Baroreceptor reflex and arterial rigidity in adolescents

The heart rate (HR) variability and pulse wave delay (PWD) in the major arteries of schoolchildren were studied. The function of ordinary coherence of the HR and PWD was used, which reflects the linear relationship between the two processes in the heart and vessels. The high tone of the sympathetic part of the autonomic nervous system (ANS) in schoolchildren causes an increase in heart performance and decreases the shift in the phase of association between HR and PWD, which leads to the appearance of a new characteristic of the system, arterial rigidity. The results of the physiological activation of the sympathetic part of ANS during passive orthostasis and pharmacological trials with blockers of ANS receptors in schoolchildren with heart arrhythmia at rest are presented.     

心力衰竭状态下的动脉压力感受器反射

心力衰竭是以心脏泵血功能降低（心输出量减少）为始动因素的临床综合征。心输出量降低首先引起动脉压力感受性反射失负荷,进而通过迷走-交感机制加快心率;同时,支配血管床的交感传出活动增强,进而增加总外周阻力。本文主要论述在心力衰竭状态下压力感受性反射在循环功能异常调控中的作用机制。本综述及我们近年的研究表明：（1）在心力衰竭状态下压力感受性反射功能明显减弱;（2）中枢血管紧张素Ⅱ和活性氧在压力感受性反射功能失调中发挥关键作用;（3）心交感传入刺激和化学感受性反射能抑制压力感受性反射;（4）适当的运动可以部分纠正异常的心血管反射活动。     

Baroreceptor influence on a spinal cardiovascular reflex

A stretch of the walls of the thoracic aorta, performed in vagotomized cats without obstructing aortic flow, induces increases in heart rate, myocardial contractility, and arterial pressure. These reflex responses are still present after high spinal section. Cats under chloralose-urethane anesthesia were vagotomized and one carotid sinus was isolated and perfused with arterial blood at constant flow. The contralateral carotid sinus nerve and both aortic nerves were sectioned. A stretch of the walls of the thoracic aorta between the 7th and 10th intercostal arteries induced a reflex increase in mean arterial pressure 29 +/- 2 mmHg (mean +/- SE). Stepwise increases of carotid sinus pressure (CSP) or electrical stimulation of the carotid sinus nerve induced stepwise decreases of this reflex response. At maximal baroreceptor stimulation (CSP 212 +/- 9 mmHg) the reflex response to aortic stretch was reduced by 42%. These experiments show that this spinal cardiovascular reflex is at least partially under the inhibitory control of the baroreceptor input.     

Baroreceptor mechanisms in rat

Baroreflex control of cardiovascular parameters was studied in control, atropine- and guanethidine-treated rats. Baroreceptor activity was tested by the relationship between the increase in blood pressure produced by a phenylephrine administration (bolus ov infusion) and the induced bradycardia. No differences were observed in basal arterial blood pressure and heart rate between treated- and control rats. Baroreceptor sensitivity was lower in atropine- or guanethidine-treated rats than in control animals. Baroreceptor activity has two components: a first, rapid, predominantly parasympathetic and a second, slower, that is mediated by both parasympathetic and sympathetic efferent pathways.     

Baroreceptor reflex modulation by circulating angiotensin II is mediated by AT1 receptors in the nucleus tractus solitarius

Circulating ANG II modulates the baroreceptor reflex control of heart rate (HR), at least partly via activation of ANG II type 1 (AT1) receptors on neurons in the area postrema. In this study, we tested the hypothesis that the effects of circulating ANG II on the baroreflex also depend on AT1 receptors within the nucleus tractus solitarius (NTS). In confirmation of previous studies in other species, increases in arterial pressure induced by intravenous infusion of ANG II had little effect on HR in urethane-anesthetized rats, in contrast to the marked bradycardia evoked by equipressor infusion of phenylephrine. In the presence of a continuous background infusion of ANG II, the baroreflex control of HR was shifted to higher levels of HR but had little effect on the baroreflex control of renal sympathetic activity. The modulatory effects of circulating ANG II on the cardiac baroreflex were significantly reduced by microinjection of candesartan, an AT1 receptor antagonist, into the area postrema and virtually abolished by microinjections of candesartan into the medial NTS. After acute ablation of the area postrema, a background infusion of ANG II still caused an upward shift of the cardiac baroreflex curve, which was reversed by subsequent microinjection of candesartan into the medial NTS. The results indicate that AT1 receptors in the medial NTS play a critical role in modulation of the cardiac baroreflex by circulating ANG II via mechanisms that are at least partly independent of AT1 receptors in the area postrema.     

