Haemodynamic Effects of Noise Exposure before and after β1-Selective and Non-Selective β-Adrenoceptor Blockade in Patients with Essential Hypertension

1981 ◽  
Vol 61 (s7) ◽  
pp. 89s-91s ◽  
Author(s):  
L. Andrén ◽  
L. Hansson ◽  
M. Björkman
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Total Peripheral Resistance ◽  
Noise Exposure ◽  
Blood Pressure Response ◽  
Peripheral Resistance ◽  
Pressure Response ◽  
Arterial Blood ◽  
Before And After ◽  
Haemodynamic Changes

1. Noise stimulation (100 dBA) for 10 min caused a significant increase in diastolic (7.0%, P < 0.001) and mean arterial blood pressure (4.3%, P < 0.01) in patients with essential hypertension. 2. The blood pressure response to noise was due to an increase in total peripheral resistance (4.8%, P < 0.02); heart rate, stroke volume and cardiac output were unchanged. 3. β1-selective adrenoceptor blockade (metoprolol) did not change the haemodynamic reaction pattern induced by noise. 4. Noise exposure during non-selective β-adrenoceptor blockade (propranolol) caused an accentuated blood pressure response with increments of both systolic and diastolic blood pressure as well as a more pronounced rise in total peripheral resistance. 5. The haemodynamic changes induced by noise stimulation at 100 dBA totally disappeared after 5 min of quiet rest at 40 dBA.

Central Haemodynamics and Plasma Prostaglandin E2 in Borderline and Sustained Essential Hypertensive Patients before and after Indomethacin

1981 ◽  
Vol 61 (s7) ◽  
pp. 323s-325s ◽  
Author(s):  
M. E. Safar ◽  
A. F. Hornych ◽  
J. A. Levenson ◽  
A. Ch. Simon ◽  
G. M. London ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Index ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Hypertensive Patients ◽  
Arterial Blood ◽  
Before And After ◽  
Haemodynamic Changes ◽  
Normotensive Subjects ◽  
Pg E2

1. In basal conditions, plasma arterial prostaglandin (PG) E2 was significantly increased in borderline hypertensive patients (BH) (28.5 ± 6.7 pg/ml) in comparison with sustained essential hypertensive patients (EH) (11.6 ± 3.2 pg/ml) and in comparison with control normotensive subjects (NTS) (5.8 ± 1.4 pg/ml). 2. Plasma arterial PGE2 was positively significantly correlated with cardiac index and negatively significantly correlated with total peripheral resistance in basal conditions. 3. Indomethacin induced more pronounced haemodynamic changes in borderline than in sustained hypertensive patients, with a significant increase in arterial blood pressure and total peripheral resistance and a significant decrease in stroke volume and cardiac index. 4. Indomethacin significantly decreased arterial PGE2 in borderline hypertensive patients. The decrease was less important in sustained hypertensive patients. 5. In the overall population, a significant positive correlation between arterial PGE2 concentration and cardiac index was observed before and after indomethacin treatment. 6. The study suggests an important role of PGE2 in the regulation of cardiac output (positive inotropic effect) and blood pressure of essential hypertensive patients.

Cardiovascular responses to oxygen inhalation after hemorrhage in anesthetized rats: hyperoxic vasoconstriction

2007 ◽  
Vol 292 (2) ◽  
pp. H776-H785 ◽  
Author(s):  
James L. Atkins ◽  
Ken B. Johnson ◽  
Frederick J. Pearce
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Pressure Response ◽  
Oxygen Inhalation ◽  
Arterial Blood ◽  
Anesthetized Rats ◽  
Initial Care ◽  
Target Pressure

Oxygen inhalation is recommended for the initial care of trauma victims. The improved survival seen in early hemorrhage is normally associated with an increase in blood pressure. Although clinical use of oxygen can occur late after hemorrhage, the effects of late administration have not been specifically examined. Anesthetized rats were studied using an isobaric hemorrhage model with target pressures of either 70 or 40 mmHg. At various times after hemorrhage, the feedback control of the blood pressure was stopped and the inspired gas was changed from room air to 100% oxygen. The results show that shortly after hemorrhage to 70 mmHg, oxygen inhalation results in an increase in mean arterial blood pressure of 60 ± 3 mmHg, which is associated with a large increase in total peripheral resistance from 0.89 ± 0.05 to 1.25 ± 0.1 peripheral resistance units. The blood pressure response is essentially unchanged with time, and it is not altered by a 10-min exposure to NG-nitro-l-arginine methyl ester. At a target pressure of 40 mmHg, the initial blood pressure response to oxygen is the same, but it gradually decreases as the animal develops a lactic acidosis. We conclude that the therapeutic value of oxygen needs to be separately evaluated for late hemorrhage.

scholarly journals Prolonged duration of blood pressure response to enalkiren, the novel dipeptide renin inhibitor, in essential hypertension.

Hypertension ◽  
1990 ◽  
Vol 15 (6_pt_2) ◽  
pp. 835-840 ◽  
Author(s):  
R S Boger ◽  
H N Glassman ◽  
J H Cavanaugh ◽  
P J Schmitz ◽  
J Lamm ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Blood Pressure Response ◽  
Pressure Response ◽  
Renin Inhibitor ◽  
The Novel ◽  
Prolonged Duration

scholarly journals 24-Hour blood pressure response to lower dose (30 mg) fimasartan in Korean patients with mild to moderate essential hypertension

2017 ◽  
Vol 32 (6) ◽  
pp. 1025-1036 ◽  
Author(s):  
Hae-Young Lee ◽  
Cheol-Ho Kim ◽  
Jae-Kwan Song ◽  
Shung Chull Chae ◽  
Myung Ho Jeong ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Blood Pressure Response ◽  
Moderate Essential Hypertension ◽  
Pressure Response ◽  
Korean Patients

Effect of sympathetic blockade on diurnal variation of hemodynamic patterns

1989 ◽  
Vol 256 (3) ◽  
pp. R778-R785 ◽  
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.

Carotid baroreceptor control of liver and spleen volume in cats

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.

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

2001 ◽  
Vol 281 (6) ◽  
pp. H2511-H2517 ◽  
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.

Effects of β-Adrenoreceptor Antagonists on Sino-Aortic Baroreflex Sensitivity and Blood Pressure in Hypertensive Man

1979 ◽  
Vol 57 (3) ◽  
pp. 241-247 ◽  
Author(s):  
R. D. S. Watson ◽  
T. J. Stallard ◽  
W. A. Littler
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Older Patients ◽  
Acute Treatment ◽  
Baroreflex Sensitivity ◽  
Chronic Treatment ◽  
Positive Relationship ◽  
Initial Pulse ◽  
Arterial Blood ◽  
Before And After

1. Sensitivity of the sino-aortic baroreflex was investigated before and after acute (23 patients) and chronic (23 patients) β-adrenoreceptor antagonism in patients with essential hypertension. 2. Sensitivity was inversely related to age (r = −0·60) and systolic blood pressure (r = −0·46); a positive relationship was noted between sensitivity and initial pulse intervals (r = 0·40). 3. Sensitivity increased significantly in patients less than 40 years of age after chronic treatment. No change occurred after acute treatment or in older patients treated chronically. 4. The fall in ambulatory intra-arterial blood pressure after chronic treatment was unrelated to alteration of baroreflex sensitivity.

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