Metabolic and Hemodynamic Markers of Endothelial Dysfunction in Patients With Hypertension and Patients With Type 2 Diabetes During the Cold Pressor Test

Abstract

Leptin, a 167-amino acid peptidic hormone secreted by adipose tissue, acts mainly in the arcuate hypothalamus nucleus as a satiety signal, but given its closed connections with inflammatory and endothelial systems, a probable regulatory role in blood pressure (BP) control by interaction with nitric oxide (NO) and C-reactive protein (CRP) has also been described. The cold pressor test (CPT) is a simple test that indirectly determines endothelial dysfunction. In this work, biochemical indicators (CRP, leptin, and NO) and hemodynamic indicators (systolic and diastolic BP) were performed and evaluated in patients with hypertension, patients with type 2, and control subjects during a single CPT for assessment of endothelial dysfunction. A total of 43 subjects aged 25 to 60 years were divided into three groups: 15 healthy volunteers, 13 patients with hypertension, and 15 patients with type 2 diabetes were included in the study. A complete clinical history was obtained from each subject and a complete physical examination, including an electrocardiogram, was carried out. During the 30-minute assay, 0.9% saline solution was infused intravenously. CPT was performed to assess the cardiovascular reactivity at 15 minutes. The cardiovascular variables (systolic and diastolic BP) were measured at 0, 16, and 30 minutes. In addition, serum variables were extracted at the beginning and at the end of the experiment and statistical analysis was performed. CPT caused in all subjects a significant increase in BP and pulse. There were no significant differences in CRP or leptin in all groups, although we observed significant differences for NO (P < 0.05). Sensibility and specificity for all biochemical variables resulted in nonsignificant statistical or clinical importance as markers of endothelial dysfunction; however, a positive association was found when leptin and NO were evaluated together (sensibility, 0.2; specificity, 0.8). CRP, leptin, and NO did not show any direct or significant association with the hemodynamic variables in this study, although a relationship was observed in NO according to group and among biochemical variables when studied together.

Effects of Varying Degrees of Intermittent Hypoxia on Proinflammatory Cytokines and Adipokines in Rats and 3T3-L1 Adipocytes

“…Leptin was significantly increased in sleep apneas compared to levels in both BMI-matched obese and normal weight subjects [41] and a reduction of serum leptin levels was observed after weeks or months of continuous positive airway pressure (CPAP) treatment [26]. Leptin, a main cytokine coded by obesity gene and secreted by adipocytes, especially higher levels in obese patients [11], is essential, and it acts not only in the arcuate hypothalamus nucleus as a satiety signal, but also in the inflammatory and endothelial systems [60]. Leptin can act at the level of the pancreas to downregulate insulin gene transcription and insulin secretion and at the peripheral tissues to increase glucose uptake [9].…”

The environmental and genetic evidence for the association of hyperlipidemia and hypertension

“…There is also increasing evidence that obesity contributes to the development as well as to the progression of chronic kidney disease [38,39]. Obesity might lead to hypertension and cardiovascular disease by activating the renin-angiotensin-aldosterone system [40], increasing sympathetic activity [41], promoting insulin resistance and leptin resistance [42,43], potentiating procoagulatory activity [44], and inducing endothelial dysfunction [45,46]. In the present study, however, we found that hyperlipidemia but not hypertension was positively correlated with BMI and alcohol consumption, whereas hypertension but not hyperlipidemia was Association of hyperlipidemia and hypertension Ruixing et al 255 positively correlated with sodium intake.…”

Several Lipid-Related Gene Polymorphisms Interact with Overweight/Obesity to Modulate Blood Pressure Levels

“…Other postulated factors include excessive caloric intake, enhanced sympathetic activity [22], and even the greater lean mass present in obese subjects. In addition, enhanced salt sensitivity [19], activated renin-angiotensin-aldosterone system [23], potentiated procoagulatory activity [24], and induced endothelial dysfunction [25,26] among obese individuals may be also responsible for the development of hypertension.…”