scholarly journals Influence of plasma osmolality on baroreflex control of sympathetic activity

2007 ◽  
Vol 293 (4) ◽  
pp. H2313-H2319 ◽  
Author(s):  
Megan M. Wenner ◽  
William C. Rose ◽  
Erin P. Delaney ◽  
Michael E. Stillabower ◽  
William B. Farquhar
Keyword(s):  
Blood Pressure ◽  
Sympathetic Activity ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Saline Infusion ◽  
Sympathetic Outflow ◽  
Intravascular Volume ◽  
Baroreflex Control ◽  
Controlled Breathing ◽  
The Relationship

The purpose of this study was to determine if plasma osmolality alters baroreflex control of sympathetic activity when controlling for a change in intravascular volume; we hypothesized that baroreflex control of sympathetic activity would be greater during a hyperosmotic stimulus compared with an isoosmotic stimulus when intravascular volume expansion was matched. Seven healthy subjects (25 ± 2 yr) completed two intravenous infusions: a hypertonic saline infusion (HSI; 3% NaCl) and, on a separate occasion, an isotonic saline infusion (ISO; 0.9% NaCl), both at a rate of 0.15 ml·kg−1·min−1. To isolate the effect of osmolality, comparisons between HSI and ISO conditions were retrospectively matched based on hematocrit; therefore, baroreflex control of sympathetic outflow was determined at 20 min of a HSI and 40 min of an ISO. Muscle sympathetic outflow (MSNA) was directly measured using the technique of peroneal microneurography; osmolality and blood pressure (Finometer) were assessed. The baroreflex control of sympathetic outflow was estimated by calculating the slope of the relationship between MSNA and diastolic blood pressure during controlled breathing. Plasma osmolality was greater during the HSI compared with the ISO (HSI: 292 ± 0.9 mosmol/kg and ISO: 289 ± 0.8 mosmol/kg, P < 0.05). Hematocrits were matched (HSI: 39.1 ± 1% and ISO: 39.1 ± 1%, P > 0.40); thus, we were successful in isolating osmolality. The baroreflex control of sympathetic outflow was greater during the HSI compared with the ISO (HSI: −8.3 ± 1.2 arbitrary units·beat−1·mmHg−1 vs. ISO: −4.0 ± 0.8 arbitrary units·beat−1·mmHg−1, P = 0.01). In conclusion, when controlling for intravascular volume, increased plasma osmolality enhances baroreflex control of sympathetic activity in humans.

Sympathetic neural responses to increased osmolality in humans

2006 ◽  
Vol 291 (5) ◽  
pp. H2181-H2186 ◽  
Author(s):  
William B. Farquhar ◽  
Megan M. Wenner ◽  
Erin P. Delaney ◽  
Allen V. Prettyman ◽  
Michael E. Stillabower
Keyword(s):  
Muscle Sympathetic Nerve Activity ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Plasma Norepinephrine ◽  
Sympathetic Outflow ◽  
Neural Responses ◽  
Burst Frequency ◽  
Norepinephrine Concentration ◽  
The Relationship ◽  
Hypertonic Saline Infusion

The purpose of this study was to examine the relationship between osmolality and efferent sympathetic outflow in humans. We hypothesized that increased plasma osmolality would be associated with increases in directly measured sympathetic outflow. Muscle sympathetic outflow was successfully recorded in eight healthy subjects during a 60-min intravenous hypertonic saline infusion (HSI; 3% NaCl) on one day and during a 60-min intravenous isotonic saline (ISO) infusion (0.9% NaCl) on a different day. The HSI provides an osmotic and volume stimulus, whereas the ISO infusion provides a volume-only stimulus. Muscle sympathetic nerve activity was quantified using the technique of peroneal microneurography. Plasma osmolality increased during the HSI but not during the ISO infusion (ANOVA, P < 0.05). Sympathetic outflow differed between the trials (ANOVA, P < 0.05); during the HSI burst, frequency initially increased from 14.6 ± 2.5 to 18.1 ± 1.9 bursts/min; during the ISO infusion, burst frequency initially declined from 14.7 ± 2.5 to 12.0 ± 2.1 bursts/min. Plasma norepinephrine concentration was greater at the end of the HSI compared with the end of the ISO infusion (HSI: 297 ± 64 vs. ISO: 202 ± 49 pg/ml; ANOVA, P < 0.05). We conclude that HSI-induced increases in plasma osmolality are associated with increases in sympathetic activity in humans.

scholarly journals Influence of increased plasma osmolality on sympathetic outflow during apnea

