Central Vasomotor Stimulation by Angiotensin

1970 ◽  
Vol 39 (2) ◽  
pp. 239-245 ◽  
Author(s):  
C. M. Ferrario ◽  
C. J. Dickinson ◽  
J. W. McCubbin
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Internal Carotid ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Direct Stimulation ◽  
Vertebral Arteries ◽  
Reflex Bradycardia ◽  
The Difference ◽  
Stimulation Of

1. When angiotensin was infused at low rates into the vertebral arteries of anaesthetized dogs, it raised the blood pressure. When infused at similar rates intravenously or into the internal carotid artery it either did not change blood pressure, or raised it only very slightly. The difference in response was highly significant over the range of 1–50 ng kg−1 min−1. 2. During intravenous infusion at higher rates, angiotensin usually produced the well-known reflex bradycardia and fall of cardiac output, but on infusion into the vertebral arteries it rapidly raised systemic arterial pressure, often increased heart rate, and usually produced a transient increase of cardiac output. 3. Angiotensin by both routes raised peripheral resistance, but noradrenaline, by contrast, produced the same response whether it was given into the vertebral arteries or into a vein. 4. These observations suggest that part of the pressor effect of intravenous angiotensin may be mediated by a direct stimulation of some part of the hind brain.

Cardiovascular effects produced by L-glutamate stimulation of the lateral hypothalamic area

1989 ◽  
Vol 257 (2) ◽  
pp. H540-H552 ◽  
Author(s):  
S. E. Spencer ◽  
W. B. Sawyer ◽  
A. D. Loewy
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Lateral Hypothalamic Area ◽  
Hypothalamic Area ◽  
Pharmacological Blockade ◽  
Stimulation Of

L-Glutamate microinjections into the tuberal region of the lateral hypothalamic area (LHAt) caused a fall in blood pressure and heart rate in pentobarbital-anesthetized rats. The bradycardia was mediated by both beta-adrenergic and muscarinic mechanisms as demonstrated with pharmacological blockade. The hypotension was due to a decrease in cardiac output, not a decrease in total peripheral resistance. In addition, there was a reduction in coronary blood flow. If heart rate was held constant by pharmacological blockade or by electrical cardiac pacing, L-glutamate stimulation of the LHAt still caused a fall in blood pressure. When the electrically paced model was used, this hypotension was due to a fall in cardiac output. In contrast, with the pharmacological blockade of the heart, the hypotension was due to a decrease in the total peripheral resistance. The cardiac output reduction in the paced condition was not mediated solely by either beta-sympathetic or parasympathetic mechanisms as determined by pharmacological blockade. With heart rate held constant by either drugs or pacing, LHAt stimulation did not alter regional blood flow or resistance in any vascular bed, including the coronary circulation. We conclude that L-glutamate stimulation of the LHAt lowers the cardiac output and heart rate by both parasympathetic and beta-adrenergic mechanisms and elicits hypotension by lowering cardiac output in the naive and electrically paced model.

Control of Blood Pressure and the Distribution of Blood Flow

1991 ◽  
Vol 7 (S1) ◽  
pp. 79-84 ◽  
Author(s):  
Hans T. Versmold
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Peripheral Resistance ◽  
Systemic Blood Pressure ◽  
Adrenergic Innervation ◽  
Systemic Blood ◽  
Low Cardiac Output ◽  
Neurohumoral Control ◽  
The Brain

Systemic blood pressure (BP) is the product of cardiac output and total peripheral resistance. Cardiac output is controlled by the heart rate, myocardial contractility, preload, and afterload. Vascular resistance (vascular hindrance × viscosity) is under local autoregulation and general neurohumoral control through sympathetic adrenergic innervation and circulating catecholamines. Sympathetic innovation predominates in organs receivingflowin excess of their metabolic demands (skin, splanchnic organs, kidney), while innervation is poor and autoregulation predominates in the brain and heart. The distribution of blood flow depends on the relative resistances of the organ circulations. During stress (hypoxia, low cardiac output), a raise in adrenergic tone and in circulating catecholamines leads to preferential vasoconstriction in highly innervated organs, so that blood flow is directed to the brain and heart. Catecholamines also control the levels of the vasoconstrictors renin, angiotensin II, and vasopressin. These general principles also apply to the neonate.

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

Hypertension ◽  
2018 ◽  
Vol 72 (5) ◽  
pp. 1103-1108 ◽  
Author(s):  
Chloe Park ◽  
Abigail Fraser ◽  
Laura D. Howe ◽  
Siana Jones ◽  
George Davey Smith ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Elevated Blood Pressure ◽  
Elevated Blood

Acute effects of caffeine ingestion at rest in humans with impaired epinephrine responses

1996 ◽  
Vol 80 (3) ◽  
pp. 999-1005 ◽  
Author(s):  
M. Van Soeren ◽  
T. Mohr ◽  
M. Kjaer ◽  
T. E. Graham
Keyword(s):  
Blood Pressure ◽  
Adenosine Receptors ◽  
Vascular Tissue ◽  
Physiological Responses ◽  
Acute Effects ◽  
Peripheral Vascular ◽  
Direct Stimulation ◽  
Spinal Cord Lesions ◽  
Caffeine Ingestion ◽  
Stimulation Of

