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Recruiting NCT04101188

Mechanisms Underlying the Protective Vascular Effects of Dietary Potassium in Humans

No phase Interventional Cardiovascular Risk Factor

For patients and families

In plain language

An automatic summary of structured registry data. It is an orientation aid, not a substitute for the official protocol or a physician assessment.

What is being studied
The protocol lists: Moderate Potassium/Low Sodium Diet, Moderate Potassium/High Sodium Diet, High Potassium/High Sodium Diet.
Who it may be relevant to
Registry conditions: Cardiovascular Risk Factor. Basic parameters: 18 years — 45 years · All.
What needs checking
Age, condition and sex are only basic indicators. Prior treatment, laboratory values and other mandatory requirements appear in the eligibility criteria below.
Where it takes place
United States
Next step
Save the trial, show it to the treating physician, and confirm current recruitment with the study center. Costs, documents and travel →

Overview

Americans continue to consume high amounts of sodium. Potassium is notable for its blood pressure lowering effects but less is known regarding its effect on the vasculature. This investigation seeks to determine the role of dietary potassium on the vasculature in the presence of a high sodium diet in salt-resistant adults.

Detailed description

Significant public health efforts have been made towards salt reduction but most have met with failure. Dietary factors such high sodium/low potassium diets contribute to the development of cardiovascular diseases (CVDs) such as atherosclerosis and high blood pressure (BP). This is important as CVD is the number one killer in the U.S. While the role of these two nutrients on BP is widely accepted, their impact on the vasculature has received less attention. Endothelial dysfunction, characterized by impaired dilation, is an important non-traditional risk factor for atherosclerosis. Evidence supporting potassium's beneficial role on vascular health remains unclear although it may be more effective in the presence of a high sodium diet. A purported mechanism responsible for sodium-induced vascular dysfunction is overproduction of reactive oxygen species (ROS) resulting in reduced nitric oxide (NO) production/bioavailability. Additionally, high sodium diets have been shown to stiffen the endothelium. This investigation will evaluate the vascular effects of dietary potassium during a high salt diet including its impact on sodium-induced oxidative stress and endothelial cell stiffness.

Interventions

  • Other Moderate Potassium/Low Sodium Diet
    Consumption of 10 days of a diet moderate in potassium and low in sodium.
  • Other Moderate Potassium/High Sodium Diet
    Consumption of 10 days of a diet moderate in potassium and high in sodium.
  • Other High Potassium/High Sodium Diet
    Consumption of 10 days of a diet high in potassium and high in sodium.

Primary outcome measures

  • Conduit artery endothelial-dependent dilation [Time frame: on day 10 of the diet]
  • Microvascular function [Time frame: on day 10 of the diet]
Secondary outcome measures (1)
  • Ambulatory BP monitoring [Time frame: on day 7 and 10 of diet]

Eligibility criteria

Inclusion criteria

  • healthy
  • normal blood pressure
  • normal resting ECG

Exclusion criteria

  • hypertension
  • history of heart disease
  • diabetes
  • kidney disease
  • obese (BMI ≥30)
  • significant weight changes in the last 6 months
  • use of tobacco products
  • pregnant
  • on a special diet (gluten free; vegan)
  • take any medications for the above conditions
  • endurance trained athletes

Criteria are shown verbatim from the registry (in English). Final eligibility is always assessed by the study center.

Healthy volunteers: Yes

Study design

Allocation
Randomized
Model
Crossover
Masking
Open label
Primary purpose
Prevention

Study locations

United States · 1 center
  • University of Delaware — Newark

Identifiers

NCT: NCT04101188 · 1472577 · 5R01HL145055-05

Primary sources (government registries)

View this study on ClinicalTrials.gov ↗