2010 ◽  
Vol 299 (4) ◽  
pp. R1091-R1096 ◽  
Author(s):  
Jody L. Greaney ◽  
Chester A. Ray ◽  
Allen V. Prettyman ◽  
David G. Edwards ◽  
William B. Farquhar
Keyword(s):  
Muscle Sympathetic Nerve Activity ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Total Activity ◽  
Baseline Period ◽  
Saline Infusion ◽  
Volume Control ◽  
Sympathetic Outflow ◽  
Burst Frequency ◽  
Absolute Increase

Animal models have shown that peripheral chemoreceptors alter their firing patterns in response to changes in plasma osmolality, which, in turn, may modulate sympathetic outflow. The purpose of this study was to test the hypothesis that increases in plasma osmolality augment muscle sympathetic nerve activity (MSNA) responses to chemoreceptor activation. MSNA was recorded from the peroneal nerve (microneurography) during a 23-min intravenous hypertonic saline infusion (3% NaCl; HSI). Chemoreceptor activation was elicited by voluntary end-expiratory apnea. MSNA responses to end-expiratory apnea were calculated as the absolute increase from the preceding baseline period. Plasma osmolality significantly increased from pre- to post-HSI (284 ± 1 to 290 ± 1 mOsm/kg H2O; P < 0.01). There was a significant overall effect of osmolality on sympathetic activity ( P < 0.01). Duration of the voluntary end-expiratory apnea was not different after HSI (pre = 40 ± 5 s; post = 41 ± 4 s). MSNA responses to end-expiratory apnea were not different after HSI, expressed as an absolute change in burst frequency ( n = 11; pre = 8 ± 2; post = 11 ± 1 burst/min) and as a percent increase in total activity (pre = 51 ± 4% AU; post = 53 ± 4% AU). A second group of subjects ( n = 8) participated in 23-min volume/time-control intravenous isotonic saline infusions (0.9% NaCl). Isotonic saline volume-control infusions yielded no change in plasma osmolality or MSNA at rest. Furthermore, MSNA responses to apnea following isotonic saline infusion were not different. In summary, elevated plasma osmolality increased MSNA at rest and during apnea, but contrary to the hypothesis, MSNA responsiveness to apnea was not augmented. Therefore, this study does not support a neural interaction between plasma osmolality and chemoreceptor stimulation.

Feedback effects of circulating norepinephrine on sympathetic outflow in healthy subjects

2005 ◽  
Vol 288 (2) ◽  
pp. H710-H715 ◽  
Author(s):  
Mikko P. Tulppo ◽  
Heikki V. Huikuri ◽  
Elli Tutungi ◽  
Derek S. Kimmerly ◽  
Adrian W. Gelb ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Sympathetic Activity ◽  
Healthy Subjects ◽  
Blood Pressure Variability ◽  
Feedback Inhibition ◽  
Adrenergic Blockade ◽  
Sympathetic Outflow ◽  
Systolic Blood Pressure Variability ◽  
Normalized Units

The amplitude of low-frequency (LF) oscillations of heart rate (HR) usually reflects the magnitude of sympathetic activity, but during some conditions, e.g., physical exercise, high sympathetic activity results in a paradoxical decrease of LF oscillations of HR. We tested the hypothesis that this phenomenon may result from a feedback inhibition of sympathetic outflow caused by circulating norepinephrine (NE). A physiological dose of NE (100 ng·kg−1·min−1) was infused into eight healthy subjects, and infusion was continued after α-adrenergic blockade [with phentolamine (Phe)]. Muscle sympathetic nervous activity (MSNA) from the peroneal nerve, LF (0.04–0.15 Hz) and high frequency (HF; 0.15–0.40 Hz) spectral components of HR variability, and systolic blood pressure variability were analyzed at baseline, during NE infusion, and during NE infusion after Phe administration. The NE infusion increased the mean blood pressure and decreased the average HR ( P < 0.01 for both). MSNA (10 ± 2 vs. 2 ± 1 bursts/min, P < 0.01), LF oscillations of HR (43 ± 13 vs. 35 ± 13 normalized units, P < 0.05), and systolic blood pressure (3.1 ± 2.3 vs. 2.0 ± 1.1 mmHg2, P < 0.05) decreased significantly during the NE infusion. During the NE infusion after PHE, average HR and mean blood pressure returned to baseline levels. However, MSNA (4 ± 2 bursts/min), LF power of HR (33 ± 9 normalized units), and systolic blood pressure variability (1.7 ± 1.1 mmHg2) remained significantly ( P < 0.05 for all) below baseline values. Baroreflex gain did not change significantly during the interventions. Elevated levels of circulating NE cause a feedback inhibition on sympathetic outflow in healthy subjects. These inhibitory effects do not seem to be mediated by pressor effects on the baroreflex loop but perhaps by a presynaptic autoregulatory feedback mechanism or some other mechanism that is not prevented by a nonselective α-adrenergic blockade.

