽

J. E. Hall

Keyword(s):

Cardiac Output ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Atrial Natriuretic Peptide ◽

Blood Cells ◽

Venous Return ◽

Control Period ◽

Peripheral Resistance ◽

Circulating Blood Volume

Atrial natriuretic peptide (ANP) may decrease cardiac output (CO) by lowering circulating blood volume (BV) or by altering the vasculature in a manner that would decrease venous return. The purpose of this study was to determine the role of decreased BV in mediating the decrease in CO during acute infusion of ANP. BV was measured by dilution of 51Cr-labeled red blood cells in seven trained conscious splenectomized dogs studied after unilateral (UNX) and total (TNX) nephrectomy. BV, hematocrit (Hct), CO, mean arterial pressure (MAP), and total peripheral resistance (TPR) were determined during a 90-min control period and 270 min of infusion of ANP (20 ng.kg-1.min-1 iv). In UNX dogs, ANP decreased BV from 60.9 +/- 1.4 to 58.6 +/- 1.4 ml/kg and increased Hct from 39.3 +/- 1.8% to 41.1 +/- 1.8% (P less than 0.05). MAP was not changed and CO fell to a low that was 86 +/- 2% of control (P less than 0.05) 240 min after starting ANP. TPR increased significantly during ANP infusion. All variables returned to control after ANP was stopped. In the same dogs studied 24 h after TNX, MAP averaged 111 +/- 5 mmHg during control and did not change during ANP infusion. CO fell to a low of 82 +/- 3% of control (P less than 0.05) after 120 min of infusion and remained reduced until after the ANP was stopped.(ABSTRACT TRUNCATED AT 250 WORDS)

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Cardiovascular Effects of Moxibustion at Jen Chung (Go-26) during Halothane Anesthesia in Dogs

The American Journal of Chinese Medicine ◽

10.1142/s0192415x75000268 ◽

1975 ◽

Vol 03 (03) ◽

pp. 245-261 ◽

Cited By ~ 9

Author(s):

Do Chil Lee ◽

Myung O. Lee ◽

Donald H. Clifford

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Stroke Volume ◽

Total Peripheral Resistance ◽

Venous Pressure ◽

Peripheral Resistance ◽

Cardiovascular Effects ◽

Halothane Anesthesia

The cardiovascular effects of moxibustion at Jen Chung (Go-26) in 10 dogs under halothane anesthesia were compared to 5 dogs under halothane anesthesia without moxibustion and 5 dogs under halothane anesthesia in which moxibustion was effected at a neutral or non-acupuncture site. Cardiac output, stroke volume, heart rate, mean arterial pressure, central venous pressure, total peripheral resistance, pH, PaCO2, PaO2 and base deficit were measured over a two-hour period. A significant increase in cardiac output and stroke volume and a significant decrease in the total peripheral resistance were observed in the group which was stimulated by moxibustion at Jen Chun (Go-26). Heart rate, mean arterial pressure and pulse pressure were significantly increase during the early part of the two-hour period in the same group. The cardiovascular effects of moxibustion at Jen Chung (Go-26) which were observed at the end of the two hours were also present in two dogs in which measurements were continued for two additional hours.

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Relative importance of venous and arterial resistances in controlling venous return and cardiac output

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1959.196.5.1008 ◽

1959 ◽

Vol 196 (5) ◽

pp. 1008-1014 ◽

Cited By ~ 59

Author(s):

Arthur C. Guyton ◽

Berry Abernathy ◽

Jimmy B. Langston ◽

Berwind N. Kaufmann ◽

Hilton M. Fairchild

Keyword(s):

Cardiac Output ◽

Arterial Pressure ◽

Total Peripheral Resistance ◽

Venous Return ◽

Peripheral Resistance ◽

Systemic Arterial Pressure ◽

Cardiovascular Reflexes ◽

Marked Rise ◽

Arterial Resistance ◽

Venous Resistance

In dogs with cardiovascular reflexes completely blocked by total spinal anesthesia, the total peripheral resistance was increased five- or more fold in two ways: first, by injecting small plastic microspheres into the arteries, thereby increasing the arterial resistance, and, second, by inflating pneumatic cuffs around the major veins, thereby increasing venous resistance. A small increase in venous resistance decreased cardiac output eight times as much as an increase in arterial resistance of similar magnitude. This difference was caused principally by a) a marked rise in systemic arterial pressure when arterial resistance was increased; this maintained the cardiac output at almost normal levels and b) a fall in systemic arterial pressure when venous resistance was increased; this promoted even more fall in cardiac output than increased total peripheral resistance alone would have caused.

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HEMODYNAMIC ALTERATIONS IN ACUTE MYOCARDIAL INFARCTION. I. CARDIAC OUTPUT, MEAN ARTERIAL PRESSURE, TOTAL PERIPHERAL RESISTANCE, “CENTRAL” AND TOTAL BLOOD VOLUMES, VENOUS PRESSURE AND AVERAGE CIRCULATION TIME 12

Journal of Clinical Investigation ◽

10.1172/jci102584 ◽

1952 ◽

Vol 31 (2) ◽

pp. 131-140 ◽

Cited By ~ 134

Author(s):

Edward D. Freis ◽

Harold W. Schnaper ◽

Robert L. Johnson ◽

George E. Schreiner

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Cardiac Output ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Total Peripheral Resistance ◽

Venous Pressure ◽

Peripheral Resistance ◽

Total Blood ◽

Blood Volumes

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Arterial pressure control after chronic carotid sinus denervation

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1988.255.4.h910 ◽

1988 ◽

Vol 255 (4) ◽

pp. H910-H916 ◽

Cited By ~ 4

Author(s):

D. S. O'Leary ◽

A. M. Scher

Keyword(s):

