This systematic review and meta-analysis with accompanying summary of non-parametric data shows elevated maternal circulating TNF-α, IL-6, and IL-10 levels in preeclampsia.

Abstract-Increasing evidence suggests elevated sympathetic outflow may be important in the genesis of hypertension. It is thought that peripheral angiotensin II, in addition to its pressor actions, may act centrally to increase sympathetic nerve activity (SNA). Without direct long-term recordings of SNA, testing the involvement of neural mechanisms in angiotensin II-induced increases in arterial pressure is difficult. Using a novel telemetry-based implantable amplifier, we made continuous recordings of renal SNA (RSNA) before, during, and after 1 week of angiotensin II-based hypertension in rabbits living in their home cages. Angiotensin II infusion (50 ng · kg Ϫ1 · min Ϫ1) caused a sustained increase in arterial pressure (18Ϯ3 mm Hg). There was a sustained decrease in RSNA from 18Ϯ2 normalized units (n.u.) before angiotensin II to 8Ϯ2 n.u. on day 2 and 9Ϯ2 n.u. on day 7 of the angiotensin II infusion (PϽ0.01) before recovering to 17Ϯ2 n.u. after ceasing angiotensin II. Analysis of the baroreflex response showed that although angiotensin II-induced hypertension led to resetting of the relationship between mean arterial pressure (MAP) and heart rate, there was no evidence of resetting of the MAP-RSNA relationship. We propose that the lack of resetting of the MAP-RSNA curve, with the resting point lying near the lower plateau, suggests the sustained decrease in RSNA during angiotensin II is baroreflex mediated. These results suggest that baroreflex control of RSNA and thus renal function is likely to play a significant role in the control of arterial pressure not only in the short term but also in the long term. Key Words: rabbits Ⅲ telemetry Ⅲ angiotensin II Ⅲ baroreflex Ⅲ sympathetic nerve activity S everal previous studies indicate that the sympathetic nervous system plays a critical role in the development of hypertension. In young or borderline hypertensive subjects, it is clear that plasma catecholamines are elevated 1-3 and muscle sympathetic activity is increased. 4,5 Importantly, it seems that rather than generalized overactivity of the sympathetic nervous system occurring, it is specifically increased renal sympathetic nerve activity (RSNA), resulting in diminished renal function, that is important. In young borderline hypertensive patients, noradrenaline spillover from the kidney is particularly elevated. 6,7 Animal models have identified that the onset of hypertension may be delayed or the magnitude of the arterial pressure elevation may be reduced by chronic renal denervation. 8 -12 Other studies have used longterm infusions of norepinephrine directly into the renal artery to mimic increased RSNA and observed the retention of sodium and water and sustained increases in arterial pressure. [13][14][15] These results have been interpreted to suggest that an integral relationship exists between functional sympathetic outflow to the kidneys and the development of hypertension.Although much progress has been made in recent years on the central nervous system pathways involved in regulating sympathetic acti...

Since the first recording of sympathetic nerve activity (SNA) early last century, numerous methods for presentation of the resulting data have developed. In this paper, we discuss the common ways of describing SNA and their application to chronic recordings. Suggestions on assessing the quality of SNA are made, including the use of arterial pressure wave-triggered averages and nasopharyngeal stimuli. Calculation of the zero level of the SNA signal from recordings during ganglionic blockade, the average level between bursts and the minimum of arterial pressure wave-triggered averages are compared and shown to be equivalent. The use of normalization between zero and maximal SNA levels to allow comparison between groups is discussed. We recommend that measured microvolt levels of integrated SNA be presented (with the zero/noise level subtracted), along with burst amplitude and frequency information whenever possible. We propose that standardization of the quantifying/reporting of SNA will allow better comparison between disease models and between research groups and ultimately allow data to be more reflective of the human situation.

Abstract-Arterial baroreflexes are well established to provide the basis for short-term control of arterial pressure;however, their role in long-term pressure control is more controversial. We proposed that if the sustained decrease in renal sympathetic nerve activity (RSNA) we observed previously in response to angiotensin II-induced hypertension is baroreflex mediated, then the decrease in RSNA in response to angiotensin II would not occur in sinoaortic-denervated (SAD) animals. Arterial pressure and RSNA were recorded continuously via telemetry in sham and SAD rabbits living in their home cages before, during, and after a 7-day infusion of angiotensin II (50 ng ⅐ kg Ϫ1 ⅐ min Ϫ1). The arterial pressure responses in the 2 groups of rabbits were not significantly different (82Ϯ3 mm Hg sham versus 83Ϯ3 mm Hg SAD before angiotensin II infusion, and 101Ϯ6 mm Hg sham versus 100Ϯ4 mm Hg SAD day 6 of angiotensin II). In sham rabbits, there was a significant sustained decrease in RSNA (53Ϯ7% of baseline on day 2 and 65Ϯ7% on day 6 of the angiotensin II). On ceasing the angiotensin II, all variables recovered to baseline. In contrast, RSNA did not change in SAD rabbits with the angiotensin II infusion (RSNA was 98Ϯ8% of baseline on day 2 and 98Ϯ8% on day 6 of the angiotensin II infusion). These results support our hypothesis that the reduction in RSNA in response to a pressor dose of angiotensin II is dependent on an intact arterial baroreflex pathway. Key Words: baroreceptors Ⅲ denervation Ⅲ rabbits Ⅲ nervous system, sympathetic renal A rterial baroreflexes are well established to provide the basis for the short-term control of arterial pressure; however, it has generally been accepted that they do not regulate long-term pressure. 1 This concept is based on 3 main lines of evidence, the first being that arterial baroreceptors reset during sustained increases in arterial pressure. 2 Second, chronic sinoaortic denervation, while producing tremendous lability in arterial pressure, does not result in higher average 24-hour pressures. 3 Finally, it is thought that the reflex gain of the baroreceptor control system is not sufficiently strong to explain the long-term constancy of arterial pressure. 4 However, a number of recent experiments have renewed interest in the role of the baroreflex in long-term arterial pressure control and suggest that arterial baroreflexes may act chronically to suppress sympathetic nerve activity. Lohmeier et al 5 studied responses to 5 days of angiotensin II infusion in dogs using a split-bladder preparation combined with denervation of 1 kidney. During angiotensin II infusion, sodium excretion from the innervated kidney significantly increased compared with the denervated kidney, indicating a decrease in renal sympathetic nerve activity (RSNA). The sustained increase in sodium excretion from the innervated kidney was proposed to be mediated by a sustained baroreflex-mediated suppression of RSNA because after cardiopulmonary and sinoaortic denervation, the sodium excretion from the innervated kid...

We have developed a system for long-term continuous monitoring of cardiovascular parameters in rabbits living in their home cage to assess what role renal sympathetic nerve activity (RSNA) has in regulating renal blood flow (RBF) in daily life. Blood pressure, heart rate, locomotor activity, RSNA, and RBF were recorded continuously for 4 wk. Beginning 4-5 days after surgery a circadian rhythm, dependent on feeding time, was observed. When averaged over all days RBF to the innervated and denervated kidneys was not significantly different. However, control of RBF around these mean levels was dependent on the presence of the renal sympathetic nerves. In particular we observed episodic elevations in heart rate and other parameters associated with activity. In the denervated kidney, during these episodic elevations, the increase in renal resistance was closely related to the increase in arterial pressure. In the innervated kidney the renal resistance response was significantly more variable, indicating an interaction of the sympathetic nervous system. These results indicate that whereas overall levels of RSNA do not set the mean level of RBF the renal vasculature is sensitive to episodic increases in sympathetic nerve activity.