Yohimbine increases sympathetic nerve activity and norepinephrine spillover in normal volunteers

1991 ◽  
Vol 260 (1) ◽  
pp. R142-R147 ◽  
Author(s):  
E. Grossman ◽  
R. F. Rea ◽  
A. Hoffman ◽  
D. S. Goldstein
Keyword(s):  
Sympathetic Nerve ◽  
Physiological Role ◽  
Normal Volunteers ◽  
Arterial Blood ◽  
The Mean ◽  
Arterial Plasma ◽  
Human Limb ◽  
Norepinephrine Spillover ◽  
Forearm Vascular Resistance

It has been difficult to examine clinically the physiological role of central and peripheral alpha 2-adrenoceptors in humans. We simultaneously measured directly recorded peroneal skeletal muscle sympathoneural activity (MSNA) and the rate of appearance (spillover) of norepinephrine (NE) in forearm venous and arterial plasma before and at 15 min during intravenous administration of the alpha 2-blocker yohimbine (Yoh, 125 micrograms/kg bolus, 1 microgram.kg-1.min-1 infusion) in seven normal volunteers. Yoh administration increased mean arterial pressure by 16% (P less than 0.005), heart rate by 8% (P less than 0.05), and forearm vascular resistance by 67% (P less than 0.05). MSNA was increased by 73% (P less than 0.05), NE spillover into arterial blood by 125% (P less than 0.05), and forearm NE spillover (FSO) by 337% (P less than 0.005). Ganglion blockade by trimethaphan during Yoh infusion decreased MSNA to below detection limits and reversed Yoh-induced increases in arterial concentrations of NE and epinephrine. The results demonstrate that Yoh administration increases sympathoadrenal outflow. Because the mean increase of FSO was much larger than that of MSNA, the results suggest that alpha 2-adrenoceptors on sympathetic nerve endings modulate the neuronal release of NE for a given amount of sympathetic nerve traffic in humans; this effect seems prominent in the human limb.

Plasma secretin concentrations in fasting and postprandial states in dog.

1979 ◽  
Vol 236 (5) ◽  
pp. E539 ◽  
Author(s):  
M S Kim ◽  
K Y Lee ◽  
W Y Chey
Keyword(s):  
Pancreatic Secretion ◽  
Physiological Role ◽  
Fasting State ◽  
Meat Meal ◽  
Duodenal Ph ◽  
The Mean ◽  
Bicarbonate Output ◽  
Marked Suppression ◽  
Sustained Increase

In four dogs with a modified Herrara pancreatic fistula and gastric cannula and three dogs with two duodenal cannulas, ingestion of a meat meal resulted in a significant and sustained increase in the mean plasma immunoreactive secretin concentrations, from mean fasting levels of less than 10 pg/ml to 25--55 pg/ml. This increase in the plasma secretin concentration coincided with a marked increase in pancreatic bicarbonate output and frequent decreases in the mean proximal duodenal pH to less than 4.5 from the range of 6.5 in the fasting state. Intravenous administration of cimetidine, 150 mg, produced a marked suppression of postprandial increases in both pancreatic bicarbonate output and plasma secretin concentration. Moreover, the postprandial duodenal pH rarely reached below 5.0 after cimetidine administration. These studies indicate that plasma secretin concentration does increase significantly after a meal. The postprandial increase in plasma secretin concentration appears to depend on the gastric acid delivered in the proximal duodenum. A possible physiological role of secretin in the pancreatic secretion after a meal is indicated by these findings.

scholarly journals A reversal of fate : unravelling the role of central 5-HT in cardiorespiratory control in neonatal and adult rodents

2018 ◽  
Author(s):  
◽  
Jennifer Magnusson
Keyword(s):  
Blood Pressure ◽  
Physiological Role ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Autonomic Tone ◽  
Neurogenic Hypertension ◽  
Cardiorespiratory Control ◽  
Arterial Blood ◽  
Lower Blood

