Forearm vasodilator mechanisms during mental stress: possible roles for epinephrine and ANP

1996 ◽  
Vol 270 (3) ◽  
pp. E393-E399 ◽  
Author(s):  
M. Lindqvist ◽  
T. Kahan ◽  
A. Melcher ◽  
P. Bie ◽  
P. Hjemdahl
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Intravenous Infusion ◽  
Mental Stress ◽  
Plasma Catecholamine ◽  
Healthy Men ◽  
Arterial Plasma ◽  
Forearm Vascular Resistance

The contribution of epinephrine (Epi) to forearm vasodilator responses to mental stress was evaluated in 12 healthy men by comparing hemodynamic and plasma catecholamine responses to mental stress and to intravenous and intra-arterial infusions of epinephrine. Mental stress decreased forearm vascular resistance (FVR) by 45%, increased arterial Epi from 0.23 to 0.44 nmol/l in arterial plasma, and increased forearm norepinephrine overflow. Intra-arterial Epi infusion decreased FVR concentration dependently by up to 43%. Intravenous Epi infusion decreased diastolic arterial pressure and increased heart rate and systolic blood pressure dose dependently. FVR decreased by up to 39% at 4.60 nmol/l Epi in arterial plasma. The average Epi contribution to forearm vasodilation during mental stress was calculated to be between 9 and 30%, depending on if responses to stress were compared with intravenous or intra-arterial Epi infusion. Arterial atrial natriuretic peptide immunoreactivity increased by 23% during stress, supporting a vasodilator influence, whereas vasopressin immunoreactivity was unaffected. Thus secretion of Epi explains only part of the stress-induced forearm vasodilation. Intravenous infusion of Epi appears to activate sympathetic counterregulation.

Hemodynamic and sympathoadrenal responses to mental stress during nitric oxide synthesis inhibition

2004 ◽  
Vol 287 (5) ◽  
pp. H2309-H2315 ◽  
Author(s):  
Madeleine Lindqvist ◽  
Anders Melcher ◽  
Paul Hjemdahl
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Mental Stress ◽  
Stress Test ◽  
Arterial Plasma ◽  
Forearm Vascular Resistance

Cardiovascular and sympathoadrenal responses to a reproducible mental stress test were investigated in eight healthy young men before and during intravenous infusion of the nitric oxide (NO) synthesis inhibitor N-monomethyl-l-arginine (l-NMMA). Before l-NMMA, stress responses included significant increases in heart rate, mean arterial pressure, and cardiac output (CO) and decreases in systemic and forearm vascular resistance. Arterial plasma norepinephrine (NE) increased. At rest after 30 min of infusion of l-NMMA (0.3 mg·kg−1·min−1 iv), mean arterial pressure increased from 98 ± 4 to 108 ± 3 mmHg ( P < 0.001) because of an increase in systemic vascular resistance from 12.9 ± 0.5 to 18.5 ± 0.9 units ( P < 0.001). CO decreased from 7.7 ± 0.4 to 5.9 ± 0.3 l/min ( P < 0.01). Arterial plasma NE decreased from 2.08 ± 0.16 to 1.47 ± 0.14 nmol/l. Repeated mental stress during continued infusion of l-NMMA (0.15 mg·kg−1·min−1) induced qualitatively similar cardiovascular responses, but there was a marked attenuation of the increase in mean arterial blood pressure, resulting in similar “steady-state” blood pressures during mental stress without and with NO blockade. Increases in heart rate and CO were attenuated, but stress-induced decreases in systemic and forearm vascular resistance were essentially unchanged. Arterial plasma NE increased less than during the first stress test. Thus the increased arterial tone at rest during l-NMMA infusion is compensated for by attenuated increases in blood pressure during mental stress, mainly through a markedly attenuated CO response and suppressed sympathetic nerve activity.

Acupuncture effects on reflex responses to mental stress in humans

2001 ◽  
Vol 280 (5) ◽  
pp. R1462-R1468 ◽  
Author(s):  
Holly R. Middlekauff ◽  
Jun Liang Yu ◽  
Kakit Hui
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Mental Stress ◽  
Animal Studies ◽  
Muscle Sympathetic Nerve Activity ◽  
Real Acupuncture ◽  
Normal Humans ◽  
Needle Acupuncture

In animal studies, acupuncture has been shown to be sympathoinhibitory, but it is unknown if acupuncture is sympathoinhibitory in humans. Nineteen healthy volunteers underwent mental stress testing pre- and postacupuncture. Muscle sympathetic nerve activity (MSNA), blood pressure, and heart rate during mental stress were compared pre- and postacupuncture. Control acupuncture consisted of acupuncture at nonacupoints and “no-needle” acupuncture. Acupuncture had no effect on resting MSNA, blood pressure, or heart rate. After real acupuncture, the increase in mean arterial pressure (pre- vs. postacupuncture 4.5 vs. 1.7 mmHg, P < 0.001), but not MSNA or heart rate, was blunted during mental stress. Similarly, following nonacupoint acupuncture, the increase in mean arterial pressure was blunted during mental stress (5.4 vs. 2.9 mmHg, P < 0.0003). No-needle acupuncture had no effect on these variables. In conclusion, acupuncture at traditional acupoints, nonacupoints, and no-needle acupuncture does not modulate baseline MSNA or MSNA responses to mental stress in normal humans. Acupuncture significantly attenuates the increase in blood pressure during mental stress. Needling nonacupoints, but not “no-needle” acupuncture, have a similar effect on blood pressure.

