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J F van Brederode

Publications and source records attributed to J F van Brederode.

At least 19 recordsLinked to original sources

GABA-evoked chloride currents do not differ between dendrites and somata of rat neocortical neurons.

1. We performed patch-clamp recordings on acutely isolated somata and dendritic segments of rat neocortical neurons, in order to compare the reversal potential (E(GABA)) and relative density of GABA(A) receptor-mediated Cl(-) currents in these two cellular compartments. 2. Currents were recorded with the Cl(-)-impermeable pore former gramicidin (25--75 microg ml(-1)) in HCO(3)(-)-free bath solution. Voltage ramps (-110 to -30 mV) from a holding potential (V(h)) of -60 mV in the absence and presence of 2 microM GABA were used to construct instantaneous current-voltage relationships. Currents were abolished by co-application of GABA with the GABA(A) receptor antagonist bicuculline (40 microM). 3. GABA conductance, normalized to membrane surface area, was not different in somata and dendrites. In addition, E(GABA) was not different in the two compartments. 4. Replacement of intracellular K(+) with Cs(+) resulted in a significantly more depolarized E(GABA) in both somata and dendrites. These results suggest that the resting intracellular Cl(-) concentration ([Cl(-)](i)) is similar in somata and dendrites and that an outward Cl(-) transporter system maintains low [Cl(-)](i).

Animals↗

Evidence of altered inhibition in layer V pyramidal neurons from neocortex of Kcna1-null mice.

Mice lacking the potassium channel subunit KCNA1 exhibit a severe epileptic phenotype beginning at an early postnatal age. The precise cellular physiological substrates for these seizures are unclear, as is the site of origin. Since KCNA1 mRNA in normal mice is expressed in the neocortex, we asked whether neurons in the neocortex of three to four week-old Kcna1-null mutants exhibit evidence of hyperexcitability. Layer V pyramidal neurons were directly visualized in brain slices with infrared differential-interference contrast microscopy and evaluated with cellular electrophysiological techniques. There were no significant differences in intrinsic membrane properties and action potential shape between Kcna1-null and wild-type mice, consistent with previous findings in hippocampal slice recordings. However, the frequency of spontaneous post-synaptic currents was significantly higher in Kcna1-null compared to wild-type mice. The frequency of spontaneous inhibitory post-synaptic currents and miniature (action-potential-independent) inhibitory post-synaptic currents was also significantly higher in Kcna1-null compared to wild-type mice. However, the frequency of spontaneous and miniature excitatory post-synaptic currents was not different in these two groups of animals. Comparison of the amplitude and kinetics of miniature inhibitory and excitatory post-synaptic currents revealed differences in amplitude, rise time and half-width between Kcna1-null and wild-type mice. Our data indicate that the inhibitory drive onto layer V pyramidal neurons is increased in Kcna1 knockout mice, either directly through an increased spontaneous release of GABA from presynaptic terminals contacting layer V pyramidal neurons, or an enhanced excitatory synaptic input to inhibitory interneurons.

Animals↗

Morphological and electrophysiological properties of atypically oriented layer 2 pyramidal cells of the juvenile rat neocortex.

We used whole-cell patch clamp recordings combined with intracellular dye-filling to examine the morphological and electrophysiological properties of atypically oriented pyramidal cells located at the layer 1/2 border of the juvenile rat neocortex. Orientation of the apical dendrite varied from oblique (>20 degrees from vertical) to truly horizontal (90 degrees from vertical). The length of the apical dendrite ranged from 150 to 400 microm. The total horizontal domain of the dendritic tree (including basal dendrites) of the longest horizontal pyramids exceeded 500 microm, but we also found short horizontal cells with horizontal dendritic domains of less than 300 microm. In addition, atypically oriented pyramids had long horizontal axon collaterals in layer 1/2. Electrophysiologically, atypically oriented pyramidal cells had intrinsic membrane properties similar to regularly oriented pyramids that have been described in the superficial layers at this age in the rat. Cells that fired repetitively were all regular spiking. In addition, we identified a subgroup of neurons (20%) in this sample, which were unable to fire more than a few spikes at the beginning of the current pulse. We suggest that the unique orientation and size of their dendritic trees and the length and arrangement of their local axons collaterals make atypically oriented pyramids in layer 2 ideally suited to perform horizontal integration of synaptic inputs in the neocortex.

Animals↗

Developmental changes in calretinin expression in GABAergic and nonGABAergic neurons in monkey striate cortex.