Effect of phentolamine on the reflex increase in arterial pressure

Experiments were carried out in anaesthetized and curarized cats to study the effects of the alpha-blocker phentolamine on arterial pressor response to stimulation of group I afferent fibers from gastrocnemius-soleus muscles. It has been found that increasing doses of phentolamine given i.v. cause a decreasing pressor response until complete disappearance occurs at 2.5 mg/Kg. It is concluded that pressor response is present only when the adrenergic control system is effective and, therefore, it is due mainly to an increase in peripheral vascular resistances.     

Somatosympathetic reflex in rats with various models of arterial hypertension

Spontaneous and reflex activities of sympathetic nerve were compared in animals with arterial hypertension of different aetiology. Reflex discharges elicited by single-shock stimulation of afferent fibres were recorded. In acute experiences on anaesthetized rats with renovascular and spontaneous (SHR) model of arterial hypertension, electric basal and evoked activity (somatosympathetic reflex) in cervical sympathetic trunk were recorded. It is shown, that the spontaneous electric activity in sympathetic nerve of hypertensive rats is larger than spontaneous activity of normotensive control animals. The somatosympathetic reflex in hypertensive rats differs from that of control animals. In rats with renovascular model of hypertension, the reflex magnitude is reduced, and in the SHR the reflex is increased. Time characteristics of the reflex in hypertensive rats differed among them. It is suggested that functional activities of the brain stem in rats with different arterial hypertension model are unequal.     

Interaction between vestibulo-cardiovascular reflex and arterial baroreflex during postural change in rats

To examine a cooperative role for the baroreflex and the vestibular system in controlling arterial pressure (AP) during voluntary postural change, AP was measured in freely moving conscious rats, with or without sinoaortic baroreceptor denervation (SAD) and/or peripheral vestibular lesion (VL). Voluntary rear-up induced a slight decrease in AP (-5.6 ± 0.8 mmHg), which was significantly augmented by SAD (-14.7 ± 1.0 mmHg) and further augmented by a combination of VL and SAD (-21 ± 1.0 mmHg). Thus we hypothesized that the vestibular system sensitizes the baroreflex during postural change. To test this hypothesis, open-loop baroreflex analysis was conducted on anesthetized sham-treated and VL rats. The isolated carotid sinus pressure was increased stepwise from 60 to 180 mmHg while rats were placed horizontal prone or in a 60° head-up tilt (HUT) position. HUT shifted the carotid sinus pressure-sympathetic nerve activity (SNA) relationship (neural arc) to a higher SNA, shifted the SNA-AP relationship (peripheral arc) to a lower AP, and, consequently, moved the operating point to a higher SNA while maintaining AP (from 113 ± 5 to 114 ± 5 mmHg). The HUT-induced neural arc shift was completely abolished in VL rats, whereas the peripheral arc shifted to a lower AP and the operating point moved to a lower AP (from 116 ± 3 to 84 ± 5 mmHg). These results indicate that the vestibular system elicits sympathoexcitation, shifting the baroreflex neural arc to a higher SNA and maintaining AP during HUT.     

Volume rigidity of the capacitance vessels of rats in local arterial hypotension]

It was shown in experiments on rats that reduction of arterial pressure in the vessels of the posterior extremity for a period of up to three months was accompanied by a decrease of the volume stiffness of the capacitance vessels of this area.     

