Renal Denervation Normalizes Arterial Pressure with No Effect on Glucose Metabolism or Renal Inflammation in Obese Hypertensive Mice

Ninitha Asirvatham-Jeyaraj, Jessica K. Fiege, Ruijun Han, Jason Foss, Christopher T. Banek, Brandon J. Burbach, Maria Razzoli, Alessandro Bartolomucci, Yoji Shimizu, Angela Panoskaltsis-Mortari, John W. Osborn

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10 Citations (Scopus)

Abstract

Hypertension often occurs in concurrence with obesity and diabetes mellitus, commonly referred to as metabolic syndrome. Renal denervation (RDNx) lowers arterial pressure (AP) and improves glucose metabolism in drug-resistant hypertensive patients with high body mass index. In addition, RDNx has been shown to reduce renal inflammation in the mouse model of angiotensin II hypertension. The present study tested the hypothesis that RDNx reduces AP and renal inflammation and improves glucose metabolism in obesity-induced hypertension. Eight-week-old C57BL/6J mice were fed either a low-fat diet (10 kcal%) or a high-fat diet (45 kcal%) for 10 weeks. Body weight, food intake, fasting blood glucose, and glucose metabolism (glucose tolerance test) were measured. In a parallel study, radiotelemeters were implanted in mice for AP measurement. High fat-fed C57BL/6J mice exhibited an inflammatory and metabolic syndrome phenotype, including increased fat mass, increased AP, and hyperglycemia compared with low-fat diet mice. RDNx, but not Sham surgery, normalized AP in high-fat diet mice (115.8±1.5 mm Hg in sham versus 96.6±6.7 mm Hg in RDNx). RDNx had no significant effect on AP in low-fat diet mice. Also, RDNx had no significant effect on glucose metabolism or renal inflammation as measured by the number of CD8, CD4, and T helper cells or levels of inflammatory cytokines in the kidneys. These results indicate that although renal nerves play a role in obesity-induced hypertension, they do not contribute to impaired glucose metabolism or renal inflammation in this model.

Original languageEnglish (US)
Pages (from-to)929-936
Number of pages8
JournalHypertension
Volume68
Issue number4
DOIs
StatePublished - Oct 1 2016

Fingerprint

Obese Mice
Denervation
Arterial Pressure
Inflammation
Kidney
Glucose
Fat-Restricted Diet
Hypertension
Obesity
High Fat Diet
Inbred C57BL Mouse
Fats
Glucose Tolerance Test
Helper-Inducer T-Lymphocytes
Angiotensin II
Hyperglycemia
Blood Glucose
Fasting
Diabetes Mellitus
Body Mass Index

Keywords

  • T cell
  • cytokines
  • glucose
  • hypertension
  • metabolic syndrome
  • renal denervation

Cite this

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title = "Renal Denervation Normalizes Arterial Pressure with No Effect on Glucose Metabolism or Renal Inflammation in Obese Hypertensive Mice",
abstract = "Hypertension often occurs in concurrence with obesity and diabetes mellitus, commonly referred to as metabolic syndrome. Renal denervation (RDNx) lowers arterial pressure (AP) and improves glucose metabolism in drug-resistant hypertensive patients with high body mass index. In addition, RDNx has been shown to reduce renal inflammation in the mouse model of angiotensin II hypertension. The present study tested the hypothesis that RDNx reduces AP and renal inflammation and improves glucose metabolism in obesity-induced hypertension. Eight-week-old C57BL/6J mice were fed either a low-fat diet (10 kcal{\%}) or a high-fat diet (45 kcal{\%}) for 10 weeks. Body weight, food intake, fasting blood glucose, and glucose metabolism (glucose tolerance test) were measured. In a parallel study, radiotelemeters were implanted in mice for AP measurement. High fat-fed C57BL/6J mice exhibited an inflammatory and metabolic syndrome phenotype, including increased fat mass, increased AP, and hyperglycemia compared with low-fat diet mice. RDNx, but not Sham surgery, normalized AP in high-fat diet mice (115.8±1.5 mm Hg in sham versus 96.6±6.7 mm Hg in RDNx). RDNx had no significant effect on AP in low-fat diet mice. Also, RDNx had no significant effect on glucose metabolism or renal inflammation as measured by the number of CD8, CD4, and T helper cells or levels of inflammatory cytokines in the kidneys. These results indicate that although renal nerves play a role in obesity-induced hypertension, they do not contribute to impaired glucose metabolism or renal inflammation in this model.",
keywords = "T cell, cytokines, glucose, hypertension, metabolic syndrome, renal denervation",
author = "Ninitha Asirvatham-Jeyaraj and Fiege, {Jessica K.} and Ruijun Han and Jason Foss and Banek, {Christopher T.} and Burbach, {Brandon J.} and Maria Razzoli and Alessandro Bartolomucci and Yoji Shimizu and Angela Panoskaltsis-Mortari and Osborn, {John W.}",
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T1 - Renal Denervation Normalizes Arterial Pressure with No Effect on Glucose Metabolism or Renal Inflammation in Obese Hypertensive Mice