The development of the calcium-binding protein calretinin (CaR) and its co-localization with GABA was studied in the striate cortex of Macaca monkeys from fetal day (Fd) 45 to adult. At Fd45, early neurons resembling Cajal-Retzius cells are stained in the marginal zone (MZ). At Fd55 the MZ is filled with CaR+ Cajal-Retzius cells and their processes, and scattered CaR+ cells are also found in deep cortical plate (CP), intermediate zone (IZ), and subventricular zone (SVZ). At Fd66, a band of CaR+ fibers appears in the IZ, corresponding to the location of the geniculocortical axons. This fiber band labels heavily until Fd130 but then ceases to be immunoreactive by postnatal (P) 16 weeks. At Fd85-101, the number of CaR+ cells in the CP, SVZ, and ventricular zone (VZ) reaches its highest cell density. After Fd130, CaR+ cells are concentrated in layer II and upper layer III, and this distribution changes little into adulthood. After mid-gestation, there is a progressive loss of CaR+ cell bodies and processes in the MZ, and these are rare in the adult cortex. Just before birth, a weakly stained CaR+ cell band appears in layer IVA at the border between layer IVA and IVB, but this band disappears immediately after birth. Another CaR+ cell band appears transiently in upper layer V just below the border with layers IV at P6 months. These results suggest that CaR is expressed early in fetal development in the cell populations that are immunoreactive for CaR in the adult. However, developmental events related to cortical maturation during late prenatal and early postnatal stages result in transient expression of CaR in neurons that are not immunoreactive for CaR in the adult. CaR-immunoreactivity is colocalized with GABA in almost all CaR+ cells with the exception of Cajal-Retzius cells in the MZ and some large cells observed at Fd70-101 in the VZ. The band of CaR+ fibers in the IZ is GABA-. At Fd90, almost all (> 96%) CaR+ cells are GABA+ in the CP and the first developed layers V/VI. This percentage declines later, so that on average 80% of CaR+ cells are GABA+ in adult cortex. At Fd135, 53% of GABA+ neurons located in layers II/III are CaR+; this percentage declines to 37% in the adult. These double-label patterns suggest that early in fetal development the majority of GABA+ cells stain for CaR and that expression of CaR may be related to the migration of these neurons into the cortical plate. Once they attain their final position in the cortex many GABA+ cells loose CaR-immunoreactivity, so that in postnatal life only a minority of GABA+ neurons contain this calcium-binding protein.

Animals↗

Differences in inhibitory synaptic input between layer II-III and layer V neurons of the cat neocortex.

1. The goal of this study was to compare the relative effectiveness of intrinsic inhibitory synaptic inputs in different layers of the cat motor cortex. Postsynaptic potentials (PSPs) were evoked in neurons located in the superficial (layer II-III) or deep layers (layer V) by local extracellular stimulation in vitro. Electrophysiological properties and intracellular filling indicated that the recorded neurons were pyramidal cells. 2. The shape and time course of the evoked PSPs differed. Layer II-III cells showed stereotyped triphasic PSPs consisting of a fast excitatory PSP (fEPSP) and a fast and slow inhibitory PSP (fIPSP and sIPSP, respectively). PSPs in layer V cells, in contrast, were much more variable, mainly depolarizing at resting membrane potential, and lacked a hyperpolarizing IPSP in 84% of neurons tested at rest. 3. Blockade of glutaminergic neurotransmission with 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and D-2-amino-5-phosphonovaleric acid (AP5) revealed that fIPSPs could be evoked in all layer V cells by local stimulation of the superficial or deep layers, even in those that showed small or no IPSPs in control perfusate. Small (< 1 mV) isolated sIPSPs were evoked in only one-fifth of layer V cells when the deep layers were stimulated, and in about one-half of the layer V cells when the superficial layers were stimulated. In layer II-III cells, stimulation of the superficial layers always resulted in fIPSP-sIPSP combinations. No IPSPs could be evoked in layer II-III neurons by stimulating the deep layers after glutaminergic blockade. Selective blockade of gamma-aminobutyric acid-A (GABAA) or GABAB receptor-mediated neurotransmission showed that in both cell types fIPSPs were due to GABAA receptor stimulation, whereas sIPSPs were mediated by GABAB receptors. 4. Isolated fIPSPs were recorded in perfusate containing CNQX, AP5, and the GABAB antagonist CGP 35348. The rise and decay times of the fIPSPs in layer II-III cells were significantly longer than those in layer V cells. Rise and decay times normalized for differences in membrane time constant were not significantly different, however, suggesting that the intrinsic membrane properties of the postsynaptic membrane account for the difference in time course of the fIPSPs in these two cell types. 5. Selective blockade of the inward rectifier current Ih with extracellular Cs+ showed that this conductance functions to shorten and attenuate fIPSPs in layer V cells. In contrast, Ih is absent or small in layer II-III cells, and, consequently, Cs+ had little or no effect on the fIPSPs evoked in these cells.(ABSTRACT TRUNCATED AT 400 WORDS)

