In this study we assessed the cardiovascular response to 13 days of irreversible inhibition of the enzyme histidine-decarboxylase (HD) with alpha-fluoro-methylhistidine (AFMH). Age-matched untreated rats were used as controls, Tail-cuff mean arterial pressure (MAP) and heart rate (HR) rose progressively in AFMH-treated rats, reaching maximal values during the study period by the 13th day of treatment. There was a reduction in urinary histamine at the day 7 and 13, and of sodium excretion at the day 7 of treatment, while the renal catecholamine excretion was increased at both days of treatment, suggesting an increase of sympathetic activity. At the 13th day of treatment, there was an activation of the renin-angiotensin-aldosterone system. In addition, the cardiovascular responses to footshock stress were determined in rats treated intraperitoneally (i.p.) or intracerebroventricularly (i.v.t.) with a single dose of AFMH. Peripheral sympathetic facilitation was found, as the hemodynamic response to footshock stress was significantly enhanced after i.p. administration, but not after i.v.t. administration of AFMH. Our results suggest that conditions of peripheral histamine deficiency may result in sympathetic facilitation, arterial hypertension and tachycardia in the rat.
Leptin is a 167 aminoacid peptidic hormone secreted by adipose tissue. It works mainly in the hypothalamus at thirst signal, but given its closed connections with inflammatory and endothelial systems, also has been postulated that it may exert a regulatory control over blood pressure (BP), interacting with nitric oxide (NO) and C reactive protein (CRP). 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 hypertensive, type 2 diabetic, and control subjects during a single CPT for assessment of endothelial dysfunction. A total of 43 subjects, males and females aged 25 to 60 years and divided in three groups, 15 healthy volunteers, 13 hypertensive patients, 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 assay of 30 minutes, 0.9% saline was infused intravenously. CPT was performed to assess the cardiovascular reactivity at minute 15. The cardiovascular variables (systolic and diastolic BP) were measured in minute 0, 16, and 30. In addition, serum variables were obtained at the beginning and at the end of the experiment, and statistical analysis was performed. CPT caused in all subjects a significant increase of BP and pulse. There were no significant differences to CPR and leptin in any group, although we observed significant differences for NO (P < 0.05). Sensitivity 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 (sensitivity: 0.2; specificity. 0.8). CRP, leptin, and NO did not shown any direct and significant association with the hemodynamic variables in this study, although a relationship was noted between NO according to group and biochemical variables when studied altogether.
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