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.

scholarly journals Reduced GABA inhibition of sympathetic function in renal-wrapped hypertensive rats

1998 ◽  
Vol 275 (5) ◽  
pp. R1523-R1529 ◽  
Author(s):  
Douglas S. Martin ◽  
Joseph R. Haywood
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Paraventricular Nucleus ◽  
Plasma Norepinephrine ◽  
Plasma Catecholamine ◽  
Hypertensive Rats ◽  
Sympathetic Function ◽  
Arterial Pressure Measurement ◽  
Gaba Function

Animals with bilateral cannulas in the paraventricular nucleus were made hypertensive by a one-kidney, figure eight renal wrap procedure or sham operated. Femoral artery and vein catheters were inserted for arterial pressure measurement and plasma catecholamine determination. After recovery and 4 days after hypertension surgery, bicuculline methiodide or muscimol was microinjected into the paraventricular nucleus. In some rats, nitroprusside was infused intravenously to reflexly stimulate the sympathetic nervous system. In control rats, bicuculline increased blood pressure, heart rate, and plasma norepinephrine and epinephrine concentrations. In contrast, in hypertensive rats blood pressure did not change while the heart rate response was maintained. Plasma norepinephrine and epinephrine responses were reduced 75 and 68%, respectively. Muscimol injections decreased arterial pressure in the hypertensive rats. Heart rate responses to nitroprusside were similar in the two groups of rats, while the plasma catecholamine responses were attenuated in the hypertensive animals. These data suggest that GABA function in the paraventricular nucleus is reduced in renal wrap hypertension.

scholarly journals The Effects of Gallamine and a Mixture of Pancuronium and Alcuronium on the Pressor and Plasma Catecholamine Responses to Tracheal Intubation

1984 ◽  
Vol 12 (1) ◽  
pp. 22-26 ◽  
Author(s):  
Mary F. Cummings ◽  
W. J. Russell ◽  
D. B. Frewin ◽  
Wendy A. Miller
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Tracheal Intubation ◽  
Arterial Pressure ◽  
Plasma Noradrenaline ◽  
Plasma Catecholamine ◽  
Plasma Adrenaline ◽  
Noradrenaline Concentration ◽  
Noradrenaline And Adrenaline

Tracheal intubation can be accompanied by significant increases in arterial pressure, heart rate and the plasma levels of noradrenaline and adrenaline. The drugs used at induction can enhance or attenuate these responses. In nine patients who had received gallamine, intubation was associated with a 45% rise in mean arterial pressure, a twofold rise in plasma adrenaline and a 49% rise in plasma noradrenaline concentration. When a mixture of pancuronium and alcuronium (in a ratio of 4:10 by weight) was used in ten patients, blood pressure fell 24% after induction and rose 49% after intubation. A 24% rise in plasma noradrenaline in response to intubation was also observed. Compared with pancuronium alone, the use of the mixture attentuates the rise in blood pressure and noradrenaline concentration associated with intubation but does not abolish them. In addition, the mixture was associated with a significant fall in blood pressure between induction and intubation, whereas this was not found with gallamine.

Cardiovascular and sympathoadrenal responses to mental stress: influence of beta-blockade

1988 ◽  
Vol 255 (6) ◽  
pp. H1443-H1451 ◽  
Author(s):  
U. Freyschuss ◽  
P. Hjemdahl ◽  
A. Juhlin-Dannfelt ◽  
B. Linde
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Mental Stress ◽  
Beta Blockade ◽  
Rate Dependent ◽  
Before And After ◽  
Peripheral Vasodilatation ◽  
Arterial Plasma

Cardiovascular, sympathoadrenal, and subjective responses to mental stress induced by a color-word conflict test (CWT) were studied in 30 healthy males before and after intravenous administration of either placebo, beta 1-blockade by metoprolol (0.15 mg/kg), or nonselective beta-blockade by propranolol (0.15 mg/kg). CWT responses were reproducible. Mean arterial pressure increased by 20%. A mainly heart rate-dependent 65% increase in cardiac output (thermodilution) was associated with 25% decreases of both systemic (SVR) and calf vascular (CVR) resistances. Arterial plasma epinephrine (Epi) was doubled, and norepinephrine (NE) increased by 50%. Self-evaluated stress score correlated positively with changes in cardiac output and inversely with changes in SVR during CWT. Both metoprolol and propranolol halved heart rate responses; whereas increases in mean arterial pressure, Epi, and NE were uninfluenced. Metoprolol reduced the increase in stroke volume, and propranolol abolished it. SVR and CVR responses were attenuated by metoprolol and abolished by propranolol. The results suggest that mental stress accelerates the heart through neurogenic mechanisms and that peripheral vasodilatation is achieved through the concerted actions of reduced vasoconstrictor activity and elevated circulating Epi.