6-Cyano-7-nitroquinoxaline-2,3-dione↗

A comparison of the electrophysiological properties of morphologically identified cells in layers 5B and 6 of the rat neocortex.

In vitro studies performed in mammalian brain slices have shown that cortical neurons differ in their intrinsic membrane properties. In the rodent cortex these properties are related to a specific cell morphology and synaptic connectivity in some cells but not in others. Due to their small size, little is known about the intrinsic membrane properties of layer 6 cells, however, and it is not clear whether cell morphology is related to electrophysiological properties in this layer. We used a combination of intracellular recording and dye-filling to study the electrophysiological and morphological characteristics of layer 6 cells of the rat sensorimotor cortex in vitro and compared their properties to those of large layer 5B pyramidal cells. Our sample of 24 filled and anatomically reconstructed cells in layer 6 confirms previous Golgi studies that showed them to be a morphologically diverse group consisting of regularly and irregularly oriented pyramidal cells and spiny nonpyramidal cells. Regular layer 6 pyramidal cells differed with respect to the length of their apical dendrites and extent of their axonal arborizations, while irregularly oriented pyramidal cells consisted of sideways or inverted pyramidal cells of variable size and morphology. Spiny nonpyramidal cells included bi-tufted and multi-polar cell types that differed in size and extent of dendritic trees. Many layer 6 cells showed long horizontal axon collaterals in layer 6, and an oblique or vertical projection to layer 4. Stimulation with intracellular constant current pulses revealed that the morphological diversity was mirrored by a similar electrophysiological diversity. Most layer 6 cells were capable of firing trains of action potentials characterized by an initial doublet or triplet followed by a train of single spikes (phasic-tonic mode). The majority of layer 6 cells could fire in either a tonic (single spikes only) mode with low strength current input and a phasic-tonic pattern with higher current strengths. A minority fired either always phasic-tonic or tonic-only spike trains. The size and sequence of spike afterpotentials during low-rate repetitive firing was highly variable in layer 6 cells suggesting that the relative importance of ionic currents responsible for spike repolarization and afterpotentials varied from cell to cell. Subthreshold responses showed prominent inward rectification, while hyperpolarizing "sag" was present in most cells tested. In comparison, large layer 5B pyramidal cells fired either phasic-tonic only or both phasic-tonic and tonic patterns. A minority of cells were capable of firing repetitive bursts, while the remainder fired repetitive single spikes.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Distribution of the calcium-binding proteins parvalbumin and calbindin-D28k in the sensorimotor cortex of the rat.

This study examined and compared the immunocytochemical distribution of the two calcium-binding proteins parvalbumin and calbindin-D28k in the primary motor and somatosensory areas of the rat neocortex. Parvalbumin-immunoreactive cells were found in all layers of the cortex except layer 1 and reached their peak density in the middle layers. The two cortical areas differed markedly in the number, cell size and morphology of immunoreactive cells. Parvalbumin-positive cells were more than twice as numerous in the somatosensory cortex compared to the motor cortex. In addition, the average size of their cell bodies was 25-30% larger in the somatosensory area. Parvalbumin cells in the motor area represented several classes of nonpyramidal cells, while the somatosensory cortex contained in addition many large cells with thick vertically oriented primary dendrites. Some of these cells resembled regular or inverted pyramidal neurons. Punctate neuropil labeling was much heavier in the upper layers of the somatosensory than in the motor cortex and was especially heavy in layer 4. Dense parvalbumin-positive perisomatic puncta surrounded large, unstained pyramidal cells in layer 5B of the motor cortex. Calbindin-D28k neuronal staining in both areas was confined to two populations. The most prominent was darkly labeled, small nonpyramidal cells confined to two bands in layers 2/3 and 5/6. There was also a lighter stained population composed of many pyramidal cells distributed throughout layers 2 and 3. In addition, the motor area contained a band of lightly stained, large pyramidal cells in layer 5B. Calbindin-D28k neuropil labeling was heaviest in layers 1 to 3. In contrast to parvalbumin, we found only minor differences in distribution, size and morphology of calbindin-D28k cell body or neuropil staining in the two cortical areas. Double-labeling immunocytochemistry showed that the large majority of immunoreactive cells contained only calbindin-D28k or parvalbumin, but a distinct population of multipolar cells in the upper layers of the somatosensory cortex contained both. The clear parcellation of parvalbumin immunoreactivity in the rat neocortex suggests that parvalbumin is preferentially associated with specific neuronal populations and terminals in the somatosensory cortex. The more general and homogeneous labeling of the upper layers of the cortex indicates that calbindin-D28k could be related to the relatively high density of calcium channels or N-methyl-D-aspartate receptors in the superficial layers of the rat cortex.