Baroreceptor afferent discharge in the pregnant rat

Pregnancy is associated with blunted reflex responses to cardiac and arterial baroreceptor stimulation. We tested the hypothesis that arterial baroreceptor afferent discharge is attenuated in response to a pressure stimulus in pregnant rats. Multifiber aortic depressor nerve activity (ADNA), mean arterial pressure (MAP), and heart rate were measured in anesthetized (pentobarbital sodium, 35 mg/kg ip) late-pregnant and virgin rats in response to increases ?phenylephrine (PE), 1.5-24 microg. kg(-1). min(-1) and 1-16 microg/kg and decreases ?sodium nitroprusside (SNP), 5-80 microg. kg(-1). min(-1) and 0.05-16 microg/kg in MAP. Resting MAP was lower in pregnant rats, but changes in MAP were similar to those in virgin rats during both PE and SNP administration. ADNA was significantly attenuated in pregnant animals during both PE and SNP infusions (P < 0.05) due to a more rapid adaptation to the pressure stimulus. Bolus drug administration evoked similar changes in MAP and ADNA in both groups; however, the maximum decrease in ADNA was achieved at the lowest dose of SNP in pregnant rats. Thus baroreceptor afferent discharge is attenuated in pregnant rats, and this involves a more rapid adaptation to a pressure stimulus.     

The Reptilian Baroreceptor and Its Role in Cardiovascular Control

Anatomical evidence for the existence of a depressor nerve inreptiles was first reported 100 years ago. Electrical stimulationof the central end of the cut nerve, however, did not producean unequivocal fall in heart rate and blood pressure, so itwas thought not to function as a depressor nerve. This remainedthe state of knowledge for fifty years when Marco Fedele performeda superb anatomical and physiological study of the depressornerves of turtles and lizards. He demonstrated that there weretwo depressor nerves from each vagus; the superior nerve originatedfrom the jugular ganglion or superior laryngeal nerve in turtlesand from the superior laryngeal nerve or vagus in lizards; theinferior nerve originated from the nodose ganglion or slightlycaudad of this ganglion. The nerves were shown to terminatein the proximal truncus arteriosus. Unlike the earlier workers,Fedele obtained a clear depressor effect on stimulating thedepressor nerves. In more recent times baroreflexes have been demonstrated inresponse to hemorrhage and body tilting in reptiles, with snakesreceiving particular attention. The evidence indicates thataquatic snakes are less effective at maintaining blood pressurethan terrestrial and arboreal forms. The sensitivity (gain)of the baroreceptor-heart rate reflex, when it is expressedas a percentage change in heart rate per unit pressure change,is approximately the same in reptiles, amphibians, and mammals.In addition, the ultrastructural appearance of the baroreceptorsof lizards is similar to that of mammals. A quantitative assessmentof the ability of reptiles to correct disturbances in bloodpressure has not yet been made, but techniques for obtainingthis information are now available.     

Cardiac sympathetic afferent stimulation augments the arterial chemoreceptor reflex in anesthetized rats.

Chronic heart failure (CHF) is well known to be associated with both an enhanced chemoreceptor reflex and an augmented cardiac "sympathetic afferent reflex" (CSAR). The augmentation of the CSAR may play an important role in the enhanced chemoreceptor reflex in the CHF state because the same central areas are involved in the sympathetic outputs of both reflexes. We determined whether chemical and electrical stimulation of the CSAR augments chemoreceptor reflex function in normal rats. Under anesthesia, renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) were recorded. The chemoreceptor reflex was tested by unilateral intra-carotid artery bolus injection of potassium cyanide (KCN) and nicotine. We found that 1) left ventricular epicardial application of capsaicin increased the pressor responses and the RSNA responses to chemoreflex activation induced by both KCN and nicotine; 2) when the central end of the left cardiac sympathetic nerve was electrically stimulated, both the pressor and the RSNA responses to chemoreflex activation induced by KCN were increased; 3) pretreatment with intracerebroventricular injection of losartan (500 nmol) completely prevented the enhanced chemoreceptor reflex induced by electrical stimulation of the cardiac sympathetic nerve; and 4) bilateral microinjection of losartan (250 pmol) into the nucleus tractus solitarii (NTS) completely abolished the enhanced chemoreceptor reflex by epicardial application of capsaicin. These results suggest that both the chemical and electrical stimulation of the CSAR augments chemoreceptor reflex and that central ANG II, specially located in the NTS, plays a major role in these reflex interactions.     

