Elevated Blood Pressure in Adolescence Is Attributable to a Combination of Elevated Cardiac Output and Total Peripheral Resistance

The hemodynamic and metabolic effects of long-term (5 day) infusion of human atrial natriuretic factor (ANF) were examined in conscious chronically instrumented sheep. Infusion of ANF at 20 micrograms/h, a rate below the threshold for an acute natriuretic effect, decreased blood pressure by 9 +/- 1 mmHg on day 5, associated with a fall in calculated total peripheral resistance. On day 1, ANF reduced cardiac output, stroke volume, and blood volume, effects that were associated with an increase in heart rate and calculated total peripheral resistance and a small decrease in blood pressure. On days 4 and 5 there was a small increase in urine volume and sodium excretion. On day 5 an increase in water intake and body weight was observed. No change was seen in plasma concentrations of renin, arginine vasopressin, glucose, adrenocorticotropic hormone, or protein. This study suggests that the short-term hypotensive effect of ANF results from a reduction in cardiac output associated with a fall in both stroke volume and effective blood volume. However, after 5 days of infusion, ANF lowers blood pressure via a reduction in total peripheral resistance.

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Effect of sympathetic blockade on diurnal variation of hemodynamic patterns

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1989.256.3.r778 ◽

1989 ◽

Vol 256 (3) ◽

pp. R778-R785 ◽

Cited By ~ 4

Author(s):

M. I. Talan ◽

B. T. Engel

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Cardiac Output ◽

Stroke Volume ◽

Total Peripheral Resistance ◽

Peripheral Resistance ◽

Base Line ◽

Sympathetic Blockade ◽

Selective Blockade ◽

Arterial Blood

Heart rate, stroke volume, and intra-arterial blood pressure were monitored continuously in each of four monkeys, 18 consecutive h/day for several weeks. The mean heart rate, stroke volume, cardiac output, systolic and diastolic blood pressure, and total peripheral resistance were calculated for each minute and reduced to hourly means. After base-line data were collected for approximately 20 days, observation was continued for equal periods of time under conditions of alpha-sympathetic blockade, beta-sympathetic blockade, and double sympathetic blockade. This was achieved by intra-arterial infusion of prazosin, atenolol, or a combination of both in concentration sufficient for at least 75% reduction of response to injection of agonists. The results confirmed previous findings of a diurnal pattern characterized by a fall in cardiac output and a rise in total peripheral resistance throughout the night. This pattern was not eliminated by selective blockade, of alpha- or beta-sympathetic receptors or by double sympathetic blockade; in fact, it was exacerbated by sympathetic blockade, indicating that the sympathetic nervous system attenuates these events. Because these findings indicate that blood volume redistribution is probably not the mechanism mediating the observed effects, we have hypothesized that a diurnal loss in plasma volume may mediate the fall in cardiac output and that the rise in total peripheral resistance reflects a homeostatic regulation of arterial pressure.

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Carotid baroreceptor control of liver and spleen volume in cats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1991.260.1.h254 ◽

1991 ◽

Vol 260 (1) ◽

pp. H254-H259

Author(s):

R. Maass-Moreno ◽

C. F. Rothe

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Cardiac Output ◽

Arterial Blood Pressure ◽

Total Peripheral Resistance ◽

Venous Pressure ◽

Peripheral Resistance ◽

Normal Brain ◽

Spleen Volume ◽

Arterial Blood

We tested the hypothesis that the blood volumes of the spleen and liver of cats are reflexly controlled by the carotid sinus (CS) baroreceptors. In pentobarbital-anesthetized cats the CS area was isolated and perfused so that intracarotid pressure (Pcs) could be controlled while maintaining a normal brain blood perfusion. The volume changes of the liver and spleen were estimated by measuring their thickness using ultrasonic techniques. Cardiac output, systemic arterial blood pressure (Psa), central venous pressure, central blood volume, total peripheral resistance, and heart rate were also measured. In vagotomized cats, increasing Pcs by 100 mmHg caused a significant reduction in Psa (-67.8%), cardiac output (-26.6%), total peripheral resistance (-49.5%), and heart rate (-15%) and significantly increased spleen volume (9.7%, corresponding to a 2.1 +/- 0.5 mm increase in thickness). The liver volume decreased, but only by 1.6% (0.6 +/- 0.2 mm decrease in thickness), a change opposite that observed in the spleen. The changes in cardiovascular variables and in spleen volume suggest that the animals had functioning reflexes. These results indicate that in pentobarbital-anesthetized cats the carotid baroreceptors affect the volume of the spleen but not the liver and suggest that, although the spleen has an active role in the control of arterial blood pressure in the cat, the liver does not.