Acute and chronic increases in osmolality increase excitatory amino acid drive of the rostral ventrolateral medulla in rats

2004 ◽  
Vol 287 (6) ◽  
pp. R1359-R1368 ◽  
Author(s):  
Virginia L. Brooks ◽  
Korrina L. Freeman ◽  
Theresa L. O’Donaughy
Keyword(s):  
Amino Acid ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Excitatory Amino Acid ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Saline Infusion ◽  
Ventrolateral Medulla ◽  
Depressor Response ◽  
Hypertonic Saline Infusion

Water deprivation is associated with increased excitatory amino acid (EAA) drive of the rostral ventrolateral medulla (RVLM), but the mechanism is unknown. This study tested the hypotheses that the increased EAA activity is mediated by decreased blood volume and/or increased osmolality. This was first tested in urethane-anesthetized rats by determining whether bilateral microinjection of kynurenate (KYN, 2.7 nmol) into the RVLM decreases arterial pressure less in water-deprived rats after normalization of blood volume by intravenous infusion of isotonic saline or after normalization of plasma osmolality by intravenous infusion of 5% dextrose in water (5DW). Water-deprived rats exhibited decreased plasma volume and elevated plasma osmolality, hematocrit, and plasma sodium, chloride, and protein levels (all P < 0.05). KYN microinjection decreased arterial pressure by 24 ± 2 mmHg ( P < 0.05; n = 17). The depressor response was not altered following isotonic saline infusion but, while still present ( P < 0.05), was reduced ( P < 0.05) to −13 ± 2 mmHg soon after 5DW infusion. These data suggest that the high osmolality, but not low blood volume, contributes to the KYN depressor response. To further investigate the action of increased osmolality on EAA input to RVLM, water-replete rats were also studied after hypertonic saline infusion. Whereas KYN microinjection did not decrease pressure immediately following the infusion, a depressor response gradually developed over the next 3 h. Lumbar sympathetic nerve activity also gradually increased to up to 167 ± 19% of control ( P < 0.05) 3 h after hypertonic saline infusion. In conclusion, acute and chronic increases in osmolality appear to increase EAA drive of the RVLM.

Intraruminal rehydration of ovine fetuses

1991 ◽  
Vol 261 (6) ◽  
pp. R1381-R1387
Author(s):  
M. G. Ross ◽  
D. J. Sherman ◽  
M. G. Ervin ◽  
L. Day
Keyword(s):  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Filtration Rate ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Distilled Water ◽  
Intravascular Volume ◽  
Fetal Plasma ◽  
Arterial Blood ◽  
Arterial Po2

During oral rehydration of adult mammals, oropharyngeal stimulation, the act of swallowing, and/or gastric factors contribute to a rapid decrease in plasma arginine vasopressin (AVP) that precedes plasma osmolality changes. To determine whether similar mechanisms are present in the developing fetus, six chronically prepared ovine fetuses were rehydrated with intraruminal (IR) distilled water infusions (1 ml.kg-1.min-1 for 60 min) after 43 +/- 3 h of maternal water deprivation. In response to maternal dehydration, significant increases were noted in maternal and fetal mean plasma osmolalities, sodium and AVP concentrations, and fetal urine osmolality. As estimated by hematocrit, fetal intravascular volume decreased by 11%. Fetal rehydration via IR distilled water infusion evoked a significant decrease in fetal plasma osmolality but no change in urine osmolality. Unexpectedly, fetal arterial blood pressure increased and arterial PO2 decreased while fetal hematocrit indicated a further 7% decrease in intravascular volume after the IR infusion. There was a nonsignificant trend toward increased fetal glomerular filtration rate, urine volume, and plasma AVP concentrations. Identical IR water infusions to five euhydrated fetuses resulted in significant decreases in fetal plasma osmolality and increases in glomerular filtration rate, urine flow, and osmolar excretion. The euhydrated fetuses also exhibited significant increases in mean arterial blood pressure and hematocrit and decreased fetal arterial PO2. These results indicate that IR water does not suppress AVP secretion in the dehydrated ovine fetus. Rather, both euhydrated and dehydrated fetuses exhibit an idiosyncratic vasoconstrictive response to IR water.