Caffeine ingestion has been demonstrated to increase circulating epinephrine (Epi) and norepinephrine (NE), elevate free fatty acids (FFAs), and alter heart rate, blood pressure (BP), and ventilation in humans. Whether these physiological responses are a result of caffeine acting through direct stimulation of specific tissues via adenosine receptors or secondary to Epi increases is not known. In the present experiment, six tetraplegics (level of spinal cord lesions C4-C6) were tested at rest for 3 h to investigate the effects of 6 mg/kg caffeine in capsule form on subjects with impaired Epi responses. Ventilatory, cardiovascular, metabolic, and hormonal data were collected every 15-20 min after caffeine ingestion. There were no significant (P > 0.05) increases in plasma Epi after caffeine ingestion [0.19 +/- 0.04 (SE) nM (preingestion); 0.20 +/- 0.04 nM (80 min postingestion)] or in plasma NE [0.53 +/- 0.16 nM (preingestion); 0.49 +/- 0.09 nM (80 min postingestion; P > 0.05)]. However, significant increases were found in serum FFAs [0.53 +/- 0.08 nM (preingestion); 1.03 +/- 0.20 mM (40 min postingestion; P < 0.05] and in glycerol. These concentrations remained elevated throughout the experiment. BP increased in the first hour postingestion. These data demonstrate that caffeine in physiological doses directly stimulates specific tissues, i.e., adipose and peripheral vascular tissue, and these effects are not secondary to increases in Epi after caffeine ingestion.

Long-term hemodynamic actions of atrial natriuretic factor (99-126) in conscious sheep

1988 ◽  
Vol 254 (4) ◽  
pp. H811-H815 ◽  
Author(s):  
D. G. Parkes ◽  
J. P. Coghlan ◽  
J. G. McDougall ◽  
B. A. Scoggins
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Blood Volume ◽  
Total Peripheral Resistance ◽  
Atrial Natriuretic Factor ◽  
Peripheral Resistance ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

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.

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

1993 ◽  
Vol 265 (5) ◽  
pp. R1132-R1140 ◽  
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.

IMMEDIATE HEMODYNAMIC EFFECTS OF ISOPROTERENOL

1963 ◽  
Vol 41 (1) ◽  
pp. 1949-1953 ◽  
Author(s):  
Margaret Beznák ◽  
P. Hacker
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Subcutaneous Injection ◽  
Direct Action ◽  
Peripheral Resistance ◽  
Oxygen Demand ◽  
Hemodynamic Effects ◽  
Hemodynamic Changes ◽  
Histological Damage

Subcutaneous injection of 40 mg/kg isoproterenol is followed within 2 minutes by a fall in blood pressure and peripheral resistance, by tachycardia, and by an increase in cardiac output. It seems likely that these hemodynamic changes are a consequence of a direct action of isoproterenol on the myocardium. Isoproterenol also causes a significant increase in the oxygen consumption of the rats. The increased oxygen demand of the tissues may play a role in maintaining the hemodynamic changes for periods of more than an hour after isoproterenol. Signs of histological damage in the myocardium begin to appear without affecting the function of the cardiovascular system, as measured by the tests used.

Blood Pressure Estimation with Considering of Stroke Volume Effect

2008 ◽  
pp. 173-180
Author(s):  
Moha’med O. Al-Jaafreh ◽  
Adel A. Al-Jumaily
Keyword(s):  
Blood Pressure ◽  
Stroke Volume ◽  
Applied Pressure ◽  
Peripheral Resistance ◽  
Volume Effect ◽  
Signal Features ◽  
Measure Blood Pressure ◽  
The Mean ◽  
The Difference ◽  
Blood Pressure Estimation

The mean arterial pressure (MAP) is a very important cardiovascular parameter for physicians to diagnose various cardiovascular diseases. Many algorithms were used to estimate MAP with different accuracy. These algorithms used different factors, such as blood level, pulses, and external applied pressure, photo-plethysmography (PPG) signal features, heart rate (HR), and other factors. In addition, some natural-based techniques were employed to minimize the difference between estimated and measured blood pressure, as well as to measure blood pressure continuously. This article presents an algorithm to estimate MAP, utilizing the HR, Stroke Volume (SV), and Total Peripheral Resistance (TPR), with considering SV changing influence; this consideration is investigated mathematically, and by the Particle Swarm Optimization (PSO) technique.

Pet CO2 inversely affects MSNA response to orthostatic stress

2001 ◽  
Vol 281 (3) ◽  
pp. H1040-H1046 ◽  
Author(s):  
J. Kevin Shoemaker ◽  
Debbie D. O'Leary ◽  
Richard L. Hughson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Orthostatic Intolerance ◽  
Muscle Sympathetic Nerve Activity ◽  
Peripheral Resistance ◽  
Burst Frequency ◽  
Head Up Tilt ◽  
End Tidal ◽  
Combined Data

Arterial hypocapnia has been associated with orthostatic intolerance. Therefore, we tested the hypothesis that hypocapnia may be detrimental to increases in muscle sympathetic nerve activity (MSNA) and total peripheral resistance (TPR) during head-up tilt (HUT). Ventilation was increased ∼1.5 times above baseline for each of three conditions, whereas end-tidal Pco 2 (Pet CO2 ) was clamped at normocapnic (Normo), hypercapnic (Hyper; +5 mmHg relative to Normo), and hypocapnic (Hypo; −5 mmHg relative to Normo) conditions. MSNA (microneurography), heart rate, blood pressure (BP, Finapres), and cardiac output (Q, Doppler) were measured continuously during supine rest and 45° HUT. The increase in heart rate when changing from supine to HUT ( P < 0.001) was not different across Pet CO2 conditions. MSNA burst frequency increased similarly with HUT in all conditions ( P < 0.05). However, total MSNA and the increase in total amplitude relative to baseline (%ΔMSNA) increased more when changing to HUT during Hypo compared with Hyper ( P < 0.05). Both BP and Q were higher during Hyper than both Normo and Hypo (main effect; P < 0.05). Therefore, the MSNA response to HUT varied inversely with levels of Pet CO2 . The combined data suggest that augmented cardiac output with hypercapnia sustained blood pressure during HUT leading to a diminished sympathetic response.

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