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Endothelin antagonist reduces hemodynamic responses to vasopressin in DOCA-salt hypertension

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2001.281.6.h2511 ◽

2001 ◽

Vol 281 (6) ◽

pp. H2511-H2517 ◽

Cited By ~ 7

Author(s):

Ming Yu ◽

Venkat Gopalakrishnan ◽

Thomas W. Wilson ◽

J. Robert McNeill

Keyword(s):

Blood Pressure ◽

Cardiac Output ◽

Angiotensin Ii ◽

Total Peripheral Resistance ◽

Peripheral Resistance ◽

Hemodynamic Responses ◽

Hypertensive Group ◽

Time Flow ◽

Before And After ◽

Vascular Responsiveness

The contribution of endothelin to the changes in blood pressure, cardiac output, and total peripheral resistance evoked by arginine vasopressin and angiotensin II was investigated in deoxycorticosterone acetate (DOCA)-salt hypertensive rats by infusing the peptides intravenously before and after pretreatment with the endothelin receptor antagonist bosentan. Blood pressure was recorded with radiotelemetry devices and cardiac output was recorded with ultrasonic transit time flow probes in conscious unrestrained animals. The dose-related decreases in cardiac output induced by vasopressin and angiotensin II were unaffected by bosentan. In contrast, the dose-related increases in total peripheral resistance evoked by vasopressin were blunted in both DOCA-salt hypertensive and sham normotensive rats, but this effect of bosentan was greater in the DOCA-salt hypertensive group. In contrast with vasopressin, bosentan failed to change hemodynamic responses to angiotensin II. The exaggerated vascular responsiveness (total peripheral resistance) of the DOCA-salt hypertensive group to vasopressin was largely abolished by bosentan. These results suggest that endothelin contributes to the hemodynamic effects of vasopressin but not angiotensin II in the DOCA-salt model of hypertension.

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Effects of phenoxybenzamine, metoprolol, captopril, and meclofenamate on cardiovascular function in deoxycorticosterone acetate hypertensive Yucatan miniature swine

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y83-022 ◽

1983 ◽

Vol 61 (2) ◽

pp. 149-153 ◽

Cited By ~ 4

Author(s):

Charles D. Ciccone ◽

Edward J. Zambraski

Keyword(s):

Blood Pressure ◽

Cardiac Output ◽

Arterial Pressure ◽

Total Peripheral Resistance ◽

Peripheral Resistance ◽

Response Curves ◽

Miniature Swine ◽

Deoxycorticosterone Acetate ◽

Adrenergic Activity ◽

Conscious Animals

Eight adult Yucatan miniature swine were implanted with deoxycorticosterone acetate (DOCA) impregnated silicone strips (100 mg∙kg−1). After 16 weeks of DOCA treatment mean arterial pressure (MAP) increased to 183 ± 4 mmHg (1 mmHg = 133.322 Pa). In four normal animals arterial pressure was 126 ± 8 mmHg. The increase in MAP in the DOCA animalas was due to an elevated total peripheral resistance (TPR) with cardiac output remaining normal. In tests with conscious animals, phenoxybenzamine (1 mg∙kg−1) significantly decreased arterial pressure via a selective decrease in TPR. Neither meclofenamate, metoprolol, nor captopril affected MAP in these DOCA hypertensive animals. Dose–response curves to exogenous norepinephrine and angiotensin II revealed that the DOCA animals had an increased pressor sensitivity to both of these agents. These data suggest that in the DOCA hypertensive Yucatan swine an increase in alpha adrenergic activity and (or) an increase in smooth muscle responsiveness to circulating catecholamines is responsible for the increase in blood pressure as a result of an increase in total peripheral resistance.

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Cardiac Output by the Dye Dilution Technique Under Thiopental Sodium-Oxygen and Ether Anesthesia

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1956.186.1.101 ◽

1956 ◽

Vol 186 (1) ◽

pp. 101-104 ◽

Cited By ~ 2

Author(s):

Esther M. Greisheimer ◽

Dorothy W. Ellis ◽

George Stewart ◽

Lydia Makarenko ◽

Nadia Oleksyshyn ◽

...

