Cardioaccelerator action of angiotensin

1962 ◽  
Vol 202 (2) ◽  
pp. 237-240 ◽  
Author(s):  
S. D. Nishith ◽  
L. D. Davis ◽  
W. B. Youmans
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Abdominal Aorta ◽  
Intravenous Infusion ◽  
Control Level ◽  
Arterial Blood ◽  
Initial Decrease ◽  
Slow Intravenous Infusion

Effects of synthetic angiotensin II on heart rate and blood pressure were determined in dogs under the influence of morphine (3 mg/kg) and chloralose (90 mg/kg). Angiotensin in total doses of 2.5–20 µg, rapidly injected intravenously in intact dogs, caused an initial decrease in heart rate followed by a rise above the control level, despite the continued elevation of arterial blood pressure. When the degree of rise in arterial pressure was buffered by a mechanical compensator connected with the abdominal aorta, rapid intravenous angiotensin injection produced no initial cardioinhibitory phase, and the magnitude of the accleration of heart rate was much greater than in the unbuffered animal. Slow intravenous infusion of angiotensin in some cases caused only a rise in heart rate. In sinoaortic denervated animals both blood pressure and heart rate were greatly increased when a total dose of 10 µg angiotensin was rapidly injected intravenously. Thus, it is demonstrated that the cardioinhibitory response to angiotensin depends largely or exclusively on reflex effects from sinoaortic pressoreceptors, and that angiotensin has a strong cardioaccelerator action which is exerted through the efferent nerves to the heart.

Effects of the angiotensin II receptor antagonist Losartan (DuP 753/MK 954) on arterial blood pressure, heart rate, plasma concentrations of angiotensin II and renin and the pressor response to infused angiotensin II in the salt-deplete dog

1992 ◽  
Vol 83 (5) ◽  
pp. 549-556 ◽  
Author(s):  
R. J. MacFadyen ◽  
M. Tree ◽  
A. F. Lever ◽  
J. L. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Pressor Response ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Plasma Angiotensin

1. The blood pressure, heart rate, hormonal and pressor responses to constant rate infusion of various doses of the angiotensin (type 1) receptor antagonist Losartan (DuP 753/MK 954) were studied in the conscious salt-deplete dog. 2. Doses in the range 0.1–3 μmin−1 kg−1 caused no change in blood pressure, heart rate or pressor response to angiotensin II (54 ng min−1kg−1), and a dose of 10 μgmin−1 kg−1 had no effect on blood pressure, but caused a small fall in the pressor response to angiotensin II. Infusion of Losartan at 30 μmin−1 kg−1 for 3 h caused a fall in mean blood arterial pressure from baseline (110.9 ± 11.2 to 95.0 ± 12.8 mmHg) and a rise in heart rate (from 84.6 ± 15.1 to 103 ± 15.2 beats/min). Baseline plasma angiotensin II (42.5 ± 11.8 pg/ml) and renin (64.5 ± 92.7 μ-units/ml) concentrations were already elevated in response to salt depletion and rose significantly after Losartan infusion to reach a plateau by 70 min. The rise in mean arterial blood pressure after a test infusion of angiotensin II (35.3 ± 11.6 mmHg) was reduced at 15 min (11.8 ± 6.8 mmHg) by Losartan and fell progressively with continued infusion (3 h, 4.3 ± 3.3 mmHg). The peak plasma angiotensin II concentration during infusion of angiotensin II was unaffected by Losartan, but the rise in plasma angiotensin II concentration during infusion was reduced because of the elevated background concentration. Noradrenaline infusion caused a dose-related rise in mean blood arterial pressure (1000 ngmin−1kg−1, +19.9 ± 8 mmHg; 2000ngmin−1 kg−1, +52.8 ± 13.9 mmHg) with a fall in heart rate (1000 ng min−1 kg−1, −27.9 ± 11.5 beats/min; 2000 ng min−1 kg−1, −31.2 ± 17.3 beats/min). During Losartan infusion the 1000 but not the 2000 ng min−1 kg−1 noradrenaline infusion caused a greater rise in mean arterial blood pressure and a greater fall in heart rate. The fall in heart rate tended to decrease with continued infusion of Losartan. Plasma catecholamine concentrations were unaffected by Losartan. In a further study, higher doses of Losartan (100, 300 and 1000 μg min−1 kg−1; 30 min) produced greater falls in mean arterial blood pressure also with a rise in heart rate and complete blockade of the pressor effect of infused angiotensin II. Some animals became disturbed at the highest dose. 3. Losartan produces rapid dose-related falls in blood pressure and a rise in heart rate and renin release with elevation of plasma angiotensin II. Pressor responses to angiotensin II are reduced at intermediate doses and are eliminated at high doses. Losartan does not appear to inhibit angiotensin II clearance from the plasma and may in some way increase it.

