Effects Of Baroreceptor Stimulation Research Articles

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Objective:Field stimulation of the carotid baroreceptors has been used successfully to induce long-term reduction in blood pressure. However, the effect of baroreceptor stimulation on short-term blood pressure regulation and circulatory hemodynamics in normotensive and hypertensive rat models is not

Effects of baroreceptor stimulation on performance of the Sternberg short-term memory task: A cardiac cycle time study

Activation of arterial baroreceptors can affect cortical activity. Cardiac cycle time studies have established that natural variations in baroreceptor activation are associated with changes in basic sensorimotor function whereas few have investigated more complex cognitive function. Aiming to improve our understanding of this phenomenon, this study examined performance on the Sternberg memory task as a function of the phase of the cardiac cycle. In each trial, participants were shown either two or six digits followed by a probe digit that either had or had not been presented previously and were required to press one of two response buttons to indicate a match and mismatch, respectively. Response latency per additional digit was greater for stimuli presented late compared to early in the cardiac cycle whereas the zero intercept was greatest at the start of the cardiac cycle and reduced as the cycle progressed. These findings provide evidence that natural baroreceptor stimulation can affect complex cognitive processes, such as serial-comparison in short-term memory, as well as basic sensorimotor processes.

Effect of baroreceptor stimulation on the respiratory pattern: Insights into respiratory–sympathetic interactions

Sympathetic nerve activity (SNA) is modulated by respiratory activity which indicates the existence of direct interactions between the respiratory and sympathetic networks within the brainstem. Our experimental studies reveal that T(E) prolongation evoked by baroreceptor stimulation varies with respiratory phase and depends on the pons. We speculate that the sympathetic baroreceptor reflex, providing negative feedback from baroreceptors to the rostral ventrolateral medulla and SNA, has two pathways: one direct and independent of the respiratory-sympathetic interactions and the other operating via the respiratory pattern generator and is hence dependent on the respiratory modulation of SNA. Our experimental studies in the perfused in situ rat preparation and complementary computational modelling studies support the hypothesis that baroreceptor activation during expiration prolongs the T(E) via transient activation of post-inspiratory and inhibition of augmenting expiratory neurones of the Bötzinger Complex (BötC). We propose that these BötC neurones are also involved in the respiratory modulation of SNA, and contribute to the respiratory modulation of the sympathetic baroreceptor reflex.

The effects of baroreceptor stimulation on central respiratory drive: A review

The neural systems that control breathing and the circulation are located in adjacent longitudinal columns in the ventrolateral medulla. They have much in common, in terms of their structure, function, and evolution. In the most part, both systems are affected by the same sensory modalities and receive input from many of the same higher centres. Indeed, such is the parallel organisation of the two systems that stimuli that alter the behaviour of the one almost invariably influence the other. It is well-known that rhythmic respiratory inputs exert powerful effects on parasympathetic and sympathetic outputs. However, the question of whether cardiovascular inputs exert any influence on respiratory rhythmogenesis is more contentious. Here, we review the effects of baroreceptor activation, classically considered a 'cardiovascular' stimulus, on respiratory drive. We show that, although subtle, baroreceptor inputs evoke reproducible prolongation of expiration in a range of preparations. The consequences of this reflex are discussed with regard to cardiorespiratory coordination.

Neuronal expression of nuclear transcription factor MafG in the rat medulla oblongata after baroreceptor stimulation

The medulla oblongata is the site of central baroreceptive neurons in mammals. These neurons express specific basic-leucine zipper transcription factors (bZIP) after baroreceptor stimulation. Previously we showed that activation of baroreceptors induced expression of nuclear transcription factors c-Fos and FosB in central baroreceptive neurons. Here we studied the effects of baroreceptor stimulation on induction of MafG, a member of small Maf protein family that functions as dimeric partners for various bZIP transcription factors by forming transcription-regulating complexes, in the rat medulla oblongata. To determine whether gene expression of MafG is induced by stimulation of arterial baroreceptors, we examined the expression of its mRNA by semi-quantitative reverse transcription-PCR method and its gene product by immunohistochemistry. We found that the number of MafG transcripts increased significantly in the medulla oblongata after baroreceptor stimulation. MafG-immunoreactive neurons were distributed in the nucleus tractus solitarii, the dorsal motor nucleus of the vagus nerve, the ambiguous nucleus and the ventrolateral medulla. The numbers of MafG-immunoreactive neurons in these nuclei were significantly greater in test rats than in saline-injected control rats. We also found approximately 20% of MafG-immunoreactive neurons coexpress FosB after baroreceptor stimulation. Our results suggest that MafG cooperates with FosB to play critical roles as an immediate early gene in the signal transduction of cardiovascular regulation mediated by baroreceptive signals in the medulla oblongata.