We seek to address the extent to which a specific loss of 5-hydroxytryptamine (5-HT) affects the control of respiration, arterial blood pressure (ABP) and heart rate (HR) across vigilance-states based on existing evidence suggesting that 5-HT defects increase the risk for Sudden Infant Death Syndrome (SIDS) and neurogenic hypertension. SIDS is the leading cause of infant mortality between 1 month and 1 year of age, occurs during sleep, and up to 70% of all SIDS cases have at least one 5-HT system abnormality. Neonatal rodents lacking central 5-HT exhibit severe apneas, and a reduced ABP and HR. Central 5-HT has been implicated in the etiology of neurogenic hypertension, presumably due to projections of 5-HT neurons within the midline raphe to vagal and presympathetic regions of the brain. However, data from studies examining the specific role of central 5-HT function is conflicting or inconclusive. Neurogenic hypertension accounts for more than 90% of all hypertensive cases and the normal fall in ABP that occurs during non-rapid eye movement sleep is absent in some patients with hypertension. Understanding the mechanisms associated with the development of hypertension is critical not only to lower blood pressure, but to lower its associated cardiovascular events. The purpose of this dissertation is to examine the role of central 5-HT in the control of ABP during sleep and reveal, mechanistically, the physiological role of 5-HT in the autonomic control of ABP in neonatal and adult rodents. The overarching hypothesis for this dissertation is that central 5-HT is required for the maintenance of ABP and autonomic tone at rest in both neonatal and adult rodents.

Ouabain is secreted by the adrenal gland in awake dogs

1993 ◽  
Vol 264 (3) ◽  
pp. E413-E419 ◽  
Author(s):  
B. R. Boulanger ◽  
M. P. Lilly ◽  
J. M. Hamlyn ◽  
J. Laredo ◽  
D. Shurtleff ◽  
...  
Keyword(s):  
Adrenal Gland ◽  
Blood Volume ◽  
Random Order ◽  
Paired Samples ◽  
Arterial Blood ◽  
Blood Volume Expansion ◽  
The Mean ◽  
Arterial Plasma ◽  
Adrenal Secretion

Ouabain has been identified in the plasma and adrenal glands of several mammals, including humans. To investigate possible adrenal secretion of ouabain in vivo, at rest, and in response to acute blood volume changes, we prepared trained adult dogs (n = 10) with splenectomy and unilateral adrenal venous (AV) cannulation. Two days later, after an overnight fast, dogs had either 1) 20% hemorrhage (hem) or 2) 20% blood volume expansion (exp; 6% Dextran 70, 0.9% NaCl) in random order. In AV and arterial plasma (ART), ouabain was measured by a ouabain-specific immunoassay, and cortisol and aldosterone were measured by radioimmunoassay. ART and AV ouabain concentration did not change after hem or exp [P = not significant (NS)]. In 94 of 97 paired samples, the concentration of ouabain in AV was greater than that in ART (Wilcoxon, P < 0.001), and the mean ouabain concentration was greater in AV (756.4 +/- 85.7 pmol/l) than ART (235.4 +/- 18.5 pmol/l; P < 0.001). The mean AV-to-ART ouabain concentration ratio was 5.7 +/- 1.29. Adrenal secretion of ouabain was not influenced by hem or exp (analysis of variance, P = NS). Adrenal secretion of cortisol and aldosterone increased after hem (P < 0.05) and was unaltered by exp (P = NS). This study demonstrates that ouabain is secreted by the adrenal gland in the awake dog. However, adrenal ouabain secretion and arterial blood ouabain are not altered by acute hem or exp.

scholarly journals Role of small conductance calcium-activated potassium channels expressed in PVN in regulating sympathetic nerve activity and arterial blood pressure in rats

2012 ◽  
Vol 303 (3) ◽  
pp. R301-R310 ◽  
Author(s):  
Le Gui ◽  
Lila P. LaGrange ◽  
Robert A. Larson ◽  
Mingjun Gu ◽  
Jianhua Zhu ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Channel Blocker ◽  
Dependent Manner ◽  
Sk Channels ◽  
Nerve Activity ◽  
Arterial Blood ◽  
Sk Channel ◽  
Small Conductance