Role of the area postrema in angiotensin II modulation of baroreflex control of heart rate in conscious mice

2003 ◽  
Vol 284 (3) ◽  
pp. H1003-H1007 ◽  
Author(s):  
Baojian Xue ◽  
Hope Gole ◽  
Jaya Pamidimukkala ◽  
Meredith Hay
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Area Postrema ◽  
Ang Ii ◽  
Baroreflex Control ◽  
Arterial Blood ◽  
Intravenous Infusions

This study reports the effects of angiotensin II (ANG II), arginine vasopression (AVP), phenylephrine (PE), and sodium nitroprusside (SNP) on baroreflex control of heart rate in the presence and absence of the area postrema (AP) in conscious mice. In intact, sham-lesioned mice, baroreflex-induced decreases in heart rate due to increases in arterial pressure with intravenous infusions of ANG II were significantly less than those observed with similar increases in arterial pressure with PE (slope: −3.0 ± 0.9 vs. −8.1 ± 1.5 beats · min−1 · mmHg−1). Baroreflex-induced decreases in heart rate due to increases in arterial pressure with intravenous infusions of AVP were the same as those observed with PE in sham animals (slope: −5.8 ± 0.7 vs. −8.1 ± 1.5 beats · min−1 · mmHg−1). After the AP was lesioned, the slope of baroreflex inhibition of heart rate was the same whether pressure was increased with ANG II, AVP, or PE. The slope of the baroreflex-induced increases in heart rate due to decreases in arterial blood pressure with SNP were the same in sham- and AP-lesioned animals. These results indicate that, similar to other species, in mice the ability of ANG II to acutely reset baroreflex control of heart rate is dependent on an intact AP.

Analysis of heart rate-based control of arterial blood pressure

1996 ◽  
Vol 271 (2) ◽  
pp. H812-H822 ◽  
Author(s):  
W. C. Rose ◽  
J. S. Schwaber
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Vascular System ◽  
Reciprocal Relation ◽  
Arterial Baroreflex ◽  
Arterial Blood ◽  
Limited Effectiveness ◽  
Filling Time

Vagal control of the heart is the most rapidly responding limb of the arterial baroreflex. We created a mathematical model of the left heart and vascular system to evaluate the ability of heart rate to influence blood pressure. The results show that arterial pressure depends nonlinearly on rate and that changes in rate are of limited effectiveness, particularly when rate is increased above the basal level. A 10% change in heart rate from rest causes a change of only 2.4% in arterial pressure due to the reciprocal relation between heart rate and stroke volume; at higher rates, insufficient filling time causes stroke volume to fall. These findings agree well with published experimental data and challenge the idea that changes in heart rate alone can strongly and rapidly affect arterial pressure. Possible implications are that vagally mediated alterations in inotropic and dromotropic state, which are not included in this model, play important roles in the fast reflex control of blood pressure or that the vagal limb of the baroreflex is of rather limited effectiveness.

The Influence of Physical Activity on Arterial Pressure during Ambulatory Recordings in Man

1980 ◽  
Vol 58 (1) ◽  
pp. 115-117 ◽  
Author(s):  
D. B. Rowlands ◽  
T. J. Stallard ◽  
R. D. S. Watson ◽  
W. A. Littler
Keyword(s):  
Physical Activity ◽  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Ambulatory Blood Pressure ◽  
Physical Activities ◽  
Hypertensive Patients ◽  
Arterial Blood ◽  
Significant Difference ◽  
Hypotensive Therapy

1. Ambulatory blood pressure recordings were made over a 48 h period on six hypertensive patients. The conditions of study were standardized, particularly with regard to physical activity, and during one period of each day the patients were randomly allocated to be active or inactive. 2. Results show that blood pressure was highest during physical activity and lowest during sleep. There was no significant difference between the arterial pressures measured during the same physical activities carried out at the same time each day. However, during the same time on consecutive days when activity was randomized, there was a significant difference between the pressure recordings during physical activity compared with those during inactivity. Heart rate changes showed a similar trend during the randomized period. 3. Physical activity and sleep have a profound effect on continuous arterial blood pressure recordings and these are independent of time alone. These observations should be taken into account when using this ambulatory system to assess hypotensive therapy.