AU - Asirvatham-Jeyaraj, Ninitha

AU - Fiege, Jessica K.

AU - Han, Ruijun

AU - Foss, Jason

AU - Banek, Christopher T.

AU - Burbach, Brandon J.

AU - Razzoli, Maria

AU - Bartolomucci, Alessandro

AU - Shimizu, Yoji

AU - Panoskaltsis-Mortari, Angela

AU - Osborn, John W.

PY - 2016/10/1

Y1 - 2016/10/1

N2 - Hypertension often occurs in concurrence with obesity and diabetes mellitus, commonly referred to as metabolic syndrome. Renal denervation (RDNx) lowers arterial pressure (AP) and improves glucose metabolism in drug-resistant hypertensive patients with high body mass index. In addition, RDNx has been shown to reduce renal inflammation in the mouse model of angiotensin II hypertension. The present study tested the hypothesis that RDNx reduces AP and renal inflammation and improves glucose metabolism in obesity-induced hypertension. Eight-week-old C57BL/6J mice were fed either a low-fat diet (10 kcal%) or a high-fat diet (45 kcal%) for 10 weeks. Body weight, food intake, fasting blood glucose, and glucose metabolism (glucose tolerance test) were measured. In a parallel study, radiotelemeters were implanted in mice for AP measurement. High fat-fed C57BL/6J mice exhibited an inflammatory and metabolic syndrome phenotype, including increased fat mass, increased AP, and hyperglycemia compared with low-fat diet mice. RDNx, but not Sham surgery, normalized AP in high-fat diet mice (115.8±1.5 mm Hg in sham versus 96.6±6.7 mm Hg in RDNx). RDNx had no significant effect on AP in low-fat diet mice. Also, RDNx had no significant effect on glucose metabolism or renal inflammation as measured by the number of CD8, CD4, and T helper cells or levels of inflammatory cytokines in the kidneys. These results indicate that although renal nerves play a role in obesity-induced hypertension, they do not contribute to impaired glucose metabolism or renal inflammation in this model.

AB - Hypertension often occurs in concurrence with obesity and diabetes mellitus, commonly referred to as metabolic syndrome. Renal denervation (RDNx) lowers arterial pressure (AP) and improves glucose metabolism in drug-resistant hypertensive patients with high body mass index. In addition, RDNx has been shown to reduce renal inflammation in the mouse model of angiotensin II hypertension. The present study tested the hypothesis that RDNx reduces AP and renal inflammation and improves glucose metabolism in obesity-induced hypertension. Eight-week-old C57BL/6J mice were fed either a low-fat diet (10 kcal%) or a high-fat diet (45 kcal%) for 10 weeks. Body weight, food intake, fasting blood glucose, and glucose metabolism (glucose tolerance test) were measured. In a parallel study, radiotelemeters were implanted in mice for AP measurement. High fat-fed C57BL/6J mice exhibited an inflammatory and metabolic syndrome phenotype, including increased fat mass, increased AP, and hyperglycemia compared with low-fat diet mice. RDNx, but not Sham surgery, normalized AP in high-fat diet mice (115.8±1.5 mm Hg in sham versus 96.6±6.7 mm Hg in RDNx). RDNx had no significant effect on AP in low-fat diet mice. Also, RDNx had no significant effect on glucose metabolism or renal inflammation as measured by the number of CD8, CD4, and T helper cells or levels of inflammatory cytokines in the kidneys. These results indicate that although renal nerves play a role in obesity-induced hypertension, they do not contribute to impaired glucose metabolism or renal inflammation in this model.

KW - T cell

KW - cytokines

KW - glucose

KW - hypertension

KW - metabolic syndrome

KW - renal denervation

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