Sympathetic Neural Mechanisms Underlying Attended and Unattended Blood Pressure Measurement

Whether blood pressure (BP) values differ when BP is measured with or without the presence of a doctor (attended and unattended BP measurements) is controversial, and no information exists on whether and to what extent neurogenic mechanisms participate at the possible BP differences between these measurements. In this study, we assessed continuous beat-to-beat finger systolic BP and diastolic BP, heart rate, muscle, and skin sympathetic nerve traffic (microneurography) before and during BP measurement by an automatic device in the presence or absence of a doctor. This was done in 18 untreated mild-to-moderate essential hypertensive patients (age, 40.2±2.8 years, mean±SEM). During attended BP measurement, there was an increase in systolic BP, diastolic BP, heart rate, and skin sympathetic nerve traffic and a muscle sympathetic nerve traffic decrease, the peak changes being +5.3%,+8.4%,+9.4%,+30.9%, and −15.2%, respectively ( P <0.05 for all). In contrast, during unattended BP measurement, systolic BP, diastolic BP, heart rate, and skin sympathetic nerve traffic were modestly, albeit in most instances significantly, reduced, whereas muscle sympathetic nerve traffic remained almost unchanged. During unattended BP measurement, peak systolic BP was 14.1 mm Hg lower, peak heart rate was 10.6 bpm lower, and peak skin sympathetic nerve traffic was 8.5 bursts/min lower than the peak values detected during attended BP measurement. Thus the cardiovascular and neural sympathetic responses to the alerting reaction elicited by BP measurement in the presence of a doctor are almost absent during unattended BP measurement, during which, if anything, a modest cardiovascular sympathoinhibition occurs. This has important implications for comparison of studies using these different BP measurement approaches as well as for decision concerning threshold and target BP values for treatment.

Decreased cardiac pacemaking and attenuated β-adrenergic response in TRIC-A knockout mice

Changes in intracellular calcium levels in the sinus node modulate cardiac pacemaking (the calcium clock). Trimeric intracellular cation (TRIC) channels are counterion channels on the surface of the sarcoplasmic reticulum and compensate for calcium release from ryanodine receptors, which play a major role in calcium-induced calcium release (CICR) and the calcium clock. TRIC channels are expected to affect the calcium clock in the sinus node. However, their physiological importance in cardiac rhythm formation remains unclear. We evaluated the importance of TRIC channels on cardiac pacemaking using TRIC-A-null (TRIC-A–/–) as well as TRIC-B+/–mice. Although systolic blood pressure (SBP) was not significantly different between wild-type (WT), TRIC-B+/–, and TRIC-A–/–mice, heart rate (HR) was significantly lower in TRIC-A–/–mice than other lines. Interestingly, HR and SBP showed a positive correlation in WT and TRIC-B+/–mice, while no such correlation was observed in TRIC-A–/–mice, suggesting modification of the blood pressure regulatory system in these mice. Isoproterenol (0.3 mg/kg) increased the HR in WT mice (98.8 ± 15.1 bpm), whereas a decreased response in HR was observed in TRIC-A–/–mice (23.8 ± 5.8 bpm), suggesting decreased sympathetic responses in TRIC-A–/–mice. Electrocardiography revealed unstable R-R intervals in TRIC-A–/–mice. Furthermore, TRIC-A–/–mice sometimes showed sinus pauses, suggesting a significant role of TRIC-A channels in cardiac pacemaking. In isolated atrium contraction or action potential recording, TRIC-A–/–mice showed decreased response to a β-adrenergic sympathetic nerve agonist (isoproterenol, 100 nM), indicating decreased sympathetic responses. In summary, TRIC-A–/–mice showed decreased cardiac pacemaking in the sinus node and attenuated responses to β-adrenergic stimulation, indicating the involvement of TRIC-A channels in cardiac rhythm formation and decreased sympathetic responses.