Augmentation of respiratory sinus arrhythmia in response to progressive hypercapnia in conscious dogs

2001 ◽  
Vol 280 (5) ◽  
pp. H2336-H2341 ◽  
Author(s):  
Fumihiko Yasuma ◽  
Jun-Ichiro Hayano
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Respiratory Sinus Arrhythmia ◽  
Physiological Response ◽  
Minute Ventilation ◽  
Control Level ◽  
Conscious Dogs ◽  
Sinus Arrhythmia ◽  
Arterial Blood

Respiratory sinus arrhythmia (RSA) may serve to enhance pulmonary gas exchange efficiency by matching pulmonary blood flow with lung volume within each respiratory cycle. We examined the hypothesis that RSA is augmented as an active physiological response to hypercapnia. We measured electrocardiograms and arterial blood pressure during progressive hypercapnia in conscious dogs that were prepared with a permanent tracheostomy and an implanted blood pressure telemetry unit. The intensity of RSA was assessed continuously as the amplitude of respiratory fluctuation of heart rate using complex demodulation. In a total of 39 runs of hypercapnia in 3 dogs, RSA increased by 38 and 43% of the control level when minute ventilation reached 10 and 15 l/min, respectively ( P < 0.0001 for both), and heart rate and mean arterial pressure showed no significant change. The increases in RSA were significant even after adjustment for the effects of increased tidal volume, respiratory rate, and respiratory fluctuation of arterial blood pressure ( P < 0.001). These observations indicate that increased RSA during hypercapnia is not the consequence of altered autonomic balance or respiratory patterns and support the hypothesis that RSA is augmented as an active physiological response to hypercapnia.

Control of blood pressure and hindlimb conductance during hemorrhage in conscious renal hypertensive rabbits

1995 ◽  
Vol 268 (6) ◽  
pp. H2302-H2310 ◽  
Author(s):  
G. Weichert ◽  
C. A. Courneya
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Similar Pattern ◽  
Ang Ii ◽  
Autonomic Nervous

We examined the response to hemorrhage in conscious normotensive and hypertensive rabbits under control conditions and during efferent blockade of 1) the hormones vasopressin (AVP) and angiotensin II (ANG II), 2) the autonomic nervous system, and 3) autonomic and hormonal inputs. We recorded mean arterial pressure, heart rate, and hindlimb conductance. The response to hemorrhage was unchanged with hormonal blockade alone. Blockade of the autonomic nervous system caused a faster rate of blood pressure decline, but the rate of decrease in hindlimb conductance was maintained at control levels. Blocking the autonomic nervous system and the hormones resulted in rapid blood pressure decline and an increase in hindlimb conductance. Although the three types of efferent blockade had a similar pattern of effects in normotensive and hypertensive rabbits, hypertensive rabbits exhibited less cardiovascular support during hemorrhage than normotensive rabbits. During hemorrhage, hypertensive rabbits had an attenuation of hindlimb vasoconstriction, a reduction in the heart rate-mean arterial pressure relationship, and reduced ability to maintain blood pressure compared with normotensive rabbits.

scholarly journals Acute Cardiovascular Effects of Epidural Spinal Cord Stimulation

2007 ◽  
Vol 5;10 (9;5) ◽  
pp. 677-685
Author(s):  
David M. Schultz
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Spinal Cord Stimulation ◽  
Statistical Significance ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Arterial Blood

Background: Several animal studies support the contention that thoracic spinal cord stimulation (SCS) might decrease arterial blood pressure. Objective: To determine if electrical stimulation of the dorsal spinal cord in humans will lower mean arterial pressure (MAP) and heart rate (HR). Design: Case Series Methods: Ten normotensive subjects that were clinically indicated for SCS testing were studied. Two of the 10 patients who underwent testing were excluded from the analysis because they did not respond to the Cold Pressor Test (CPT). Systolic blood pressure, diastolic blood pressure, and heart rate were measured continuously at the wrist (using the Vasotrac device). SCS was administered with quadripolar leads implanted into the epidural space under fluoroscopic guidance. SCS was randomly performed either in the T1-T2 or T5-T6 region of the spinal cord during normal conditions as well as during transient stress induced by CPT. The CPT was conducted by immersing the non-dominant hand in ice-cold water for 2 minutes. Results: There were moderate decreases in MAP and HR during SCS at the T5-T6 region compared to baseline that did not reach statistical significance. However, SCS at the T1-T2 region tended to increase MAP and HR compared to baseline but the change did not reach statistical significance. Arterial blood pressure was transiently elevated by 9.4 ± 3.8 mmHg using CPT during the control period with SCS turned off and also during SCS at either the T1-T2 region or T5-T6 region of the spinal cord (by 9.2 ± 5 mmHg and 10.7 ± 8.4 mmHg, respectively). During SCS at T5-T6, the CPT significantly increased MAP by 5.9±7.1 mmHg compared to control CPT (SCS off). Conclusion: This study demonstrated that SCS at either the T1-T2 or T5-T6 region did not significantly alter MAP or HR compared to baseline (no SCS). However, during transcient stress (elevated sympathetic tone) induced by CPT, there was a significant increase in MAP and moderate decrease in HR during SCS at T5-T6 region, which is not consistent with previous data in the literature. Acute SCS did not result in adverse cardiovascular responses and proved to be safe. Key words: Spinal cord stimulation, mean arterial pressure, heart rate, cold pressor test