Small conductance Ca2+-activated K+ (SK) channels regulate membrane properties of rostral ventrolateral medulla (RVLM) projecting hypothalamic paraventricular nucleus (PVN) neurons and inhibition of SK channels increases in vitro excitability. Here, we determined in vivo the role of PVN SK channels in regulating sympathetic nerve activity (SNA) and mean arterial pressure (MAP). In anesthetized rats, bilateral PVN microinjection of SK channel blocker with peptide apamin (0, 0.125, 1.25, 3.75, 12.5, and 25 pmol) increased splanchnic SNA (SSNA), renal SNA (RSNA), MAP, and heart rate (HR) in a dose-dependent manner. Maximum increases in SSNA, RSNA, MAP, and HR elicited by apamin (12.5 pmol, n = 7) were 330 ± 40% ( P < 0.01), 271 ± 40% ( P < 0.01), 29 ± 4 mmHg ( P < 0.01), and 34 ± 9 beats/min ( P < 0.01), respectively. PVN injection of the nonpeptide SK channel blocker UCL1684 (250 pmol, n = 7) significantly increased SSNA ( P < 0.05), RSNA ( P < 0.05), MAP ( P < 0.05), and HR ( P < 0.05). Neither apamin injected outside the PVN (12.5 pmol, n = 6) nor peripheral administration of the same dose of apamin (12.5 pmol, n = 5) evoked any significant changes in the recorded variables. PVN-injected SK channel enhancer 5,6-dichloro-1-ethyl-1,3-dihydro-2H-benzimidazol-2-one (DCEBIO, 5 nmol, n = 4) or N-cyclohexyl- N-[2-(3,5-dimethyl-pyrazol-1-yl)-6-methyl-4-pyrimidin]amine (CyPPA, 5 nmol, n = 6) did not significantly alter the SSNA, RSNA, MAP, and HR. Western blot and RT-PCR analysis of punched PVN tissue showed abundant expression of SK1-3 channels. We conclude that SK channels expressed in the PVN play an important role in the regulation of sympathetic outflow and cardiovascular function.

Surges of muscle sympathetic nerve activity during obstructive apnea are linked to hypoxemia

1995 ◽  
Vol 79 (2) ◽  
pp. 581-588 ◽  
Author(s):  
U. Leuenberger ◽  
E. Jacob ◽  
L. Sweer ◽  
N. Waravdekar ◽  
C. Zwillich ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Matched Control ◽  
Sleep Stage ◽  
Muscle Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Obstructive Apnea ◽  
Arterial Blood ◽  
Obstructive Sleep

Obstructive sleep apnea (OSA) is associated with oscillations of arterial blood pressure (BP) that occur in phase with irregularities of respiration. To explore the role of the sympathetic nervous system in these responses, we studied muscle sympathetic nerve activity (MSNA; peroneal microneurography), an index of vasoconstrictor nerve traffic, and BP during awake regular breathing and during spontaneous apneas in patients with OSA. To determine the role of the arterial chemoreflex, we also examined the effects of 100% O2 (hyperoxia) on MSNA and BP. In awake regularly breathing patients with OSA (n = 12), resting MSNA was markedly higher than in an age-matched control population (n = 15) [41 +/- 23 (SD) vs. 24 +/- 17 bursts/min; P < 0.05] and was unchanged during hyperoxia (n = 9). Apneas during sleep (n = 8) were associated with surges in MSNA followed by transient rises in BP when breathing resumed. In contrast to room air apneas, hyperoxic apneas of similar duration were associated with attenuated MSNA responses (+82 +/- 84% vs. +5 +/- 25% compared with awake baseline; P < 0.05; n = 6), even though O2 did not affect sleep stage and the occurrence of arousal. Thus the BP oscillations that occur with apnea during sleep may in part be mediated by intermittent surges of sympathetic activity resulting in vasoconstriction. Because the MSNA responses to obstructive apnea are blunted during O2 administration, they appear to be linked to intermittent arterial hypoxemia and stimulation of arterial chemoreceptors.

Effect of changes in carotid sinus pulse pressure on catecholamine blood levels

1963 ◽  
Vol 204 (3) ◽  
pp. 467-470 ◽  
Author(s):  
Jiro Nakano ◽  
Christian De Schryver
Keyword(s):  
Pulse Pressure ◽  
Plasma Levels ◽  
Carotid Sinus ◽  
Blood Levels ◽  
Arterial Pulse ◽  
Arterial Blood ◽  
The Common ◽  
The Mean ◽  
Common Carotid Arteries

A study was made on the effect of changes in arterial pulse pressure per se on catecholamine secretion in the anesthetized dog. "Elasticity" bottles were inserted bilaterally in the common carotid arteries in order to change the magnitude of the pulse pressure in the carotid sinus areas without changing the mean arterial blood pressure. It was observed that a marked decrease in the pulse pressure resulted in significant increases in heart rate ( P < 0.005) and catecholamine plasma levels ( P < 0.005). The mechanism and role of this increase in plasma levels of catecholamines are discussed.

