This study evaluated the relationship between baroreceptor reflex sensitivity and cognitive performance. Twenty normal subjects performed the Uchida-Kraepelin test, a serial arithmetic task. Baroreceptor reflex sensitivity during a 5-min Uchida-Kraepelin test was assessed in minute periods by spectral analysis using the maximum-entropy method. During the task, baroreceptor reflex sensitivity was significantly reduced. There was an inverse between-subjects association between baroreceptor reflex sensitivity and the level of performance (number of additions completed) both at different time periods of the Uchida-Kraepelin test and during the whole task (r=-.51). This finding supports the existence of a pathway mediating mutual cardiovascular-central nervous system influences through the baroreceptors, establishing an essential mechanism facilitating adaptive reactions to stressful conditions.

Leptin is a key mediator in the neuroendocrine regulation of energy homeostasis and appetite. An in vivo study that raised leptin concentrations at high altitudes associated with loss of appetite (1) led us to speculate that low oxygen (hypoxia) might be the key stimulus for leptin secretion from adipocytes. Because leptin has angiogenic effects as well as vascular endothelial growth factor (2) and leptin secretion from non-adipocytes, human trophoblastic cells (3) are increased in culture under hypoxic conditions (4).We investigated the effect of hypoxia on leptin production and on lipogenic activity and glucose uptake in primary cultures of rat adipocytes. To determine the effects of hypoxia on leptin secretion, adipocytes were exposed to 10% or 20% O 2 atmosphere for 48 hours and the levels of leptin released from adipocytes were determined by radioimmunoassay. Hypoxia suppressed the secretion of leptin by ϳ50% compared with adipocytes exposed to normoxia (3.8 Ϯ 0.8 vs. 8.4 Ϯ 1.4 ng/mL per milligram protein, mean Ϯ SEM, five experiments, p Ͻ 0.05). To examine the effects of hypoxia on lipogenesis and glucose uptake, adipocytes were exposed to either 10% or 20% O 2 atmosphere for 48 hours and glycero-3-phosphate dehydrogenase activity of lipogenic enzyme, triglyceride content, and glucose uptake were measured spectrophotometrically, by H 2 O 2 colorimetric assay and enzymatically, respectively. Hypoxia resulted in a significant reduction of glycero-3-phosphate dehydrogenase activity (10% O 2 : 1.4 Ϯ 0.5; 20% O 2 : 4.6 Ϯ 0.9 U/mg protein, five experiments, p Ͻ 0.05) and accumulation of triglyceride (10% O 2 : 39.0 Ϯ 10.7; 20% O 2 : 106.4 Ϯ 22.1 mg/dL per milligram protein, five experiments, p Ͻ 0.05). However, hypoxia did not significantly affect the amount of glucose uptake by adipocytes (10% O 2 : 392.7 Ϯ 69.8; 20% O 2 : 655.6 Ϯ 128.9 mg/dL per milligram protein, five experiments, p ϭ 0.11).Our results show that hypoxia does not stimulate leptin secretion from adipocytes; it rather decreased leptin secretion from adipocytes associated with a concomitant reduction in lipogenic response of adipocytes in vitro. These results indicate that the high leptin levels circulating in individuals with anorexia at high altitude are not simply attributable to the direct effect of hypoxia on secretion of leptin in adipocytes. The comprehensible mechanisms are at least three factors: increased production of leptin in adipocytes indirectly stimulated by the other hormones or cytokines induced by hypoxia; delayed clearance of leptin from circulation due to binding its soluble receptor, which increases its half-life; and changed tissue distribution of leptin/leptin shift to circulation from other tissues (5,6). But according to our results, the first factor is improbable unless the hormones or cytokines, which have a potent effect to stimulate the leptin release from adipocytes to overcome the inhibitory effect of hypoxia on the leptin release, are upregulated by hypoxia.Our results also indicated that glucose uptake by adipocy...

Baroreceptor-cardiac reflex, which consists of baroreceptor-induced chronotropic and inotropic actions, is a very useful index of cardiac sympathovagal balance. Baroreceptor-heart rate reflex sensitivity, which reflects baroreceptor-induced chronotropic action, has been used as a marker of baroreceptor-cardiac reflex. However, it cannot be used in patients with chronotropic incompetence and/or implanted cardiac pacemaker. We hypothesized that baroreceptor-stroke volume (SV) reflex sensitivity, which reflects baroreceptor-induced inotropic action, may also be a useful method for measurement of baroreceptor-cardiac reflex, similar to the baroreceptor-heart rate reflex sensitivity. To test this hypothesis, we measured baroreceptor-SV reflex sensitivity expressed as ratio of low frequency (LF) power to total power of SV fluctuation (LF/TP(SV): %/mmHg) by spectral analysis of mean blood pressure and SV fluctuations, the gain in low-frequency band between two signals in supine and 60 degrees upright positions, and compared these values to baroreceptor-heart rate reflex sensitivity in 14 healthy subjects. Baroreceptor-SV reflex sensitivity correlated significantly with baroreceptor-heart rate reflex sensitivity (r = 0.73, p < 0.0001). In addition, baroreceptor-SV reflex sensitivity correlated significantly and positively with high frequency (HF) power (r = 0.57, p < 0.005) and negatively with LF/HF ratio (r = -0.57, p < 0.005) in power spectral analysis of R-R interval variability. Moreover, baroreceptor-SV reflex sensitivity in LF/TP(SV) correlated positively with the R-R interval (r = 0.70, p < 0.0001) and negatively with diastolic blood pressure (r = -0.50, p < 0.01). We conclude that baroreceptor-SV reflex sensitivity in LF/TP(SV) can be used as a quantitative probe of baroreceptor-cardiac reflex, similar to the baroreceptor-heart rate reflex sensitivity in healthy subjects, and it may enable us to estimate inotropic aspect in baroreceptor-cardiac reflex in patients with chronotropic incompetence and/or implanted pacemaker.

Fixed-rate AV sequential pacing did not blunt the decrease in baroreceptor-SV reflex sensitivity consistent with the arterial baroreflex gain response to upright posture. The decreased baroreceptor-SV reflex sensitivity occurring with the upright posture may reflect a baroreflex-induced inotropic effect secondary to vagal withdrawal and sympathetic activation.

In this study, we assessed whether baroreflex sensitivity (BRS) is influenced by risk factors of cardiovascular disease. Subjects of this study were 95 elderly people (40 males and 55 females; mean age +/- SD, 66.6+/-1.6 years) who underwent a medical check-up. BRS was determined as the gain of transfer function in baroreflex arc by spectral analysis of mean blood pressure and R-R interval variabilities in low-frequency band (0.04-0.15 Hz). Gender-related differences in BRS and relationships between BRS and various risk factors of cardiovascular disease were investigated. The value of BRS was significantly higher in males [10.7+/-3.7 (SD) ms/mmHg] than in females [9.0+/-4.0 ms/mmHg, p< 0.05]. However, this gender-related difference disappeared when other variables were taken into account in the multivariate model. Multiple regression analyses showed independent inverse relationships between BRS and heart rate [b=-0.016+/-0.004 (SE) bpm, beta=-0.39], and between BRS and platelet count [b=-0.002+/-0.001 x 103/ micro l, beta=-0.22]. Our results indicated that BRS is inversely related to platelet count in the elderly population. The precise mechanism of this correlation is unknown, but platelet factors released from platelet aggregates can potentially influence vascular function and modify BRS, or there is a common underlying determinant responsible for the covariation.