Hypotensive and Regional Haemodynamic Effects of Exercise, Fasted and after Food, in Human Sympathetic Denervation

1998 ◽  
Vol 94 (1) ◽  
pp. 49-55 ◽  
Author(s):  
Sharmini Puvi-Rajasingham ◽  
Gareth D. P. Smith ◽  
Adeola Akinola ◽  
Christopher J. Mathias
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Superior Mesenteric Artery ◽  
Vascular Resistance ◽  
Mesenteric Artery ◽  
Autonomic Failure ◽  
Sympathetic Denervation ◽  
Stroke Distance

1. In human sympathetic denervation due to primary autonomic failure, food and exercise in combination may produce a cumulative blood pressure lowering effect due to simultaneous splanchnic and skeletal muscle dilatation unopposed by corrective cardiovascular reflexes. We studied 12 patients with autonomic failure during and after 9 min of supine exercise, when fasted and after a liquid meal. Standing blood pressure was also measured before and after exercise. 2. When fasted, blood pressure fell during exercise from 162 ± 7/92 ± 4 to 129 ± 9/70 ± 5 mmHg (mean arterial pressure by 22 ± 5%), P < 0.0005. After the meal, blood pressure fell from 159 ± 8/88 ± 6 to 129 ± 6/70 ± 4 mmHg (mean arterial pressure by 22 ± 3%), P < 0.0001, and further during exercise to 123 ± 6/61 ± 3 mmHg (mean arterial pressure by 9 ± 3%), P < 0.01. The stroke distance—heart rate product, an index of cardiac output, did not change after the meal. During exercise, changes in the stroke distance—heart rate product were greater when fasted. 3. Resting forearm and calf vascular resistance were higher when fasted. Calf vascular resistance fell further after exercise when fasted. Resting superior mesenteric artery vascular resistance was lower when fed; 0.19 ± 0.02 compared with 032 ± 0.06, P < 0.05. After exercise, superior mesenteric artery vascular resistance had risen by 82%, to 0.53 ± 0.12, P < 0.05 (fasted) and by 47%, to 0.29 ± 0.05, P < 0.05 (fed). 4. On standing, absolute levels of blood pressure were higher when fasted [83 ± 7/52 ± 7 compared with 71 ± 2/41 ± 3 (fed), each P < 0.05]. Subjects were more symptomatic on standing post-exercise when fed. 5. In human sympathetic denervation, exercise in the fed state lowered blood pressure further than when fasted and worsened symptoms of postural hypotension.

Haemodynamic responses to psychosocial stress during the menstrual cycle

1991 ◽  
Vol 81 (1) ◽  
pp. 17-22 ◽  
Author(s):  
Karin Manhem ◽  
Christina Jern ◽  
Martin Pilhall ◽  
Guy Shanks ◽  
Sverker Jern
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Menstrual Cycle ◽  
Systolic Blood Pressure ◽  
Psychosocial Stress ◽  
Mental Stress ◽  
Luteal Phase ◽  
Follicular Phase ◽  
Two Phases ◽  
Plasma Catecholamine Concentrations

1. The haemodynamic effects of hormonal changes during the menstrual cycle were examined in 11 normotensive women (age 20–46 years). The subjects were studied on days 2–8 (follicular phase) and days 18–26 (luteal phase) in a randomized order. A standardized mental stress test and a 24 h recording of ambulatory blood pressure and heart rate were performed. 2. Pre-stress resting levels of heart rate and blood pressure were similar during the two phases of the menstrual cycle. 3. During mental stress, the heart rate response was significantly greater during the luteal phase than during the follicular phase (14.7 versus 9.7 beats/min; P < 0.05). 4. Blood pressure, plasma catecholamine concentrations and subjective stress experience increased significantly in response to stress, without any significant differences between the two phases. 5. During 24 h ambulatory monitoring, higher levels of systolic blood pressure and heart rate were observed in the luteal phase than in the follicular phase (P < 0.005 and P < 0.0001, respectively). 6. These data indicate that cyclic variations in female sex hormones not only affect systolic blood pressure and heart rate, but also alter the haemodynamic responses to psychosocial stress.

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