Background: Vasovagal syncope is the most common cause of syncope in children and adults, accounting for 50-66% of unexplained syncope. There are no studies establishing the relationship between syncope, baseline heart rate, and blood pressure.Objective: To identify a possible association between baseline blood pressure and heart rate with syncope.Design/Methods: We conducted a questionnaire-based chart review study. A questionnaire was distributed to the guardian of children between eight and 18 years of age who attended the Pediatric Ambulatory Care Clinic at Flushing Hospital Medical Center. Based on the responses in the questionnaire, subjects were classified either as cases (positive for syncope) or controls (negative for syncope). Children and adolescents with neurological, cardiac, or any medical condition that can cause syncopal episodes were excluded from the study. Data collected from the questionnaire included age, gender, ethnicity, medical history, family history of syncope, and the amount of salt used in food. Anthropometric and vital signs for the current visit (height, weight, BMI, blood pressure, and heart rate) and vital signs from two previous visits were collected from electronic medical records. The data was analyzed using t-test and chi-square test with Microsoft Excel software (Microsoft Office Standard, v. 14, Microsoft; 2010); p<0.05 was considered significant.Results: A total of 197 subjects were included in this study. There were 18 cases and 179 controls. Of the cases, (4/18) 22.2% were more likely to have a systolic blood pressure lower than the 10th percentile for their gender, age, and height as compared with controls (7/179) 3.9%, p = 0.003. The subjects with a history of syncope were more likely to add salt to their food (p = 0.004). There were no significant differences between cases and controls for age, gender, ethnicity between cases and controls for systolic blood pressure. No significant difference was observed between the heart rates of cases and controls.Conclusions: Children and adolescents with syncope were more likely to have a systolic blood pressure lower than the 10th percentile, and there was no difference in the baseline heart rate. In addition, children with syncope were more likely to add salt to their food.
Objective: The present study tested the hypothesis that genetic deletion of angiotensin II (Ang II) AT1 (AT1a) receptors selectively in the renomemdullary interstitial cells (RMICs) of the kidney medulla attenuates the development of Ang II-induced hypertension in mice. Design and method: To test the hypothesis, we used inducible Tenascin-C-CreER2 and Agtr1a-floxed recombination approach to generate a novel mouse model with deletion of AT1a receptors selectively in the RMICs of the kidney (RMIC-Agtr1a-/-). Adult male wildtype (WT) and RMIC-Agtr1a-/- mice (n = 10 per group) were implanted with a telemetry probe and infused with or without Ang II via an osmotic minipump (∼500 μg/kg/day, i.p.) for 2 weeks. Results: Mice with deletion of AT1a receptors selectively in RMICs of the kidney medulla were fertile and grew normally without apparent structural or histological abnormality in the kidney medulla. However, telemetry systolic, diastolic, and mean blood pressure were significantly lower in adult male RMIC-Agtr1a-/- than WT mice (WT: 122 ± 4 mmHg vs. RMIC-Agtr1a-/-: 102 ± 3 mmHg, P < 0.01). Interestingly, this hypotensive phenotype in RMIC-Agtr1a-/- mice was associated with significant decreases in 24 h urine output (WT: 1.56 ± 0.15 mL/24 h vs. RMIC-Agtr1a-/-: 0.98 ± 0.13 mL/24 h, P < 0.01), urinary sodium (WT: 207.9 ± 7.3 μmol/24 h vs. RMIC-Agtr1a-/-: 145.2 ± 5.4 μmol/24 h, P < 0.01), and potassium excretion (WT: 221.0 ± 6.7 μmol/24 h vs. RMIC-Agtr1a-/-: 160.8 ± 10.6 μmol/24 h, P < 0.01), respectively. Moreover, urine osmolality was markedly decreased in RMIC-Agtr1a-/-mice (WT: 1724 ± 335 mOsm/Kg H2O vs. RMIC-Agtr1a-/-: 1128 ± 102 mOsm/Kg H2O, P < 0.01). Ang II infusion significantly increased telemetry systolic blood pressure to 148 ± 5 mmHg in WT mice, but it increased systolic blood pressure only to 129 ± 8 mmHg in RMIC-Agtr1a-/- mice (P < 0.01). Furthermore, infusion of Ang II for 2 weeks failed to restore urine osmolality in RMIC-Agtr1a-/- mice (1226 ± 110 mOsm/Kg H2O, n.s.). Conclusions: In conclusion, the results of the present study support the hypothesis that AT1a receptors in the RMICs of the kidney medulla plays a critical role in maintaining basal blood pressure homeostasis and the development of Ang II-induced hypertension.
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