A neural set point for the long-term control of arterial pressure: beyond the arterial baroreceptor reflex

Arterial baroreceptor reflex control of renal sympathetic nerve activity (RSNA) has been proposed to play a role in long-term control of arterial pressure. The hypothesis that the "set point" of the acute RSNA baroreflex curve determines the long-term level of arterial pressure is presented and challenged. Contrary to the hypothesis, studies on the long-term effects of sinoaortic denervation (SAD) on arterial pressure and RSNA, as well as more recent studies of chronic baroreceptor "unloading" on arterial pressure, suggest that the basal levels of sympathetic nerve activity and arterial pressure are regulated independent of arterial baroreceptor input to the brainstem. Studies of the effect of SAD on the long-term salt sensitivity of arterial pressure are consistent with a short-term role, rather than a long-term role for the arterial baroreceptor reflex in regulation of arterial pressure during changes in dietary salt intake. Renal denervation studies suggest that renal nerves contribute to maintenance of the basal levels of arterial pressure. However, evidence that baroreflex control of the kidney plays a role in the maintenance of arterial pressure during changes in dietary salt intake is lacking. It is proposed that a "baroreflex-independent" sympathetic control system must exist for the long-term regulation of sympathetic nerve activity and arterial pressure. The concept of a central nervous system "set point" for long-term control of mean arterial pressure (CNS-MAP set point), and its involvement in the pathogenesis of hypertension, is discussed.     

Receptor Targeting in Medullary Nuclei Mediating Baroreceptor Reflexes

The sympathoinhibitory component of the baroreceptor reflex prominently involves glutamatergic visceral afferents terminating in the nuclei of the solitary tract (NTS) and C1 adrenergic neurons of the rostral ventrolateral medulla (RVLM). As reviewed, we have used electron microscopic immunocytochemical dual labeling in these regions to precisely analyze (1) the cellular sites for synergistic or opposing responses attributed to activation of different receptor subtypes on single neurons and (2) interactions involving monoaminergic neurons identified by their content of neurotransmitter synthesizing enzymes, vesicular monoamine transporter, and frequent coexpression of endogenous opioid peptides. The summarized results provide important cellular substrates for N-methyl-D-aspartate (NMDA)-mediated glutamatergic transmission and activation of either serotoninergic (5-HT2A), adrenergic (alpha 2A), or mu- or delta opioid receptors within the baroreceptor reflex circuit.     

Roles of baroreflex and vestibulosympathetic reflex in controlling arterial blood pressure during gravitational stress in conscious rats

Gravity acts on the circulatory system to decrease arterial blood pressure (AP) by causing blood redistribution and reduced venous return. To evaluate roles of the baroreflex and vestibulosympathetic reflex (VSR) in maintaining AP during gravitational stress, we measured AP, heart rate (HR), and renal sympathetic nerve activity (RSNA) in four groups of conscious rats, which were either intact or had vestibular lesions (VL), sinoaortic denervation (SAD), or VL plus SAD (VL + SAD). The rats were exposed to 3 G in dorsoventral axis by centrifugation for 3 min. In rats in which neither reflex was functional (VL + SAD group), RSNA did not change, but the AP showed a significant decrease (-8 +/- 1 mmHg vs. baseline). In rats with a functional baroreflex, but no VSR (VL group), the AP did not change and there was a slight increase in RSNA (25 +/- 10% vs. baseline). In rats with a functional VSR, but no baroreflex (SAD group), marked increases in both AP and RSNA were observed (AP 31 +/- 6 mmHg and RSNA 87 +/- 10% vs. baseline), showing that the VSR causes an increase in AP in response to gravitational stress; these marked increases were significantly attenuated by the baroreflex in the intact group (AP 9 +/- 2 mmHg and RSNA 38 +/- 7% vs. baseline). In conclusion, AP is controlled by the combination of the baroreflex and VSR. The VSR elicits a huge pressor response during gravitational stress, preventing hypotension due to blood redistribution. In intact rats, this AP increase is compensated by the baroreflex, resulting in only a slight increase in AP.