Blood pressure and norepinephrine spillover during propranolol infusion in humans

1985 ◽  
Vol 248 (4) ◽  
pp. R400-R406 ◽  
Author(s):  
J. D. Best ◽  
J. B. Halter
Keyword(s):  
Blood Pressure ◽  
Control Period ◽  
Normal Subjects ◽  
Plasma Norepinephrine ◽  
Base Line ◽  
Adrenergic Blockade ◽  
Arterial Blood ◽  
Norepinephrine Infusion ◽  
Arterial Plasma ◽  
Norepinephrine Spillover

To determine whether a reflex increase of sympathetic nervous system activity contributes to maintenance of blood pressure during acute beta-adrenergic blockade, we measured plasma norepinephrine levels and norepinephrine kinetics during propranolol administration. During a 90-min infusion of propranolol (10 mg iv + 80 micrograms/min) in 12 normal subjects, heart rate fell from 56 +/- 2 to 49 +/- 2 (SE) beats/min (P less than 0.001), but there was no fall in mean arterial blood pressure (84 +/- 3 mmHg before and 86 +/- 3 mmHg after propranolol). Arterial plasma norepinephrine levels rose from 183 +/- 20 to 250 +/- 29 pg/ml during propranolol (P less than 0.001), suggesting increased sympathetic vasoconstrictor tone. However, isotope dilution studies using tritiated norepinephrine infusion showed that arterial plasma levels of tritiated norepinephrine rose from 743 +/- 78 to 1,002 +/- 101 dpm/ml during propranolol (P less than 0.001), indicating a reduction in the rate of norepinephrine clearance from plasma. The calculated fall in clearance from 1.90 +/- 0.13 to 1.42 +/- 0.11 1/min (P less than 0.001) entirely accounted for the rise in plasma norepinephrine, since the calculated rate of norepinephrine spillover into plasma remained at the base-line level of 340 +/- 40 ng/min during propranolol. In control studies on four subjects, arterial plasma norepinephrine levels and norepinephrine kinetics did not change from base line during the control period. We conclude that maintenance of blood pressure during propranolol infusion is not due to a reflex generalized increase of sympathetic vasoconstrictor tone.

Effects of vasomotor- and mediator-induced hypotension on bronchomotor tone in swine

1989 ◽  
Vol 66 (4) ◽  
pp. 1852-1859 ◽  
Author(s):  
S. R. White ◽  
J. S. Blake ◽  
T. M. Murphy ◽  
M. M. Mack ◽  
N. M. Munoz ◽  
...  
Keyword(s):  
Plasma Norepinephrine ◽  
Base Line ◽  
Adrenergic Blockade ◽  
Plasma Epinephrine ◽  
Induced Hypotension ◽  
Arterial Blood ◽  
Lung Resistance ◽  
Induced Changes ◽  
Mast Cell Degranulating

We studied the sympathetic neural response on airways to hypotensive stimuli in 19 swine in vivo. The effects of pharmacologically induced hypotension with nitroprusside (NTP) and hypotension elicited by intravenous compound 48/80 (48/80), a mast cell degranulating agent, were compared after equivalent reductions in mean arterial blood pressure (MAP). Reduction of the MAP to 60% of base line with NTP in six swine caused an increase in plasma epinephrine (E) from 60 +/- 28 to 705 +/- 276 pg/ml (P = 0.032) and plasma norepinephrine (NE) from 270 +/- 46 to 796 +/- 131 pg/ml (P = 0.032). Comparable reduction in MAP elicited with 48/80 in six other swine caused a substantially greater increase in both plasma E (9,581 +/- 4,147 pg/ml; P = 0.012 vs. NTP group) and plasma NE (2,239 +/- 637 pg/ml; P = 0.041 vs. NTP group). Catecholamine secretion attenuated mediator-induced changes in lung resistance (RL). In animals receiving 48/80, RL increased from 2.97 +/- 0.31 to 7.44 +/- 0.56 cmH2O.l-1.s. In animals having ganglionic blockade with 7.5 mg/kg iv hexamethonium and beta-adrenergic blockade with propranolol (4.0 mg/kg iv followed by 40 micrograms/kg-1.min-1), comparable doses of 48/80 caused an increase in RL to 18.6 +/- 4.55 cmH2O.l-1.s (P less than 0.04 vs. swine receiving neither hexamethonium nor propranolol).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular responses to ice-cold showers