Angels of Mercy and the Angel of History

This chapter explores Jayne Anne Phillips’s Lark and Termite and Chang-rae Lee’s The Surrendered, which focus on the suffering of civilians during the Korean War by subversively reiterating the dominant ways in which US liberal depictions conveyed the plight of refugees—and especially orphans—during the Korean War. Korean noncombatants were framed at midcentury within a humanitarian Orientalism, casting them as objects of humanitarian care whose deaths—even when the result of US actions that were essentially war crimes—were to be recognized as a necessary though tragic by-product of conflict. These novels’ protagonists resemble the salvific figures lionized in such representations and become the focus of readers’ sympathetic responses. However, these works engage in a subversive project of cultural memory by disfiguring the humanitarian identifications they elicit and feature Korean subjects who respond to the putative benevolence extended to them with a self-immolating violence and rage. This chapter argues that Lark and Termite and The Surrendered strive to compel their readers to adopt an excruciating identification with the angel of history as rendered by Walter Benjamin rather than angels of mercy and thus to see the past as a chain of catastrophes in which they are fundamentally implicated.

Music and the Soul

The belief that music can affect the human soul was deeply rooted in ancient Greece. Many philosophers tried to describe the sympathetic responses of human beings to musical performances and their ethical consequences, even without framing their remarks within a consistent and systematic theory. “Music and the Soul” aims at analyzing the cultural background and the contemporary intellectual milieu in which Plato operated, in order to assess earlier or alternative views of the ethical power of mousikē overshadowed by his influential theorization. To this end, the chapter focuses on the role of music in the early Pythagorean environment and the evidence for sophistic (in the broadest sense) epideixeis on the psychagogic effects of music and the anti-ethical reaction documented by the fourth-century Hibeh papyrus.

Abstract P136: Effects Of Sex Hormones On The Hemodynamic And Sympathetic Responses To Centrally Administered Tumor Necrosis Factor-α In Rats

Inflammation plays an important role in the pathophysiology of cardiovascular dysfunction and neurohumoral excitation in heart failure and hypertension. Growing evidence has demonstrated significant sex differences in the inflammatory response and immune processes, with estrogen exerting an anti-inflammatory effects and testosterone potentially having pro-inflammatory influence. We previously reported that central administration of tumor necrosis factor-α (TNF-α) elicited different effects on blood pressure (BP), heart rate (HR) and renal sympathetic nerve activity (RSNA) in male and female rats. Whether the sex steroids estrogen and testosterone contribute to the observed differences in TNF-α-induced hemodynamic and sympathetic responses remains unknown. We hypothesized that estrogen protects against TNF-α-induced sympathetic excitation and pressor responses while testosterone enhances these excitatory outcomes in response to TNF-α. Female or male Sprague Dawley rats (10-12 weeks) anesthetized with ketamine plus xylazine underwent bilateral ovariectomy or castration, respectively, 2 weeks prior to study. Sham-operated (Sham) female or male animals served as controls. TNF-α (100 ng) was administered intracerebroventricularly (ICV). BP (mmHg), HR (bpm) and RSNA (% change) were recorded in urethane anesthetized rats. In ovariectomized female rats (n=6), ICV TNF-α induced significantly (*p<0.05 vs. Sham) larger increases in BP (19.3 ± 1.4* vs. 12.8 ± 1.2 ), HR (76.3 ± 4.8* vs. 51.5 ± 4.3) and RSNA (104.8 ± 6.9* vs. 72.4 ± 5.1), compared with Sham-female rats, that began within 20-30 mins and peaked at 90-120 mins after ICV injection. In castrated male rats (n=6), ICV TNF-α-elicited significantly smaller increases in BP (15.2 ± 1.3* vs. 21.8 ± 1.6), HR (57.7 ± 4.2* vs. 82.6 ± 4.1) and RSNA (72.6 ± 4.3* vs. 110.3 ± 4.7), compared with Sham-male animals. These data indicate a distinct role of sex hormones estrogen and testosterone in central inflammation-driven cardiovascular and sympathetic activation and suggest a protective effect of estrogen and a harmful effect of testosterone in the development of hypertension and heart failure.

Increased sympathetic responses induced by chronic obstructive sleep apnea are caused by sleep fragmentation

Obstructive sleep apnea causes a hyperactive chemoreflex, with increased sympathetic activation. However, it is not clear whether this pathophysiologic mechanism is due to repeated hypoxia or to sleep disruption. The present study suggests that sleep fragmentation contributes importantly to increased sympathetic activation after chemoreceptor stimulation. This suggests that sleep fragmentation has an important role in the sympathetic activation seen in sleep apnea patients.