Keyword(s):

Blood Pressure ◽

Cardiac Output ◽

Arterial Blood Pressure ◽

Total Peripheral Resistance ◽

Peripheral Resistance ◽

Stroke Index ◽

Ether Anesthesia ◽

Dye Dilution ◽

Arterial Blood ◽

Thiopental Sodium

One hundred-twenty determinations of cardiac output by the dye dilution technic utilizing the cuvette oximeter were made on 20 dogs. Of these, 60 were done under thiopental sodium-oxygen analgesia and 60 were done after supplementing with ether. Arterial blood pressure was recorded by strain gauge. Electrocardiograms were taken periodically. Concentrations of thiopental and ether in arterial blood were determined. Cardiac output began to increase under thiopental analgesia and continued to increase when ether was administered. Arterial blood pressure and heart rate decreased slightly when ether was administered. Stroke index increased when ether was administered. Total peripheral resistance decreased markedly under thiopental analgesia, and continued to decrease when ether was administered. When compared with an earlier study in which cyclopropane was used as the supplementing agent, it was found that cyclopropane and ether exert opposite effects on cardiac output and peripheral resistance despite the fact that the effect on arterial blood pressure is similar under the two agents. Increase in cardiac output was found to be parallel with decrease in total peripheral resistance in this study. Amount of dye injected did not influence cardiac output. Under the conditions of this study, cardiac output was in no way dependent on the concentration of thiopental in the blood nor on the amount injected. Level of ether in the blood did not show much effect, if any, on cardiac output. It is probable that the changes observed in this study are comparable with those which obtain clinically when thiopental-oxygen analgesia is supplemented with ether. Systolic blood pressure is not an infallible guide to other cardiovascular functions since it may remain fairly steady while cardiac output and peripheral resistance undergo marked changes under anesthesia.

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Contribution of Stenosis Resistance to the Rise in total Peripheral Resistance during Experimental Renal Hypertension in Conscious Dogs

Clinical Science ◽

10.1042/cs0610663 ◽

1981 ◽

Vol 61 (6) ◽

pp. 663-670 ◽

Cited By ~ 24

Author(s):

W. P. Anderson ◽

P. I. Korner ◽

J. A. Angus ◽

C. I. Johnston

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Cardiac Output ◽

Plasma Renin Activity ◽

Renal Artery ◽

Total Peripheral Resistance ◽

Peripheral Resistance ◽

Plasma Renin ◽

Vascular Beds ◽

Renal Vascular

1. Mild, moderate and severe renal artery stenosis was induced in uninephrectomized conscious dogs by inflating a renal artery cuff to lower distal pressure to 60, 40 or 20 mmHg respectively. The renal artery was narrowed progressively over the next 3 days by further inflation of the cuff to relower the distal renal artery pressure to the initial values. 2. Graded progressive stenosis produced graded progressive rises in blood pressure, plasma renin activity and total renal resistance to flow over the 3 day period, followed by a return to control values 24 h after cuff deflation. 3. The rise in total renal resistance to flow was almost entirely due to the stenosis, with only small changes occurring in renal vascular resistance. 4. in moderate and severe stenosis cardiac output did not alter significantly and thus increases in blood pressure were due to increases in total peripheral resistance. in these groups the resistance to blood flow of the stenosis accounted respectively for about 36 and 26% of the rises in total peripheral resistance. Vasoconstriction of the other non-renal vascular beds accounted for the remainder of the increase in total peripheral resistance. 5. in mild stenosis the changes in both cardiac output and total peripheral resistance were variable and not statistically significant. in this group the rise in stenosis resistance was compensated by vasodilatation of the non-renal vascular beds. 6. in all groups rises in plasma renin activity and blood pressure correlated with the haemodynamic severity of the stenosis. 7. Thus the resistance to blood flow of the moderate and severe renal artery stenoses accounted for one-quarter to one-third of the increases in total peripheral resistance. The remainder of the increase in total peripheral resistance was due to vasoconstriction of nonrenal beds.