1964 ◽  
Vol 19 (6) ◽  
pp. 1145-1150 ◽  
Author(s):  
William R. Keatinge ◽  
Malcolm B. McIlroy ◽  
Alan Goldfien
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Cold Water ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Cardiovascular Responses ◽  
Normal Subjects ◽  
Plasma Norepinephrine ◽  
Arterial Blood ◽  
Sympathetic Nervous

A shower of ice-cold water (0@#X2013;2.5 C) over the chest caused large increases in systolic and diastolic arterial pressures, pulse pressure, and pulse rate in normal subjects. Cardiac output rose by 59 and 100% in the two subjects in whom it was measured. The changes in pressure were considerably larger than those caused by a cold pressor test or by anxiety. The changes appear to be due to sympathetic nervous reflexes to the heart and blood vessels rather than release of adrenal catecholamines, as plasma epinephrine did not increase and plasma norepinephrine rose only by 0.32 @#X00B5;g/liter. Hyperventilation and evidence of peripheral venoconstriction occurred during the showers, but neither voluntary hyperventilation nor increased venous return from a change in posture produced the changes in blood pressure seen during shower arterial blood pressure; cardiac output; catecholamines; sympathetic nervous reflexes; hyperventilation; peripheral venoconstriction Submitted on March 10, 1964

scholarly journals Increased superoxide levels in ganglia and sympathoexcitation are involved in sarafotoxin 6c-induced hypertension

2008 ◽  
Vol 295 (5) ◽  
pp. R1546-R1554 ◽  
Author(s):  
Melissa Li ◽  
Xiaoling Dai ◽  
Stephanie Watts ◽  
David Kreulen ◽  
Gregory Fink
Keyword(s):  
Blood Pressure ◽  
Sympathetic Innervation ◽  
Sympathetic Ganglia ◽  
Plasma Norepinephrine ◽  
Sprague Dawley ◽  
Surgical Ablation ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
Induced Hypertension ◽  
Hypertension Development

Endothelin (ET) type B receptors (ETBR) are expressed in multiple tissues and perform different functions depending on their location. ETBR mediate endothelium-dependent vasodilation, clearance of circulating ET, and diuretic effects; all of these should produce a fall in arterial blood pressure. However, we recently showed that chronic activation of ETBR in rats with the selective agonist sarafotoxin 6c (S6c) causes sustained hypertension. We have proposed that one mechanism of this effect is constriction of capacitance vessels. The current study was performed to determine whether S6c hypertension is caused by increased generation of reactive oxygen species (ROS) and/or activation of the sympathetic nervous system. The model used was continuous 5-day infusion of S6c into male Sprague-Dawley rats. No changes in superoxide anion levels in arteries and veins were found in hypertensive S6c-treated rats. However, superoxide levels were increased in sympathetic ganglia from S6c-treated rats. In addition, superoxide levels in ganglia increased progressively the longer the animals received S6c. Treatment with the antioxidant tempol impaired S6c-induced hypertension and decreased superoxide levels in ganglia. Acute ganglion blockade lowered blood pressure more in S6c-treated rats than in vehicle-treated rats. Although plasma norepinephrine levels were not increased in S6c hypertension, surgical ablation of the celiac ganglion plexus, which provides most of the sympathetic innervation to the splanchnic organs, significantly attenuated hypertension development. The results suggest that S6c-induced hypertension is partially mediated by sympathoexcitation to the splanchnic organs driven by increased oxidative stress in prevertebral sympathetic ganglia.

Effect of chronic left ventricular failure on beta-endorphin

1992 ◽  
Vol 73 (6) ◽  
pp. 2675-2680 ◽  
Author(s):  
E. Mellow ◽  
E. Redei ◽  
K. Marzo ◽  
J. R. Wilson
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Chronic Heart Failure ◽  
Left Ventricular ◽  
Plasma Norepinephrine ◽  
Endogenous Opiates ◽  
Beta Endorphin ◽  
Arterial Blood ◽  
Norepinephrine Concentration ◽  
C 30