Thirst and fluid regulatory responses to hypertonicity in older adults

1996 ◽  
Vol 271 (3) ◽  
pp. R757-R765 ◽  
Author(s):  
N. S. Stachenfeld ◽  
G. W. Mack ◽  
A. Takamata ◽  
L. DiPietro ◽  
E. R. Nadel
Keyword(s):  
Older Adults ◽  
Hypertonic Saline ◽  
Rating Scale ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Free Water ◽  
Saline Infusion ◽  
Renal Handling ◽  
Aging Adults ◽  
Hypertonic Saline Infusion

To assess the fluid regulatory responses in aging adults, we measured thirst perception and osmoregulation during and after infusion of hypertonic NaCl) saline in older (72 +/- 2 yr, n = 6) and younger (26 +/- n = 6) subjects. Hypertonic saline was infused at 0.1 min-1.kg-1 for 120 min. On a separate day, the same subjects were infused identically with isotonic saline as a control. After infusion and a 30-min equilibration period, the drank water ad libitum for 180 min. Hypertonic infusion led to graded increases in plasma osmolality (Posm; 18 +/- 2 and 20 +/- 2 mosmol/kgH2O) and percent changes plasma volume (16.2 +/- 1.9 and 18.0 +/- 1.2%) that were in older and younger subjects. Osmotically stimulated increases in thirst (94.8 +/- 18.9 and 88.3 +/- 25.6 mm), assessed on a line rating scale, and plasma arginine vasopressin concentration (6.08 +/- 1.50 and 4.51 +/- 1.37 pg/ml, for older younger, respectively) were also unaffected by age. subsequent hypervolemia, both groups of subjects sufficient water to restore preinfusion levels of Posm. Renal handling of free water and sodium was also unaffected by age during recovery from hypertonic saline infusion, but was significantly lower in older subjects during recovery from saline infusion, resulting in net fluid retention and a significant fall in Posm (6 mosmol/kgH2O). In contrast to earlier reports of a blunted thirst response to dehydration hypertonicity, we found that osmotically stimulated thirst and renal osmoregulation were intact in older adults after hypertonic saline infusion.

S  (+)-Ketamine Increases Muscle Sympathetic Activity and Maintains the Neural Response to Hypotensive Challenges in Humans

2001 ◽  
Vol 94 (2) ◽  
pp. 252-258 ◽  
Author(s):  
Peter Kienbaum ◽  
Thorsten Heuter ◽  
Goran Pavlakovic ◽  
Martin C. Michel ◽  
Jürgen Peters
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Concentration ◽  
Arterial Pressure ◽  
Sodium Nitroprusside ◽  
Arterial Blood Pressure ◽  
Sympathetic Activity ◽  
Sympathetic Outflow ◽  
Arterial Blood ◽  
Ketamine Anesthesia

Background S(+)-Ketamine is reported to exert twofold greater analgesic and hypnotic effects but a shorter recovery time in comparison with racemic ketamine, indicating possible differential effects of stereoisomers. However, cardiovascular regulation during S(+)-ketamine anesthesia has not been studied. Muscle sympathetic activity (MSA) may be an indicator of the underlying alterations of sympathetic outflow. Whether S(+)-ketamine decreases MSA in a similar manner as the racemate is not known. Thus, the authors tested the hypothesis that S(+)-ketamine changes MSA and the muscle sympathetic response to a hypotensive challenge. Methods Muscle sympathetic activity was recorded by microneurography in the peroneal nerve of six healthy participants before and during anesthesia with S(+)-ketamine (670 microg/kg intravenously followed by 15 microg x kg(-1) x min(-1)). Catecholamine and ketamine plasma concentrations, heart rate, and arterial blood pressure were also determined. MSA responses to a hypotensive challenge were assessed by injection of sodium nitroprusside (2-10 microg/kg) before and during S(+)-ketamine anesthesia. In the final step, increased arterial pressure observed during anesthesia with S(+)-ketamine was adjusted to preanesthetic values by sodium nitroprusside infusion (1-6 microg x kg(-1) x min(-1)). Results Anesthesia with S(+)-ketamine (ketamine plasma concentration 713 +/- 295 microg/l) significantly increased MSA burst frequency (mean +/- SD; 18 +/- 6 to 35 +/- 11 bursts/min) and burst incidence (32 +/- 10 to 48 +/- 15 bursts/100 heartbeats) and was associated with a doubling of norepinephrine plasma concentration (from 159 +/- 52 to 373 +/- 136 pg/ml) parallel to the increase in MSA. Heart rate and arterial blood pressure also significantly increased. When increased arterial pressure during S(+)-ketamine was decreased to awake values with sodium nitroprusside, MSA increased further (to 53 +/- 24 bursts/min and 60 +/- 20 bursts/100 heartbeats, respectively). The MSA increase in response to the hypotensive challenge was fully maintained during anesthesia with S(+)-ketamine. Conclusions S(+)-Ketamine increases efferent sympathetic outflow to muscle. Despite increased MSA and arterial pressure during S(+)-ketamine anesthesia, the increase in MSA in response to arterial hypotension is maintained.