Animals↗

Effects of epinephrine on firing characteristics of two functionally different types of carotid baroreceptors.

Sympathetic stimulation and catecholamine exposure have been shown to sensitize the arterial baroreceptors, but the extent or importance of this effect is not known. We performed this study to investigate the effects of sympathetic feedback on the carotid sinus baroreceptors, specifically examining the effect of the stimulation on the two different functional types of baroreceptors characterized in an earlier study. The existence of two baroreceptor function-response curves has suggested that the roles of the two functionally different baroreceptors may not be the same. If true, the effects of epinephrine exposure on baroreceptor firing characteristics may contribute to differential roles played by each baroreceptor type in the control of blood pressure. Single-fiber baroreceptor activity from a vascularly isolated carotid sinus was recorded during slow increases in carotid sinus pressure before and during exposure to epinephrine (10(-8) to 10(-6) M). Baroreceptor firing characteristics were determined from function curves plotting carotid sinus pressure versus nerve activity, with curve-fitting analysis of the hyperbolic type I and sigmoidal type II baroreceptor curves used to obtain threshold (Pth) and saturation (Psat) pressures, threshold (Fth) and saturation (Fsat) firing rates, and sensitivity (slope) for each baroreceptor before and during epinephrine exposure. The possible mechanisms of observed changes were examined using our previously published baroreceptor computer model. Epinephrine exposure was found to significantly increase sensitivity, Fth, and Fsat of both types of baroreceptors, with a relatively greater effect on type I sensitivity and on type II Fth and Fsat. Epinephrine also was found to increase the level of spontaneous discharge for type II baroreceptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Firing characteristics of single-fiber carotid sinus baroreceptors.

This study examined firing patterns of single-fiber carotid baroreceptors in response to slow ramp increases in carotid sinus pressure (1-2 mm Hg/sec) in vascularly isolated carotid sinus preparations in thiopental-anesthetized dogs (25 mg/kg, plus 10 mg/kg/hr). Two general types of baroreceptor discharge patterns were obtained: 1) type I, a discontinuous, hyperbolic pattern characterized by a sudden onset of discharge at threshold pressure with a relatively high threshold frequency, which gradually increased to a higher saturation firing rate and 2) type II, a continuous, sigmoidal pattern characterized by a gradual increase in discharge above threshold pressure and a relatively low threshold frequency and saturation firing rate. Type II baroreceptor curves typically showed spontaneous discharge below threshold pressure and significantly lower sensitivities, threshold frequency, saturation firing rate, and threshold pressure than those of type I receptors. However, the saturation pressures and operating ranges of the type II receptors were greater than those of type I receptors, and the pressure at which type II receptors had their greatest sensitivity was greater than that for type I receptors. Type I baroreceptors generally had large myelinated afferent A fibers; type II baroreceptors generally had smaller A and unmyelinated C fibers, based on conduction velocities. The presence of spontaneous activity with type II baroreceptors, combined with significantly lower sensitivities and wider pressure operating ranges seen relative to type I baroreceptors, suggests that these receptors may primarily serve to provide information on tonic, or baseline, levels of arterial blood pressure to the central cardiovascular centers. The sudden onset of discharge, higher sensitivities, and narrower operating ranges of type I baroreceptors suggest that their primary role may be to provide information on dynamic, sudden changes in arterial pressure.

Afferent Pathways↗

Experimental and modeling study of the excitability of carotid sinus baroreceptors.