Role of hypotension in altering blood coagulability after endotoxin

1962 ◽  
Vol 202 (3) ◽  
pp. 519-522 ◽  
Author(s):  
Frank A. Carozza ◽  
J. Dixon Hills
Keyword(s):  
Isotonic Saline ◽  
Treated Group ◽  
Base Line ◽  
E Coli ◽  
Arterial Blood ◽  
Blood Pressures ◽  
Blood Coagulability ◽  
The Mean ◽  
Specific Reactions

Because hypotension, regardless of etiology, profoundly influences blood coagulation, the role of hypotension in altering blood coagulability after endotoxin was investigated. By means of femoral artery catheterization, serial whole blood clotting times were determined in siliconized tubes at 37 C and correlated with mean arterial blood pressures in 1-kg albino rabbits. After duplicate base-line determinations, 200 µg/kg E. coli endotoxin was injected intravenously into nine animals; this quantity of endotoxin was the largest dose not lethal to normal rabbits of the strain employed. Nine control animals received isotonic saline. Blood from the endotoxin-treated group exhibited some accelerated coagulability between 1–2 hr after endotoxin injection and became significantly hypercoagulable ( P < 0.05) during the 3rd and 4th hr. The observed hypercoagulability could not be correlated with the hypotensive arterial blood pressure levels, the mean coefficient of correlation being –0.18. These data suggest that endotoxin-induced hypercoagulability in the rabbit results from specific reactions that are mediated by mechanisms distinct from those known to operate during the hypotensive state per se.

Response of phosphoenolpyruvate cycle activity to fasting and to hyperinsulinemia in human subjects

1996 ◽  
Vol 271 (1) ◽  
pp. E159-E176 ◽  
Author(s):  
R. R. Wolfe ◽  
D. Chinkes ◽  
H. Baba ◽  
J. Rosenblatt ◽  
X. J. Zhang
Keyword(s):  
Human Subjects ◽  
Physiological Role ◽  
Forward Direction ◽  
Metabolic Adaptation ◽  
Tracer Technique ◽  
Short Term ◽  
Isotopic Tracer ◽  
Normal Volunteers ◽  
Net Flux

We have used a new isotopic tracer technique to investigate the physiological role of the phosphoenolpyruvate (PEP) cycle in metabolic adaptation to fasting and to hyperinsulinemia. The forward direction of the PEP cycle is the conversion of oxaloacetate (OAA) to PEP, and the net flux of the cycle is the rate at which PEP from OAA goes on to form glucose or glycogen, as opposed to being recycled to pyruvate and then OAA. Normal volunteers (n = 6) were studied after an overnight fast and then again after 3 days of fasting, and five additional subjects were studied during a hyperinsulinemic clamp (insulin concentration = 568 +/- 25 microU/ml, glucose infusion = 14.2 +/- 0.55 mg.kg-1.min-1). After an overnight fast, 35.4 +/- 6.7% of PEP from OAA was recycled to pyruvate-lactate. Short-term fasting caused a significant increase in the conversion of OAA to PEP and also a drop in the percentage of PEP from OAA that went to pyruvate-lactate to 15.2 +/- 4.0%. The principal response to hyperinsulinemia was a decrease in the recycling of OAA to lactate, because there was no significant change in the conversion of OAA to PEP. We conclude that changes in both directions of the PEP cycle are important in regulating gluconeogenic-glyconeogenic flux.

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.

The Role of Plasma Volume in the Increase of Aldosterone Secretion Rate during Sodium Deprivation

1975 ◽  
Vol 48 (3) ◽  
pp. 161-165 ◽  
Author(s):  
T. G. Dalakos ◽  
D. H. P. Streeten
Keyword(s):  
Plasma Volume ◽  
Upright Posture ◽  
Aldosterone Secretion ◽  
Normal Volunteers ◽  
Sodium Diet ◽  
Albumin Infusion ◽  
Significant Difference ◽  
The Mean ◽  
Secretion Rates

1. 24 h aldosterone secretion rates (ASR) have been measured in six normal volunteers while recumbent all day and while standing for 12 h, on 200 and 10 mmol/day sodium diets and after salt-poor albumin infusions (75 g in 150 ml), which significantly expanded plasma volume. 2. The mean ASR on the 10 mmol/day sodium diet, both without and with the salt-poor albumin infusion, was highly significantly increased above the mean ASR on the 200 mmol/day sodium diet, both in the recumbent and in the upright posture. 3. There was no significant difference between the mean ASR values on the 10 mmol/day sodium diet alone and after the infusion of albumin either in the recumbent or in the upright posture. 4. The above observations suggest that sodium deprivation raises ASR by a mechanism or mechanisms unrelated to plasma volume.

Sign in / Sign up

Export Citation Format

Share Document