Plasma renin activity, angiotensin II, and aldosterone during intense heat stress

1976 ◽  
Vol 41 (3) ◽  
pp. 323-327 ◽  
Author(s):  
K. J. Kosunen ◽  
A. J. Pakarinen ◽  
K. Kuoppasalmi ◽  
H. Adlercreutz
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Arterial Blood ◽  
Main Components ◽  
Intense Heat

Plasma renin activity (PRA), angiotensin II, and aldosterone levels, arterial blood pressure, and heart rate of six male students were investigated during and after heat stress in a sauna bath. Increased PRA, angiotensin II, and aldosterone levels were found both during and after sauna. The greatest mean increases in PRA (94.9 +/- 10.4% SE, P less than 0.005) and angiotensin II (196 +/- 54.7% SE, P less than 0.02) were observed at the end of the heat stress (at 20 min), and that in plasma aldosterone (505 +/- 209% SE, P less than 0.02) 30 min after the sauna. The heart rate roughly doubled during the heat stress and there was a transient increase followed by a decrease in systolic blood pressure and a decrease in diastolic blood pressure. This study demonstrates that intense heat stress can cause remarkable changes in the three main components of the renin-angiotensin-aldosterone system.

Heart rate and oxygen uptake response to angiotensin in the squirrel monkey at 10 degrees C

1977 ◽  
Vol 233 (1) ◽  
pp. H10-H14
Author(s):  
N. Wasserstrum ◽  
J. A. Herd
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Intravenous Infusion ◽  
Squirrel Monkeys ◽  
Arterial Blood ◽  
Baroreceptor Stimulation ◽  
The Central Nervous System ◽  
Total Body ◽  
Total Body Oxygen ◽  
Oxygen Uptake Response

Unanesthetized squirrel monkeys exposed to an ambient temperature of 10 degrees C showed elevations in total body oxygen consumption (VO2), systemic arterial blood pressure (BP), and heart rate (hr) above values recorded at 28 degrees C. Further elevation of BP in the cold by intravenous infusion of phenylephrine (5-50 microgram/kg-min) was accompanied by reduction in both VO2 and HR, and the changes in VO2 were proportional to those in HR. When BP was raised by intravenous infusion of angiotensin (0.05-1.0 microgram/kg-min), large elevations in BP were again accompanied by reductions in HR and VO2. However, for equivalent elevations in BP, the depressions in both HR and VO2 were much smaller with angiotensin than they were with phenylephrine. Previous studies in this laboratory have demonstrated that in response to experimental elevation of BP, reflexes originating at the sinoaortic baroreceptors depress not only HR but also VO2. The present results suggest that angiotensin modulates baro-reflexive responses to elevation in BP. The reductions in HR and VO2 that ordinarily occur in response to baroreceptor stimulation may be modified by an action of angiotensin on the central nervous system.

Comparative study of pressor and heart rate responses to angiotensin II and noradrenaline in pregnant and non-pregnant women

1992 ◽  
Vol 82 (2) ◽  
pp. 157-162 ◽  
Author(s):  
Margaret Ramsay ◽  
Fiona Broughton Pipkin ◽  
Peter Rubin
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Pregnant Women ◽  
Arterial Blood Pressure ◽  
Vascular Reactivity ◽  
Pressor Response ◽  
Arterial Blood ◽  
Diastolic Arterial Blood Pressure ◽  
In Pregnancy

1. Twenty-eight healthy non-pregnant women and 28 women in the first or second trimester of pregnancy were studied. They were given an incremental intravenous infusion of either noradrenaline or angiotensin II. Pressor and heart rate responses were documented. 2. Dose-pressor response curves were constructed for the two agents in pregnant and non-pregnant women (n=14 in each group). The regression parameters of slope and intercept were calculated, and were used to derive the variables of dose required to elicit a 10 mmHg rise in systolic or diastolic blood pressure. 3. The pressor response to angiotensin II was diminished in pregnancy, with approximately twice the dose being required to raise the systolic or diastolic arterial blood pressure as in non-pregnant subjects. 4. The systolic pressor response to noradrenaline was slightly diminished in pregnancy, but the diastolic pressor response was unchanged. There were no significant differences between the doses of noradrenaline required to elicit a 10 mmHg rise in systolic or diastolic arterial blood pressure in pregnant or non-pregnant subjects. 5. There was a diminution in the bradycardia evoked in response to both hormones in pregnancy. 6. We conclude that the well-documented pressor insensitivity to angiotensin II during pregnancy is a specific phenomenon, not a manifestation of a generalized reduction in vascular reactivity.

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