Blood Pressure ◽

Cardiac Output ◽

Arterial Pressure ◽

Carotid Sinus ◽

Peripheral Resistance ◽

Pressure Control ◽

Base Line ◽

Baroreflex Control ◽

Atrial Rate ◽

Arterial Blood

This study examines the control of arterial blood pressure in conscious, instrumented dogs with atrioventricular block before and greater than or equal to 9 days after carotid sinus baroreceptor denervation. Strength of reflex control of blood pressure was quantitated by measuring the changes in peripheral resistance and atrial rate after square wave changes in cardiac output. Surprisingly, nine or more days after carotid denervation, the strength of baroreflex control of peripheral resistance and atrial rate were not different (P greater than 0.05) from the values before denervation. This was not due to a change in the base-line levels of arterial pressure, atrial rate, cardiac output, or peripheral resistance. Bilateral vagal block after carotid denervation removed reflex effects from remaining baroreceptors and virtually eliminated changes in peripheral resistance in response to changes in arterial pressure. Therefore, the compensatory responses observed after carotid denervation were mediated by the remaining baroreceptors. Thus, after chronic carotid sinus denervation, there is no decrease in the strength of baroreflex control of peripheral resistance or heart rate.

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Carotid baroreflex pressor responses at rest and during exercise: cardiac output vs. regional vasoconstriction

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2001.280.2.h642 ◽

2001 ◽

Vol 280 (2) ◽

pp. H642-H648 ◽

Cited By ~ 37

Author(s):

Heidi L. Collins ◽

Robert A. Augustyniak ◽

Eric J. Ansorge ◽

Donal S. O'Leary

Keyword(s):

Cardiac Output ◽

Arterial Pressure ◽

Pressor Response ◽

Linear Regression Analysis ◽

Vascular Conductance ◽

Renal Vasoconstriction ◽

Peripheral Vasoconstriction ◽

Bilateral Carotid Occlusion ◽

Carotid Baroreflex ◽

Bilateral Carotid

The arterial baroreflex mediates changes in arterial pressure via reflex changes in cardiac output (CO) and regional vascular conductance, and the relative roles may change between rest and exercise and across workloads. Therefore, we quantified the contribution of CO and regional vascular conductances to carotid baroreflex-mediated increases in mean arterial pressure (MAP) at rest and during mild to heavy treadmill exercise (3.2 kph; 6.4 kph, 10% grade; and 8 kph, 15% grade). Dogs ( n = 8) were chronically instrumented to measure changes in MAP, CO, hindlimb vascular conductance, and renal vascular conductance in response to bilateral carotid occlusion (BCO). At rest and at each workload, BCO caused similar increases in MAP (average 35 ± 2 mmHg). In response to BCO, neither at rest nor at any workload were there significant increases in CO; therefore, the pressor response occurred via peripheral vasoconstriction. At rest, 10.7 ± 1.4% of the rise in MAP was due to vasoconstriction in the hindlimb, whereas 4.0 ± 0.7% was due to renal vasoconstriction. Linear regression analysis revealed that, with increasing workloads, relative contributions of the hindlimb increased and those of the kidney decreased. At the highest workload, the decrease in hindlimb vascular conductance contributed 24.3 ± 3.4% to the pressor response, whereas the renal contribution decreased to only 1.6 ± 0.3%. We conclude that the pressor response during BCO was mediated solely by peripheral vasoconstriction. As workload increases, a progressively larger fraction of the pressor response is mediated via vasoconstriction in active skeletal muscle and the contribution of vasoconstriction in inactive beds (e.g., renal) becomes progressively smaller.

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Characterization of baroreflex impairment in conscious dogs with pacing-induced heart failure

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1993.265.5.r1132 ◽

1993 ◽

Vol 265 (5) ◽

pp. R1132-R1140 ◽

Cited By ~ 14

Author(s):

N. B. Olivier ◽

R. B. Stephenson

Keyword(s):

Heart Failure ◽

Blood Pressure ◽

Heart Rate ◽

Cardiac Output ◽

Peripheral Resistance ◽

Open Loop ◽

Ventricular Pacing ◽

Baroreflex Control ◽

Rapid Ventricular Pacing ◽

Reflex Control

Open-loop baroreflex responses were evaluated in eight conscious dogs before and during congestive heart failure to determine the effects of failure on baroreflex control of blood pressure, heart rate, cardiac output, and total peripheral resistance. Heart failure was induced by rapid ventricular pacing. Baroreflex function was determined by calculation of the range and gain of the open-loop stimulus-response relationships for the effect of carotid sinus pressure on blood pressure, heart rate, cardiac output, and total peripheral resistance. The range and gain of blood pressure responses were substantially reduced as early as 3 days after induction of heart failure (161 +/- 6 to 99 +/- 8 mmHg and -2.7 +/- 0.3 to -1.5 +/- 0.1, respectively) and remained depressed for the 21 days of heart failure. This depression in baroreflex control of blood pressure was associated with similar depressions in reflex range and gain for heart rate (125 +/- 9 to 78 +/- 11 beats/min and -2.05 +/- 0.2 to -1.16 +/- 0.2 beats/min, respectively) and cardiac output (1.74 +/- 0.2 to 0.46 +/- 0.2 l/min and -0.81 +/- 0.02 to -0.027 +/- 0.008 l/min, respectively). The group-averaged range and gain for reflex control of vascular resistance were not altered by heart failure. In three dogs, discontinuation of rapid ventricular pacing led to resolution of heart failure within 7 days and partial restoration of the range and gain of reflex control of blood pressure. We conclude that heart failure reversibly depresses baroreflex control of blood pressure principally through a concurrent reduction in reflex control of cardiac output, whereas reflex control of vascular resistance is not consistently affected.

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