Effects of baroreceptor stimulation and opioids on the auditory startle reflex

We examined (a) whether carotid baroreceptor stimulation attenuates the auditory startle response and its modulation by preceding affective pictures, and (b) whether these effects are mediated by endogenous opioids. Seventy-eight young normotensive adults with or without a parental history of hypertension received brief exposures to affective pictures and noise bursts during phasic manipulation of the carotid baroreceptors. In each participant, opioids were blocked by naltrexone in half of the sessions. Baroreceptor stimulation had a strong dampening effect on the startle response. This effect was not influenced by opioid blockade, sex, or parental history of hypertension. No baroreceptor effects were obtained regarding ratings of the affective pictures or startle modulation by the pictures. The baroreceptor stimulation effects seem to be mediated by the basal primary acoustic startle circuit rather than by higher affective circuits.

Effects of baroreceptor stimulation on sensorimotor control of the hand.

Finger movements are presumed to be controlled by somatosensory and motor areas of neocortex via the corticospinal tract. Since baroreceptor activation appears to reduce central nervous system activity, an effect on sensorimotor control during precise manual manipulations is expected. To test this hypothesis, motor responses to slow and fast perturbations during grasping of a small object (precision grip) were examined. Baroreceptor activation was manipulated with the phase-related external suction (PRES) technique, which allows the application of baroreceptor stimulation and control conditions in a well-controlled and indiscernible way. Motor reactions following slow perturbations were influenced in the expected way in good-performance subjects. The time to stop slow perturbations was longer and the electromyographic (EMG) activity of the small thumb muscles was lower during baroreceptor stimulation than in the control condition. These effects did not appear in the fast-perturbation task. Fast perturbations were followed by EMG activity onset after about 50 msec, which indicates that a prominent part of the EMG activity must be attributed to a more automatic motor response. EMG activity following slow perturbations began after about 90 msec, and it may be assumed that these motor reactions are primarily under voluntary control. The fact that we found effects of baroreceptor stimulation in slow but not in fast perturbations could have been caused by at least partially different pathways utilized for automatic versus voluntary motor responses, which seem to be differentially vulnerable to baroreceptor activation. An electrocortical sign that precedes voluntary movements is the Bereitschaftspotential, or readiness potential. Since this potential is a slow brain potential, and baroreceptor activation is known to reduce slow brain potentials, it is plausible that baroreceptor activation primarily affects motor responses following slow but not fast perturbations.

Direct observations of the effects of baroreceptor stimulation on skeletal muscle circulation of the rat.

1. In anaesthetized rats, supramaximal baroreceptor stimulation by carotid sinus inflation evoked a reflex fall in arterial pressure and an increase in vascular conductance and flow of muscles of the hindquarters. 2. Simultaneously, main arteries, primary and secondary arterioles (13-90 microns, internal diameter (i.d.)) and terminal arterioles (7-13 microns) of the spinotrapezius muscle all showed a diameter increase that reached a peak as arterial pressure neared its zenith; terminal arterioles then showed a diameter decrease to below control level. These responses were abolished by local application of phentolamine or guanethidine to the spinotrapezius, or by crushing the paravascular nerve supply. 3. It is suggested that the diameter increases were mediated by reflex inhibition of sympathetic tone, while the secondary diameter decrease in terminal arterioles was induced by a fall in local concentrations of vasodilator metabolites, caused by an increase in muscle blood flow. 4. But after sympathetic blockade 25% of all arterial vessels showed a diameter increase beginning as the fall in arterial pressure neared its zenith. These responses may be attributed to vasodilator metabolites accumulating as a consequence of a reduction in muscle blood flow secondary to the reflex reduction in perfusion pressure. 5. No venous vessels, from venules (9-18 microns) to main veins (65-130 microns) that drain the muscle, showed a diameter change in response to baroreceptor stimulation, in accord with evidence that they have no sympathetic supply. 6. These results accord with and can provide explanation for changes in blood flow, regional blood volume and capillary filtration evoked by baroreceptor stimulation in studies on whole-limb muscle. They support suggestions that active changes in capacity of venous vessels of muscle play a minor role in the baroreceptor reflex; both active and passive changes in vascular capacity may be due to large veins outside of muscle proper.

Direct observations of effects of baroreceptor stimulation on mesenteric circulation of the rat.

