Negative effects of chlorthalidone on sympathetic nervous system and insulin resistance in hypertensive patients may be avoided with spironolactone: further studies are still needed

2015 ◽  
Vol 184 (4) ◽  
pp. 727-729 ◽  
Author(s):  
Y. Castro-Torres ◽  
A. Fleites-Pérez ◽  
R. Carmona-Puerta ◽  
R. G. Jiménez-Garrido
Keyword(s):  
Insulin Resistance ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Negative Effects ◽  
Hypertensive Patients ◽  
Sympathetic Nervous

Hypertension and insulin resistance: role of sympathetic nervous system activity

1992 ◽  
Vol 263 (5) ◽  
pp. E935-E942 ◽  
Author(s):  
M. A. Supiano ◽  
R. V. Hogikyan ◽  
L. A. Morrow ◽  
F. J. Ortiz-Alonso ◽  
W. H. Herman ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Multiple Regression Model ◽  
Metabolic Effects ◽  
Plasma Norepinephrine ◽  
Intravenous Glucose ◽  
Arterial Blood ◽  
Sympathetic Nervous ◽  
Intravenous Glucose Tolerance Tests

he purpose of this study was to test the hypothesis that heightened sympathetic nervous system (SNS) activity contributes to the mechanism by which hypertension is associated with insulin resistance in humans. We performed frequently sampled intravenous glucose tolerance tests to determine tissue sensitivity to metabolic effects of insulin (SI) and measured plasma norepinephrine (NE) levels in 21 normotensive and 14 hypertensive Caucasian subjects. Compared with the normotensive subjects, hypertensive subjects had decreased SI (5.4 +/- 0.5 vs. 4.0 +/- 0.7 x 10(-5) x min-1 x pM-1; P = 0.03) but similar plasma NE levels (normotensive: 1.82 +/- 0.12 vs. hypertensive: 1.73 +/- 0.16 nM; P = 0.23). In a multiple regression model, only body mass index (BMI) and mean arterial blood pressure (MABP) were significant independent predictors of SI [SI = (-0.513)(BMI) + (-0.058)(MABP) + 23.6; r = 0.748; P = 0.0001]; age, plasma glucose, epinephrine, and NE level did not enter this model. As an additional test of this hypothesis, seven hypertensive subjects were restudied after 10 days of guanadrel therapy to determine whether SI would increase during suppression of SNS activity by guanadrel. Despite a significant reduction in plasma NE levels with guanadrel (baseline: 1.63 +/- 0.18 vs. guanadrel: 0.99 +/- 0.14 nM; P = 0.01), there was no significant change in SI (baseline: 2.97 +/- 0.78 vs. guanadrel: 2.41 +/- 0.54 x 10(-5).min-1 x pM-1; analysis of variance P = 0.57). We conclude that, in the Caucasian population we studied, heightened SNS activity is not essential for the insulin resistance observed in hypertensive humans.

scholarly journals Suppression of Cardiac Sympathetic Nervous System during Dental Surgery in Hypertensive Patients.

2000 ◽  
Vol 23 (3) ◽  
pp. 207-212 ◽  
Author(s):  
Keiko MIURA ◽  
Kiyoshi MATSUMURA ◽  
Yoshito NAKAMURA ◽  
Hideo KUROKAWA ◽  
Minoru KAJIYAMA ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Dental Surgery ◽  
Hypertensive Patients ◽  
Sympathetic Nervous

scholarly journals Obesity-Related Metabolic Syndrome: Mechanisms of Sympathetic Overactivity

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Maria Paola Canale ◽  
Simone Manca di Villahermosa ◽  
Giuliana Martino ◽  
Valentina Rovella ◽  
Annalisa Noce ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Sympathetic Overactivity ◽  
Area Of Interest ◽  
The Metabolic Syndrome ◽  
Sympathetic Nervous ◽  
Permissive Role

