Activation of Bradykinin‐Sensitive Pericardial Afferents Increases Systemic Venous Tone and Cardiac Output

We tested the hypothesis that the changes in venous tone induced by changes in arterial blood oxygen or carbon dioxide require intact cardiovascular reflexes. Mongrel dogs were anesthetized with sodium pentobarbital and paralyzed with veruronium bromide. Cardiac output and central blood volume were measured by indocyanine green dilution. Mean circulatory filling pressure, an index of venous tone at constant blood volume, was estimated from the central venous pressure during transient electrical fibrillation of the heart. With intact reflexes, hypoxia (arterial Pao2 = 38 mmHg), hypercapnia (Paco2 = 72 mmHg), or hypoxic hypercapnia (Pao2 = 41; Paco2 = 69 mmHg) (1 mmHg = 133.32 Pa) significantly increased the mean circulatory filling pressure and cardiac output. Hypoxia, but not normoxic hypercapnia, increased the mean systemic arterial pressure and maintained the control level of total peripheral resistance. With reflexes blocked with hexamethonium and atropine, systemic arterial pressure supported with a constant infusion of norepinephrine, and the mean circulatory filling pressure restored toward control with 5 mL/kg blood, each experimental gas mixture caused a decrease in total peripheral resistance and arterial pressure, while the mean circulatory filling pressure and cardiac output were unchanged or increased slightly. We conclude that hypoxia, hypercapnia, and hypoxic hypercapnia have little direct influence on vascular capacitance, but with reflexes intact, there is a significant reflex increase in mean circulatory filling pressure.Key words: cardiovascular reflex, vascular capacitance, hypoxia, hypercapnia, mean circulatory filling pressure, venoconstriction.

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Hemodynamic effects of head-down tilt in normal subjects and sustained hypertensive patients

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1983.245.2.h194 ◽

1983 ◽

Vol 245 (2) ◽

pp. H194-H202 ◽

Cited By ~ 5

Author(s):

G. M. London ◽

J. A. Levenson ◽

M. E. Safar ◽

A. C. Simon ◽

A. P. Guerin ◽

...

Keyword(s):

Cardiac Output ◽

Plasma Renin Activity ◽

Central Venous Pressure ◽

Baroreflex Sensitivity ◽

Venous Pressure ◽

Plasma Renin ◽

Arterial Baroreflex ◽

Central Venous ◽

Venous Tone ◽

Hypertensive Patients

Central and forearm arterial and venous hemodynamics, arterial baroreflex sensitivity, plasma renin activity, and catecholamines were studied in supine position and after -10 degrees head-down tilt in 29 patients with sustained essential hypertension and in 29 normotensive controls of the same age and sex. In both populations, blood pressure, heart rate, and arterial baroreflex sensitivity did not change during the maneuver. Head-down tilt induced a similar increase in cardiopulmonary blood volume in controls and hypertensives, whereas the increase in central venous pressure, cardiac output, and forearm blood flow was higher in hypertensives. Forearm venous tone decreased in controls (from 16.6 +/- 0.8 to 13.8 +/- 0.9 mmHg X ml-1 X 100 g-1; P less than 0.01) but did not change in hypertensive patients (24.9 +/- 1.6 vs. 25.1 +/- 1.9. The magnitude of forearm vascular resistance changes induced by head-down tilt were significantly related to the basal venous tone in the overall population (P less than 0.01). The decrease in plasma renin activity and plasma catecholamines was similar in the two groups. The study provides the evidence that the higher increase in cardiac output and local flow observed in head-down tilt in hypertensive patients is probably due to a higher change in central venous pressure related to a decrease in venous distensibility.

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Cardiovascular responses to blockade of angiotensin and alpha-adrenergic receptors

AJP Renal Physiology ◽

10.1152/ajprenal.1978.235.3.f199 ◽

1978 ◽

Vol 235 (3) ◽

pp. F199-F202

Author(s):

L. J. Borucki ◽

D. Levenson ◽

N. K. Hollenberg

Keyword(s):

Blood Pressure ◽

Cardiac Output ◽

Arterial Blood Pressure ◽

Total Peripheral Resistance ◽

Peripheral Resistance ◽

Cardiovascular Responses ◽

Adrenergic Blockade ◽

Venous Tone ◽

Arterial Blood ◽

Adrenergic Blocking

Both angiotensin and alpha-adrenergic blocking agents reduce arterial blood pressure in hypovolemic states. We have compared the effects of an angiotensin antagonist (saralasin) and an alpha-adrenergic blocking agent (phenoxybenzamine) in supramaximal dosage on cardiac output, total peripheral resistance, and venous tone in rabbits rendered hypovolemic by restriction of sodium intake, supplemented by a furosemide-induced diuresis 48 h prior to study. Saralasin (10 microgram/kg per min) reduced arterial blood pressure significantly (-15 +/- 1.2 mmHg) despite an unchanged cardiac output (P less than 0.025) due to a fall in total peripheral resistance. Phenoxybenzamine (5 mg/kg) induced a much larger fall in arterial blood pressure (-28 +/- 3.6 mmHg), despite an identical reduction in total peripheral resistance, because cardiac output also fell (+/- 9 ml/kg per min). The reduction in cardiac output was associated with a significant increase in hindlimb venous distensibility (P less than 0.001) after alpha-adrenergic blockade. Saralasin, conversely, had no influence on venous tone. Adrenergic mechanisms contribute to cardiovascular homeostasis through an influence on both arteriolar and venous tone, whereas the effect of angiotensin is directed entirely to the arteriolar side of the circulation.

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