In this study we examined the effects of blockade of a transient K+ current with 4-aminopyridine (4-AP) on the static stimulus-response relation of myelinated carotid sinus baroreceptors (n = 8), using a vascularly isolated sinus preparation in sodium thiopental-anesthetized dogs. In one class of baroreceptors (type I), which did not fire spontaneously below the pressure threshold (Pth), 4-AP (10(-5) to 10(-4) M) decreased Pth in a dose-dependent manner and transformed the stimulus-response relation from a discontinuous, hyperbolic shape to a sigmoidal, continuous curve. After exposure to 10(-4) M of 4-AP, baroreceptors were spontaneously active below Pth. These effects of 4-AP were more pronounced in baroreceptors with a high control Pth and were independent of enhanced neurotransmitter release or changes in carotid sinus distensibility. In contrast, 4-AP had relatively little effect on type II baroreceptors, which under control conditions are characterized by a continuous, sigmoidal stimulus-response curve. We believe that these effects of 4-AP on baroreceptor discharge were mediated by blockade of a transient K+ conductance that was present at the receptor spike-initiation zone. This hypothesis was examined using a mathematical model based on the Hodgkin-Huxley axon, but modified to include the transient K+ conductance. The modeling results showed that the minimum current necessary to elicit action potential firing is an extremely sensitive function of the magnitude of this K+ conductance, supporting our experimental results obtained with 4-AP. Our findings suggest that a transient K+ conductance might play a role in the determination of Pth and that differences between type I and II receptors could be the result of differences in the effectiveness of this conductance in controlling spike-initiation zone excitability.

4-Aminopyridine↗

The lectin Vicia villosa labels a distinct subset of GABAergic cells in macaque visual cortex.

The morphology and distribution of neurons labeled specifically by the lectin, Vicia villosa (VVA), were examined in striate cortex of adult macaque monkeys. Following incubation with VVA conjugated to histochemical markers, fine punctate reaction product appears to cover the surface of the soma and proximal dendrites of a population of cortical neurons. Although a small number of VVA-labeled cells are located in layers 2, 3A, 5, and 6, approximately 75% are located in a strip of cortex overlying layers 3B through 4Ca. Layers 1 and 4C beta are virtually devoid of labeled cells. The morphology of labeled cells varies throughout the layers. In the supragranular layers, the labeled cells generally display a round or multipolar soma with a small number of radially disposed dendrites. In deeper layers, labeled cells are multipolar or horizontal, and their proximal dendrites are often more densely labeled. There is no clear correlation between the distribution of labeled cells and the pattern of cytochrome oxidase staining in supragranular layers. Double labeling of single sections for VVA and for GABA (gamma-aminobutyric acid) immunoreactivity revealed that most VVA-labeled cells are also immunoreactive for GABA. The double-labeled cells comprise approximately 30% of all GABA immunoreactive cells. Soma size analysis of double-labeled cells shows that medium-to-large GABA cells in each layer are labeled by VVA. The soma size, laminar distribution, and morphology of the VVA-labeled GABA cells suggest that they include the large basket cells originally observed in Golgi preparations.

Animals↗

Mechanisms of initial blood pressure response to postural change.

The influence of supine rest on the blood pressure response to standing and 70 degrees head-up tilt was studied in detail for the first 30 s after the change of posture. Following 20 min of supine rest, the active transition to standing was accompanied by an immediate increase in systolic pressure of 29 +/- 6 mmHg (mean +/- SEM). This was followed by large fluctuations in systolic pressure: to -28 +/- 2 mmHg below control after 7 s and to 22 +/- 2 mmHg above control after 22 s (17 mmHg in excess of the systolic pressure level after head-up tilt). Following 1 min of supine rest, there was no difference in the immediate increase in systolic pressure. However, the magnitude of the subsequent changes was significantly diminished. With head-up tilt the immediate increase in blood pressure was absent and afterwards small changes were found that were also significantly influenced by the period of prior rest. Taken in conjunction with earlier studies, the following mechanisms are suggested. The immediate blood pressure increase resulted from compression of arteries by the contracting postural muscles. The subsequent blood pressure fall was caused by at least two mechanisms: (a) the fall was predominantly of reflex origin, because the immediate pressure increase stimulated the systemic baroreceptors; (b) supine rest possibly augmented the translocation of blood from the thorax which contributed, approx. 5 s from standing, to the reflex fall of blood pressure.