The prevalence of the metabolic syndrome has increased worldwide over the past few years. Sympathetic nervous system overactivity is a key mechanism leading to hypertension in patients with the metabolic syndrome. Sympathetic activation can be triggered by reflex mechanisms as arterial baroreceptor impairment, by metabolic factors as insulin resistance, and by dysregulated adipokine production and secretion from visceral fat with a mainly permissive role of leptin and antagonist role of adiponectin. Chronic sympathetic nervous system overactivity contributes to a further decline of insulin sensitivity and creates a vicious circle that may contribute to the development of hypertension and of the metabolic syndrome and favor cardiovascular and kidney disease. Selective renal denervation is an emerging area of interest in the clinical management of obesity-related hypertension. This review focuses on current understanding of some mechanisms through which sympathetic overactivity may be interlaced to the metabolic syndrome, with particular regard to the role of insulin resistance and of some adipokines.

Abstract 114: Renal Denervation Reduces Monocyte Activation: An Anti-inflammatory Effect Relevant for Cardiovascular Risk

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Maria Teresa Kristina Zaldivia ◽  
Jennifer Rivera ◽  
Dagmara Hering ◽  
Petra Marusic ◽  
Petra Marusic ◽  
...  
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Systemic Inflammation ◽  
Sympathetic Activity ◽  
Inflammatory Markers ◽  
Renal Denervation ◽  
Monocyte Activation ◽  
Hypertensive Patients ◽  
Post Procedure ◽  
Sympathetic Nervous

Background: Over-activation of renal sympathetic nervous system and low-grade systemic inflammation are thought to be common features of hypertension. Renal Denervation (RDN) reduces sympathetic activity in patients with resistant hypertension. However, its effect on systemic inflammation has not been investigated. Aim: To determine the effect of RDN-induced sympathetic inhibition on monocyte activation and systemic inflammation in hypertensive patients. Methods: Peripheral blood was obtained from 42 patients who underwent RDN for uncontrolled blood pressure (BP) at baseline, at 3 months and 6 months post-procedure. Ambulatory BP, overall activation status of monocyte as well as monocyte subsets and inflammatory markers were assessed at each time point. Results: RDN significantly lowered 24-hour ambulatory BP at 3 months (150.5/81.0 mmHg to 144.7/77.9 mmHg), which was sustained at 6 months (144.7/78.6 mmHg). The overall monocyte activation was significantly decreased (3 months, 4079.4 MFI to 3182.0 MFI; 6 months, 3457.62 MFI) post-RDN, specifically in the subset of classical monocytes (6 months, 4696.8 MFI to 3958.8 MFI). In line with this, reduction of several inflammatory markers were observed, including monocyte-platelet aggregates at 3 months (34% [680 of 2000 monocyte events] to 11.85% [237 of 2000 monocyte events]) and plasma levels of MCP-1 (3 months, 144.9 pg/ml to 100.1 pg/ml; 6 months, 122.2 pg/ml), IL-1β (3 months, 18.3 pg/ml to 10.8 pg/ml; 6 months, 12.2 pg/ml), TNF-α (3 months, 167.5 pg/ml to 78.4 pg/ml; 6 months, 111.1 pg/ml), IL-12 (3 months, 59.8 pg/ml to 9.9 pg/ml; 6 months, 21.4 pg/ml) and IL-6 (3 months, 2.4 pg/ml to 1.5pg/ml; 6 months, 1.9 pg/ml). A positive correlation was observed between baseline muscle sympathetic nerve activity and monocyte activation (R=0.62) and changes observed at both time points (3 months, R=0.63; 6 months, R=0.88) post-procedure. Conclusions: Inhibition of sympathetic activity via RDN is associated with a reduction of monocyte activation and other circulating inflammatory markers in hypertensive patients. These findings point to a direct interaction between the inflammatory and sympathetic nervous system, which is of central relevance for the understanding of beneficial cardiovascular effects of RDN.

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