Short-Term Angiotensin Subtype 1 Receptor Blockade Does Not Alter the Circulatory Responses to Sympathetic Nervous System Modulation in Healthy Volunteers Before and During Sevoflurane Anesthesia: Results of a Pilot Study

2016 ◽  
Vol 30 (6) ◽  
pp. 1479-1484
Author(s):  
Shahbaz R. Arain ◽  
Julie K. Freed ◽  
Jutta Novalija ◽  
Paul S. Pagel ◽  
Thomas J. Ebert
2007 ◽  
Vol 293 (6) ◽  
pp. E1511-E1516 ◽  
Author(s):  
Darleen A. Sandoval ◽  
Bin Gong ◽  
Stephen N. Davis

The aim of this study was to test the hypothesis that antecedent short-term administration of estradiol or progesterone into the central nervous system (CNS) reduces levels of neuroendocrine counterregulatory hormones during subsequent hypoglycemia. Conscious unrestrained male Sprague-Dawley rats were studied during randomized 2-day experiments. Day 1 consisted of an 8-h lateral ventricle infusion of estradiol (1 μg/μl; n = 9), progesterone (1 μg/μl; n = 9), or saline (0.2 μl/min; n = 10). On day 2, a 2-h hyperinsulinemic (30 pmol·kg−1·min−1) hypoglycemic (2.9 ± 0.2 mM) clamp was performed on all rats. Central administration of estradiol on day 1 resulted in significantly lower plasma epinephrine levels during hypoglycemia compared with saline, whereas central administration of progesterone resulted in increased levels of plasma norepinephrine and decreased levels of corticosterone both at baseline and during hypoglycemia. Glucagon responses during hypoglycemia were unaffected by prior administration of estradiol or progesterone. Endogenous glucose production following day 1 estradiol was significantly lower during day 2 hypoglycemia, and consequently, the glucose infusion rate to maintain the glycemia was significantly greater after estradiol administration compared with saline. These data suggest that 1) CNS administration of both female reproductive hormones can have rapid effects in modulating levels of counterregulatory hormones during subsequent hypoglycemia in conscious male rats, 2) forebrain administration of reproductive hormones can significantly reduce pituitary adrenal and sympathetic nervous system drive during hypoglycemia, 3) reproductive steroid hormones produce differential effects on sympathetic nervous system activity during hypoglycemia, and 4) reduction of epinephrine resulted in significantly blunted metabolic counterregulatory responses during hypoglycemia.


2019 ◽  
Vol 133 (9) ◽  
pp. 1097-1113 ◽  
Author(s):  
Ken Chen ◽  
Dongdong Sun ◽  
Shuang Qu ◽  
Yue Chen ◽  
Jialiang Wang ◽  
...  

Abstract Environmental temperature plays a role in the variation of blood pressure. Maternal cold stress could affect the physiological phenotype of the offspring, including blood pressure elevation. In the present study, we found that adult offspring of dams exposed to cold have increased systolic and diastolic blood pressure, and decreased urine volume and sodium excretion, accompanied by increased heart rate and heart rate variability, secondary to increased activity of the sympathetic nervous system. Renal denervation or adrenergic receptor blockade decreased blood pressure and increased sodium excretion. The increase in peripheral sympathetic nerve activity can be ascribed to the central nervous system because administration of clonidine, a centrally acting α2 adrenergic receptor agonist, lowered blood pressure to a greater degree in the prenatal cold-exposed than control offspring. Moreover, these prenatal cold-exposed offspring had hypothalamic paraventricular nucleus (PVN) disorder because magnetic resonance spectroscopy showed decreased N-acetylaspartate and increased choline and creatine ratios in the PVN. Additional studies found that prenatal cold exposure impaired the balance between inhibitory and excitatory neurons. This led to PVN overactivation that was related to enhanced PVN-angiotensin II type 1 (AT1) receptor expression and function. Microinjection of the AT1 receptor antagonist losartan in the PVN lowered blood pressure to a greater extent in prenatal cold-exposed that control offspring. The present study provides evidence for overactive peripheral and central sympathetic nervous systems in the pathogenesis of prenatal cold-induced hypertension. Central AT1 receptor blockade in the PVN may be a key step for treatment of this type hypertension.


2004 ◽  
Vol 286 (3) ◽  
pp. R584-R590 ◽  
Author(s):  
Julia A. Moffitt ◽  
Alan Kim Johnson

Data in humans indicate that individuals with orthostatic hypotension that are refractory to other traditional forms of therapy are responsive to selective serotonin reuptake inhibitor (SSRI) treatment. We tested the hypothesis that SSRI administration would help correct the attenuated baroreflex control of sympathetic nervous system activity in the hindlimb-unloaded (HU) rat model of cardiovascular deconditioning. An initial study was conducted to determine the time course of effects of fluoxetine (Flu) administration on baroreflex control of lumbar sympathetic nerve activity (LSNA) in conscious, chronically instrumented rats. Animals received either vehicle (Veh, sterile water) or 10 mg/kg Flu for 1, 4, or 16 days of treatment. Data indicate that while 1-day and 16-day Flu administration did not affect baroreflex function, baroreflex control of LSNA was enhanced after 4-day (short term) Flu administration. HU rats were then treated with Flu for 4 days and compared with HU rats receiving Veh and to casted control rats maintained in the normal posture that received either Veh or short-term Flu treatment. Similar to pilot data, short-term Flu treatment enhanced baroreflex control of LSNA in both HU rats and control rats. These data taken together indicate that baroreflex control of sympathetic nervous system activity is a possible mechanism responsible for the successful treatment of orthostatic intolerance with Flu.


2013 ◽  
Vol 110 (12) ◽  
pp. 4786-4791 ◽  
Author(s):  
L. Bellocchio ◽  
E. Soria-Gomez ◽  
C. Quarta ◽  
M. Metna-Laurent ◽  
P. Cardinal ◽  
...  

2021 ◽  
Vol 80 (4) ◽  
pp. 1675-1685
Author(s):  
Linda H.G. Pagen ◽  
Tom Smeets ◽  
Lisa Schmiedek ◽  
Michael A. Yassa ◽  
Frans R.J. Verhey ◽  
...  

Background: Reductions in memory practice effects have gained interest as risk factor for future cognitive decline. Practice effects vary with age and can be moderated by factors such as individual variability in arousal or stress experience acting as an additional cognitive load. Objective: In the current pilot study, we examined whether sympathetic nervous system activation moderates the relationship between age and practice effects. Methods: Thirty cognitively healthy individuals aged 40–70 years performed a mnemonic discrimination task twice. Salivary alpha amylase (sAA) samples were obtained at different time points as a proxy of sympathetic activity. Spearman correlations examined the relation between practice effects and sAA. Subsequently, age by sAA interactions on practice scores were explored with bootstrapped linear regression models. Additionally, participants were divided in learners (exhibiting practice effects) and non-learners based on the difference in mnemonic discrimination performance. Results: Higher age and baseline SNS activity were independently related to lower practice effects. The non-learners showed significantly higher sAA scores at all time points compared to learners. Among the learners, baseline-adjusted lower levels of sAA after encoding were associated with greater practice effects, particularly in middle-aged individuals. No such interaction was observed for non-learners. Conclusion: These results show that higher baseline sympathetic activation is associated with worse practice effects independently of age. Additionally, in a subgroup of middle-aged learners practice effects were observed when sympathetic activity remained low during learning. These findings suggest that elevated sympathetic nervous system activation may be a promising indicator of imminent cognitive decline.


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