Adult↗

Relationship between impaired parasympathetic and sympathetic cardiovascular control in diabetes mellitus.

We have investigated the relationship between vagal and sympathetic lesions in 62 diabetic patients and compared the results with those from 37 healthy subjects. Vagal function was assessed by heart rate changes with forced breathing. Sympathetic control was measured by the heart rate and blood pressure changes after standing and the concomitant plasma catecholamine response. The integrity of the postganglionic sympathetic neuron was evaluated separately by testing sudomotor function. Impaired sympathetic control was found only in 15 diabetic patients with severely impaired or absent vagal heart rate control. In 12 patients the chief abnormalities consisted of a delayed and diminished heart rate increase, an excessive fall in systolic blood pressure (greater than 20 mmHg) in combination with an abnormally small noradrenaline increment (less than 120 ng/l) and a lesion of the postganglionic sympathetic neuron. Three patients with severely impaired parasympathetic heart rate control in combination with an intact postganglionic sympathetic neuron demonstrated a large noradrenaline increase on standing (greater than 700 ng/l). Measurement of vagal heart rate control and testing of sudomotor function makes it possible to classify a spectrum of abnormal cardiovascular responses to standing in diabetic patients.

Adult↗

Testing for autonomic neuropathy: heart rate changes after orthostatic manoeuvres and static muscle contractions.

1. The initial heart rate (HR) response evoked by standing, 70 degrees head-up tilt, handgrip and contraction of abdominal and leg muscles was analysed in diabetic patients with autonomic neuropathy and in matched controls. 2. In healthy subjects standing induced an immediate, large, HR increase lasting 20s that far exceeded the small HR rise induced by tilt. The HR response with handgrip and to contraction of abdominal and leg muscles was strikingly similar for the first 5 s to the HR increase after standing. 3. In diabetic patients handgrip and standing induced a small HR increase starting after 2-3 s. Contraction of abdominal and leg muscles evoked little or no HR changes. The HR rise after tilt up was delayed by 10 s compared with healthy controls. 4. It is concluded that the circulatory response to active and passive changes of posture differs fundamentally. Standing and handgrip are superior to head-up tilt as a test for vagal HR control. An abrupt and large HR increase after standing excludes cardiac parasympathetic neuropathy. A modified response, however, may be due to afferent as well as to efferent lesions, e.g. in muscle afferents or in vagal afferents from cardiopulmonary receptors.

Adult↗

Reflex control of heart rate in normal subjects in relation to age: a data base for cardiac vagal neuropathy.

We examined the heart rate changes induced by forced breathing and by standing up in 133 healthy subjects in the age range 10-65 years in order to establish a data base for studies on parasympathetic heart rate control in autonomic neuropathy. Test results declined with age. Log-transformation was used to define the lower limit of normal (P0.10) and an uncertainty range (values between P0.10 and P0.025). The lower limit of normal decreased from 22 to 11 beats/min for forced breathing and from 26 to 16 beats/min for standing up, with age increasing from 10 to 65 years. No subject scored below and only two subjects scored in or below the uncertainty range for both tests. Lack of correlation between both tests (r = 0.17) documents the different afferent mechanisms of the reflex heart rate changes. In combination these two tests form a simple and reliable bedside method to establish cardiac vagal neuropathy.

Adolescent↗

Mechanisms of initial heart rate response to postural change.

We explored in 43 healthy subjects the afferent mechanisms of the initial heart rate response to standing by comparing free standing, 70 degrees head-up tilt, handgrip, and contraction of abdominal and leg muscles. The results indicate the following. 1) Standing evokes an immediate, large, bimodal increase of heart rate (HR) of about 20 s duration that far exceeds the gradual HR rise induced by 70 degrees head-up tilt. 2) The immediate HR increase with active standing is due to the exercise reflex and results in a first peak about 3 s after standing briskly. 3) The secondary, more gradual HR increase after 5 s of standing and the subsequent rapid decrease of HR between about 12 and 20 s corresponds through the baroreceptor reflex with a striking fall, recovery, and sometimes overshoot of arterial pressure. 4) The maximum HR increase found after about 12 s of standing is augmented and delayed after rest. 5) The time course of the initial HR response is not modified by physical training. We conclude that active and passive changes of posture result in fundamentally different cardiovascular effects for about 20 s and that "central command," muscle receptors, high-pressure receptors, low-pressure receptors, and the plasma catecholamine level are probably all involved in the initial HR response to standing.

Acclimatization↗