Stimulation of endogenous opiate secretion worsens circulatory dysfunction in several forms of shock, in part by inhibiting sympathetic activity. To investigate whether endogenous opiates have a similar effect in chronic heart failure (HF), we measured beta-endorphin concentrations and hemodynamic responses to naloxone infusion (2 mg/kg bolus + 2 mg.kg-1 x h-1) in six control (C) dogs and eight dogs with low-output HF produced by 3 wk of rapid ventricular pacing. The dogs with HF exhibited reduced arterial blood pressure (C, 123 +/- 4 vs. HF, 85 +/- 7 mmHg; P < 0.01) and cardiac outputs (C, 179 +/- 14 vs. HF, 76 +/- 2 ml.min-1 x kg-1; P < 0.01) and elevated plasma norepinephrine concentrations (C, 99 +/- 12 vs. HF, 996 +/- 178 pg/ml; P < 0.01) but normal beta-endorphin concentrations (C, 30 +/- 11 vs. HF, 34 +/- 12 pg/ml; P = NS). Naloxone produced similar transitory increases in blood pressure (C, 14 +/- 5 vs. HF, 26 +/- 25%) and cardiac output (C, 37 +/- 13 vs. HF, 22 +/- 15%) in both groups (both P = NS). No significant changes in norepinephrine concentration or systemic vascular resistance were observed in either group. These findings suggest that beta-endorphin secretion does not exacerbate circulatory dysfunction in chronic heart failure.

Enhancement of the Antihypertensive Effect of Hydrochlorothiazide in Dogs after Suppression of Renin Release by Beta-Adrenergic Blockade

1975 ◽  
Vol 48 (2) ◽  
pp. 147-151
Author(s):  
C. S. Sweet ◽  
M. Mandradjieff
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Arterial Blood Pressure ◽  
Antihypertensive Effect ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Antihypertensive Activity ◽  
Adrenergic Blockade ◽  
Arterial Blood

1. Renal hypertensive dogs were treated with hydrochlorothiazide (8−2 μmol/kg or 33 μmol/kg daily for 7 days), or timolol (4.6 μmol/kg daily for 4 days), a potent β-adrenergic blocking agent, or combinations of these drugs). Changes in mean arterial blood pressure and plasma renin activity were measured over the treatment period. 2. Neither drug significantly lowered arterial blood pressure when administered alone. Plasma renin activity, which did not change during treatment with timolol, was substantially elevated during treatment with hydrochlorothiazide. 3. When timolol was administered concomitantly with hydrochlorothiazide, plasma renin activity was suppressed and blood pressure was significantly lowered. 4. These observations suggest that compensatory activation of the renin-angiotensin system limits the antihypertensive activity of hydrochlorothiazide in renal hypertensive dogs and suppression of diuretic-induced renin release by timolol unmasks the antihypertensive effect of the diuretic.

The relationship of blood flow velocity fluctuations to intracranial pressure B waves

1992 ◽  
Vol 76 (3) ◽  
pp. 415-421 ◽  
Author(s):  
David W. Newell ◽  
Rune Aaslid ◽  
Renate Stooss ◽  
Hans J. Reulen
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Intracranial Pressure ◽  
Arterial Blood Pressure ◽  
Wave Amplitude ◽  
Transcranial Doppler Ultrasound ◽  
Normal Subjects ◽  
Content Type ◽  
Arterial Blood ◽  
Flow Fluctuations

✓ Intracranial pressure (ICP) and continuous transcranial Doppler ultrasound signals were monitored in 20 head-injured patients and simultaneous synchronous fluctuations of middle cerebral artery (MCA) velocity and B waves of the ICP were observed. Continuous simultaneous monitoring of MCA velocity, ICP, arterial blood pressure, and expired CO2 revealed that both velocity waves and B waves occurred despite a constant CO2 concentration in ventilated patients and were usually not accompanied by fluctuations in the arterial blood pressure. Additional recordings from the extracranial carotid artery during the ICP B waves revealed similar synchronous fluctuations in the velocity of this artery, strongly supporting the hypothesis that blood flow fluctuations produce the velocity waves. The ratio between ICP wave amplitude and velocity wave amplitude was highly correlated to the ICP (r = 0.81, p < 0.001). Velocity waves of similar characteristics and frequency, but usually of shorter duration, were observed in seven of 10 normal subjects in whom MCA velocity was recorded for 1 hour. The findings in this report strongly suggest that B waves in the ICP are a secondary effect of vasomotor waves, producing cerebral blood flow fluctuations that become amplified in the ICP tracing, in states of reduced intracranial compliance.