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Clinical and Haemodynamic Study of Atenolol (Tenormin) in Essential Hypertension

Clinical Science ◽

10.1042/cs051525s ◽

1976 ◽

Vol 51 (s3) ◽

pp. 525s-526s

Author(s):

H. Æ. Jensen ◽

K. Rasmussen ◽

N. Mosbæk

Keyword(s):

Blood Pressure ◽

Cardiac Output ◽

Essential Hypertension ◽

Side Effects ◽

Total Peripheral Resistance ◽

Peripheral Resistance ◽

Blocking Agent ◽

Pronounced Decrease ◽

Daily Range ◽

Haemodynamic Study

1. The β1-adrenoreceptor-blocking agent atenolol was studied in the treatment of twelve out-patients with essential hypertension. 2. With a mean dose of 110 mg of atenolol daily (range 75–200 mg/day) we observed a pronounced decrease in blood pressure. 3. Only minimal side effects were seen. 4. Cardiac output decreased from 4·6 to 3·4 l/min during treatment. This decrease did not correlate with the decrease in blood pressure but correlated well with the changes in calculated total peripheral resistance.

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The Haemodynamic Response to Salt and Water Loading in Patients with End-Stage Renal Disease and Anephric Man

Clinical Science ◽

10.1042/cs051223s ◽

1976 ◽

Vol 51 (s3) ◽

pp. 223s-225s ◽

Cited By ~ 2

Author(s):

K. E. Kim ◽

G. Onesti ◽

E. T. Delguercio ◽

J. Greco ◽

M. Fernandes ◽

...

Keyword(s):

Blood Pressure ◽

Cardiac Output ◽

Renal Disease ◽

End Stage Renal Disease ◽

Total Peripheral Resistance ◽

Peripheral Resistance ◽

Initial Rise ◽

Anephric Patients ◽

Stage Renal Disease ◽

End Stage

1. Patients with end-stage renal disease and anephric patients underwent expansion and depletion of body fluids with salt and water. This resulted in four different sequential haemodynamic patterns: (i) no significant increase in blood pressure; (ii) increase in blood pressure associated with a rise in cardiac output and no effect on total peripheral resistance; (iii) increase in cardiac output followed by a rise in blood pressure and total peripheral resistance; (iv) increase in total peripheral resistance and blood pressure without significant changes in cardiac output. 2. It is concluded that an initial rise in cardiac output is not necessary to increase blood pressure in either anephric man or patients with end-stage renal disease.

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Autonomic Cardiovascular Dysregulation at Rest and During Stress in Chronically Low Blood Pressure

Journal of Psychophysiology ◽

10.1027/0269-8803/a000204 ◽

2019 ◽

Vol 33 (1) ◽

pp. 39-53 ◽

Cited By ~ 1

Author(s):

Stefan Duschek ◽

Alexandra Hoffmann ◽

Casandra I. Montoro ◽

Gustavo A. Reyes del Paso

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Heart Rate Variability ◽

Cardiac Output ◽

Stroke Volume ◽

Total Peripheral Resistance ◽

Baroreflex Sensitivity ◽

Peripheral Resistance ◽

Control Group ◽

Low Blood Pressure

Abstract. Chronic low blood pressure (hypotension) is accompanied by symptoms such as fatigue, reduced drive, faintness, dizziness, cold limbs, and concentration difficulties. The study explored the involvement of aberrances in autonomic cardiovascular control in the origin of this condition. In 40 hypotensive and 40 normotensive subjects, impedance cardiography, electrocardiography, and continuous blood pressure recordings were performed at rest and during stress induced by mental calculation. Parameters of cardiac sympathetic control (i.e., stroke volume, cardiac output, pre-ejection period, total peripheral resistance), parasympathetic control (i.e., heart rate variability), and baroreflex function (i.e., baroreflex sensitivity) were obtained. The hypotensive group exhibited markedly lower stroke volume, heart rate, and cardiac output, as well as higher pre-ejection period and baroreflex sensitivity than the control group. Hypotension was furthermore associated with a smaller blood pressure response during stress. No group differences arose in total peripheral resistance and heart rate variability. While reduced beta-adrenergic myocardial drive seems to constitute the principal feature of the autonomic impairment that characterizes chronic hypotension, baroreflex-related mechanisms may also contribute to this state. Insufficient organ perfusion due to reduced cardiac output and deficient cardiovascular adjustment to situational requirements may be involved in the manifestation of bodily and mental symptoms.

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