Cardiac- and noncardiac-related coherence between sympathetic drives to muscles of different human limbs

1999 ◽  
Vol 276 (6) ◽  
pp. R1608-R1616 ◽  
Author(s):  
Bernat Kocsis ◽  
Tomas Karlsson ◽  
B. Gunnar Wallin
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Sympathetic Activity ◽  
Partial Coherence ◽  
Coherence Analysis ◽  
Sympathetic Outflow ◽  
Related Factors ◽  
Arterial Blood ◽  
The Common ◽  
Resting Muscle

Partial coherence analysis was used to evaluate the extent to which coherence between resting muscle sympathetic activity (MSA) in different pairs of limbs in humans is explained by the common baroreceptor input and by other noncardiac-related factors. Multiunit MSA in two or three nerves, arterial blood pressure, and electrocardiogram were recorded simultaneously. Correlated MSA consisted of a sharp periodic component at the heart rate and a wideband component of relatively low power distributed between 0 and 2–2.5 Hz. Quantitative analysis revealed stronger coupling between MSAs in close limbs than in distant limbs (peak coherence leg-leg, 0.94 ± 0.03; arm-leg, 0.76 ± 0.11). Furthermore, the wideband component, unaffected by partialization with circulatory signals, was significantly stronger between leg-leg (0.67 ± 0.10) than between arm-leg pairs (0.29 ± 0.10), i.e., noncardiac-related components explained 71% of leg-leg and 38% of arm-leg coherences at the frequency of the heart. Our results indicate that nonuniform relationship exists between resting sympathetic outflow to muscles in close and distant extremities which is, however, partially masked by the effect of the common rhythmic baroreceptor input.

Role of renal nerves in regulation of vasopressin secretion and blood pressure in conscious rabbits

1990 ◽  
Vol 258 (4) ◽  
pp. F821-F830 ◽  
Author(s):  
S. Matsukawa ◽  
L. C. Keil ◽  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Hypertonic Saline ◽  
Water Deprivation ◽  
Renal Denervation ◽  
Saline Infusion ◽  
Renal Nerves ◽  
Vasopressin Secretion ◽  
The Relationship ◽  
Nitroprusside Infusion ◽  
Hypertonic Saline Infusion

The observation that electrical stimulation of the renal nerves increases vasopressin secretion raises the possibility that the renal nerves may participate in the control of vasopressin secretion. In the present investigation, the effects of renal denervation on the vasopressin response to two reflex stimuli (nitroprusside infusion and hemorrhage) and two osmotic stimuli (hypertonic saline infusion and water deprivation) were studied in conscious, chronically prepared rabbits. Nitroprusside infusion in 13 intact and 14 denervated rabbits caused similar decreases in mean arterial pressure (MAP) and the increase in plasma arginine vasopressin concentration (PAVP) in intact (2.6 +/- 0.3 to 5.8 +/- 0.9 pg/ml, P less than 0.01) and denervated (2.8 +/- 0.3 to 5.7 +/- 1.3 pg/ml, P less than 0.01) rabbits was not significantly different. Hemorrhage (20 ml/kg) in 15 intact and 14 denervated rabbits caused similar decreases in MAP. Again, the increase in PAVP from 2.7 +/- 0.3 to 159.0 +/- 37.1 pg/ml (P less than 0.01) in intact and from 5.0 +/- 1.7 to 115.4 +/- 45.6 pg/ml (P less than 0.01) in denervated rabbits was not significantly different, nor was the relationship between PAVP and MAP in the two groups. In seven intact rabbits, hypertonic saline infusion increased PAVP from 4.0 +/- 0.9 to 10.9 +/- 2.8 pg/ml (P less than 0.05). The change in six denervated rabbits was not significantly different, nor was the relationship between PAVP and plasma osmolality. During water deprivation (24 h) in six intact rabbits, PAVP increased from 4.0 +/- 0.7 to 6.9 +/- 0.6 pg/ml (P less than 0.05). Again, the increase in PAVP in six denervated rabbits was not significantly different from that in the intact rabbits. The change in MAP during water deprivation in the two groups was also not significantly different. Renal cortical norepinephrine concentration in denervated kidneys was less than 10 ng/g wet wt. These results indicate that, in conscious rabbits, renal denervation does not impair the osmotic or reflex regulation of vasopressin secretion, nor does it interfere with blood pressure regulation during hypovolemia or hypotension.

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