1. In anaesthetized rats, supramaximal baroreceptor stimulation by carotid sinus inflation evoked a reflex fall in systemic arterial pressure and an increase in gross mesenteric vascular conductance, but no significant change in gross mesenteric blood flow. 2. Principal arteries (80-350 microns internal diameter (i.d.)) which supply the intestine and mesentery, small arteries (30-40 microns) and some terminal arterioles (18-30 microns) of the mesentery showed a diameter increase beginning with the fall in arterial pressure, but remaining terminal arterioles and precapillary arterioles (10-18 microns) showed a diameter increase beginning when arterial pressure neared its lowest level. 3. Application of phentolamine to the mesentery abolished diameter increases that began with the reflex fall in arterial pressure. Thereafter, 50% of small arteries and terminal and precapillary arterioles showed diameter increases that began when the fall in arterial pressure neared its zenith. 4. It is proposed that the proximal arterial vessels, which are known to be sympathetically innervated, predominantly showed dilatation mediated by reflex inhibition of sympathetic tone, while more distal arterioles showed myogenic dilatation secondary to the fall in systemic arterial pressure. 5. Small veins (30-50 microns) of the mesentery and principal veins (100-560 microns) that drain mesentery and intestine also showed a diameter increase beginning with the reflex fall in systemic arterial pressure. Since they are known to have a sympathetic noradrenergic supply, and in the absence of changes in mesenteric blood flow likely to cause passive changes in venous diameter, they apparently showed dilatation due to inhibition of sympathetic tone. 6. The above responses are all compatible with, and so suggest underlying mechanisms for, changes in blood flow, regional blood volume, and capillary filtration evoked by baroreceptor stimulation in studies of whole mesenteric circulation, i.e. intestine as well as mesentery.

Baroreceptor control of pressure-flow relationships during hypoxemia.

In the absence of peripheral chemoreceptors, the effects of graded hypoxemia on the carotid sinus control of central and regional hemodynamics were studied in anesthetized mongrel dogs. Baroreceptor stimulation was effected by carotid sinus isolation and perfusion under controlled pressure. Blood flows were measured in the aorta and the celiac, mesenteric, left renal, and right iliac arteries. Carotid sinus reflex set-point pressures were well maintained until hypoxemia was severe. Carotid sinus reflex set-point gain was maximal during mild hypoxemia. Reflex operating point regional flows were unaffected by hypoxemia. A factorial analysis of overall reflex increases in mean aortic pressure, flow, and power during reduced baroreceptor stimulation showed potentiation by increasing hypoxemia. Corresponding effects of baroreceptor stimulation and hypoxemia on aortic resistance and heart rate were additive. Celiac, renal, and iliac blood flows increased during both hypoxemia and reduced baroreceptor stimulation. Only in the celiac bed were blood flow changes independent of concomitant changes in cardiac output. Thus, at maximum sympathetic stimulation (low carotid sinus pressure) during hypoxemia, the cardiovascular system maintained both central and regional blood flows at high systemic blood pressures independent of the peripheral chemoreceptors.

Modification of arterial baroreflexes by captopril in essential hypertension

Captopril lowers blood pressure without increasing heart rate and plasma norepinephrine, which suggests that this drug may potentiate arterial baroreflexes. In eight subjects with untreated essential hypertension, blood pressure was monitored intraarterially and the effects of baroreceptor stimulation or deactivation were assessed by measuring (1) the slopes of the relations between increase or reduction in systolic pressure (intravenous phenylephrine or nitroglycerin) and the resulting lengthening or shortening in R-R interval, and (2) the increase or decrease in mean arterial pressure induced by increasing and decreasing carotid transmural pressure (neck chamber). The measurements were made before and after a hypotensive oral dose of captopril (50 mg). Before captopril, the slopes of the R-R interval changes with increase and reduction in systolic pressure were 8 and 4 ms/mm Hg, respectively. The slopes of the mean arterial pressure changes with increase and reduction in carotid transmural pressure were 0.51 and 0.40 mm Hg, respectively. After captopril, the responses to baroreceptor stimulation were unaltered but those to baroreceptor deactivation were augmented. The presser and heart rate responses to hand-grip and cold exposure were unchanged by captopril. Administration of captopril is accompanied by a baroreflex potentiation which involves the lower portion of the stimulus-response curve of the reflex. This phenomenon (which may originate at the afferent baroreceptor fibers or centrally) may avoid a reduction in the tonic baroreflex influence during captopril-induced hypotension, thus contributing to the hemodynamic effects of the drug.

Changes in pattern of breathing following baroreceptor stimulation in cats.

The effects of baroreceptor stimulation produced by a sudden rise in arterial pressure on respiratory pattern were studied at various levels of PaCO2 and PaO2 in 8 anesthetized cats. A sudden rise in arterial pressure decreased both tidal volume and respiratory frequency. For a given increase in arterial pressure, the decrease in tidal volume was constant at all levels of PaCO2 and PaO2 examined, whereas the decrease in respiratory frequency became progressively lower as the level of chemical drive increased, regardless of the type of chemical stimuli. Analysis of respiratory duration revealed that the decrease in respiratory frequency during baroreceptor stimulation was solely due to prolongation of expiration. These observations were obtained in the intact as well as in the vagotomized animals but were not seen after bilateral sinus nerve section. They suggest that the central respiratory mechanisms controlling respiratory frequency are directly involved in the reduction in respiratory frequency during baroreceptor stimulation.