Bradykinin and renal function in normal man: effects of adrenergic blockade

1965 ◽  
Vol 209 (4) ◽  
pp. 844-848 ◽  
Author(s):  
John R. Gill ◽  
Kenneth L. Melmon ◽  
Louis Gillespie ◽  
Frederic C. Bartter
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Normal Subjects ◽  
Adrenergic Blockade ◽  
Disease States ◽  
Lower Blood ◽  
Normal Man ◽  
Endogenous Release ◽  
Infusion Of Norepinephrine ◽  
As Effects

Renal function was studied in five normal subjects during the infusion of bradykinin at 0.1 and 0.4 µg/kg per min, and in four additional normal subjects during the infusion of norepinephrine at dosages beginning with 1–3 µg/ min. Bradykinin at both dosages decreased glomerular filtration rate (GFR) and tended to increase renal blood flow (ERPF). It increased sodium excretion (UNaV) at the lower dosage, but did not increase it further at the higher dosage. At all dosages, norepinephrine decreased ERPF and UNaV. The effects of bradykinin cannot be explained solely as effects of norepinephrine released by the bradykinin. During adrenergic blockade produced by guanethidine, bradykinin, 0.1 µg/kg per min, slightly decreased GFR and UNaV; at 0.4 µg/kg per min, it further decreased GFR and UNaV and tended to decrease ERPF as well. It did not lower blood pressure. The data suggest that in normal man, bradykinin increases UNaV only at low dosages. During adrenergic blockade, endogenous release of angiotensin could have prevented bradykinin from lowering blood pressure and could have caused the decreases in GFR, ERPF, and UNaV. A possible role is suggested for bradykinin in the physiologic control of renal function, and as a causative agent in producing the changes in renal function found in certain disease states characterized by excessive production of kinins.

Blood pressure during routine activity, stress, and feeding in black racer snakes (Coluber constrictor)

1993 ◽  
Vol 264 (1) ◽  
pp. R79-R84 ◽  
Author(s):  
J. N. Stinner ◽  
D. L. Ely
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Acute Stress ◽  
Pressor Response ◽  
Routine Activity ◽  
Plasma Norepinephrine ◽  
Arterial Blood ◽  
Coluber Constrictor ◽  
S Peak ◽  
Hematological Changes

The pressor response to normal daily behaviors and acute stress was studied in black racer snakes (Coluber constrictor) at 30 degrees C. In addition, hematological changes during the stress response were assessed. Mean nighttime systemic arterial blood pressure (SABP) in undisturbed snakes was lower than daytime pressure (26 +/- 3 vs. 32 +/- 9 mmHg, P < 0.001). When snakes were fed mice, SABP increased 3.5- to 4-fold and heart rate increased approximately 3-fold above resting values within approximately 30 s (peak SABP, 99 +/- 18 mmHg; peak heart rate, 99 +/- 12 beats/min). Killing and ingesting the mice required 6-15 min, during which time mean SABP and heart rate were 84 +/- 16 mmHg and 92 +/- 12 beats/min. Pulmonary blood pressure also increased but remained 40-50 mmHg lower than SABP. During stress elicited by tapping the snakes for 5-8 min, heart rate was 94 +/- 6 beats/min but SABP averaged only 44 +/- 11 mmHg. Plasma norepinephrine and epinephrine increased 51- and 26-fold. Plasma glucose increased 58%, hematocrit increased 19%, and plasma volume decreased 19%. It is concluded that blood pressure is markedly affected by behavior and that the sympathetic nervous system appears to play a key role.

Effects of the cold pressor test on short-term fluctuations of finger arterial blood pressure and heart rate in normal subjects

1993 ◽  
Vol 3 (5) ◽  
pp. 303-310 ◽  
Author(s):  
Frank Weise ◽  
Dominique Laude ◽  
Arlette Girard ◽  
Philippe Zitoun ◽  
Jean-Philippe Siché ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Normal Subjects ◽  
Short Term ◽  
Pressor Test ◽  
Arterial Blood

Suctioning and Cerebral Blood Flow

PEDIATRICS ◽  
1984 ◽  
Vol 73 (5) ◽  
pp. 737-737
Author(s):  
JEFFREY M. PERLMAN ◽  
JOSEPH J. VOLPE
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Flow Velocity ◽  
Arterial Blood Pressure ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Base Line ◽  
Arterial Blood

In Reply.— Marshall misread a critical piece of information in the text. His interpretation of the data would be correct, if the intracranial pressure, arterial blood pressure, and cerebral blood flow velocity changes occurred simultaneously. However, as we stated in the text (see section on "Temporal Features of Changes with Suctioning"), the intracranial pressure fell to base-line values immediately following suctioning, whereas the changes in arterial blood pressure and cerebral blood flow velocity occurred more slowly over an approximately two-minute period.

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