Ignite Creation Date:
2025-12-24 @ 3:54 PM
Ignite Modification Date:
2025-12-26 @ 10:32 PM
Study NCT ID:
NCT04648592
Status:
UNKNOWN
Last Update Posted:
2021-02-12
First Post:
2020-11-23
Is NOT Gene Therapy:
True
Has Adverse Events:
False
Brief Title:
Salt Intake, Microbiota, Immune Response and Endothelial Function in Hypertension
Sponsor:
Hospital Clínico Universitario de Valladolid
Organization:
Study Overview
Official Title:
Impact of Salt Intake on Gut Microbiota, Th17 Immune Response and Endothelial Function in Hypertensive Patients
Status:
UNKNOWN
Status Verified Date:
2021-02
Last Known Status:
RECRUITING
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
Hypertension is a significant cardiovascular risk factor which affects 45% of the adult population. Salt intake is essential in the development and progression of hypertension. A reduction in salt intake is associated with a reduction in blood pressure and a 25% lower risk of suffering a cardiovascular event. The mechanisms involved in the association between salt intake and blood pressure are a topic of discussion. Increased salt intake can modify cardiovascular function, inducing endothelial dysfunction, modyfing the activity of the immune system and increasing inflammation or oxidative stress.
In recent years, dietary salt intake has been linked to intestinal depletion of certain genera of bacteria such as Lactobacillus. Tryptophan metabolites formed by these bacteria have been shown to modulate the activity of pro-inflammatory cells such as Th17/CD4+, interleukin 17a producing cells. Studies in animal models have demonstrated that interleukin 17a is able to raise blood pressure by hindering endothelium-dependent vasodilation mechanisms. It is also able to cause sodium and water retention, increase albuminuria, induce renal microvascular injury and vasoconstriction and promote vascular stiffening, cardiac hypertrophy and fibrosis.
The main objective of this trial is to describe the relationship between salt intake, gut commensal microbiota, Th17 activity, endothelial dysfunction and blood pressure evolution in a sample of patients with essential hypertension.
In recent years, dietary salt intake has been linked to intestinal depletion of certain genera of bacteria such as Lactobacillus. Tryptophan metabolites formed by these bacteria have been shown to modulate the activity of pro-inflammatory cells such as Th17/CD4+, interleukin 17a producing cells. Studies in animal models have demonstrated that interleukin 17a is able to raise blood pressure by hindering endothelium-dependent vasodilation mechanisms. It is also able to cause sodium and water retention, increase albuminuria, induce renal microvascular injury and vasoconstriction and promote vascular stiffening, cardiac hypertrophy and fibrosis.
The main objective of this trial is to describe the relationship between salt intake, gut commensal microbiota, Th17 activity, endothelial dysfunction and blood pressure evolution in a sample of patients with essential hypertension.
Detailed Description:
None
Study Oversight
Has Oversight DMC:
False
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
False
Is an FDA AA801 Violation?: