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J T Potts

Publications and source records attributed to J T Potts.

At least 19 recordsLinked to original sources
PubMed2005

Discharge patterns of somatosensitive neurons in the nucleus tractus solitarius of the cat.

Encoding of sensory information by nucleus of the solitary tract (NTS) neurons is incompletely understood. Using extracellular single-unit recording in alpha-chloralose-urethane anesthetized cats, we have examined the discharge characteristics of NTS neurons to activation of somatic Adelta and C fiber afferents by skeletal muscle contraction evoked by electrical stimulation of lower lumbar/upper sacral ventral roots. Generally, somatic afferent stimulation evoked two distinct firing patterns. The first population (36/43 cells) increased their firing rate to brief somatic stimuli. A subset (21/27 cells) exhibited a rapid decay of their firing rate during sustained somatic stimulation. Peak instantaneous firing frequency (F(p)) increased proportionally with the intensity of somatic stimulation (105+/-4 vs. 119+/-4 vs. 139+/-4 Hz, 10, 20 and 40 Hz, respectively, P<0.0001), whereas steady-state firing frequency (F(ss)) was not altered (25+/-2 vs. 27+/-2 vs. 27+/-2 Hz, 10, 20 and 40 Hz, respectively, P=0.72). Two indices were derived to quantify the decay properties. The decay rate constant (obtained from exponential curve fitting) was not altered by stimulation frequency (461+/-10 vs. 442+/-14 vs. 429+/-26 ms, 10, 20 and 40 Hz, respectively, P=0.415), nor was the decay index (derived to express the percent reduction in firing rate with respect to the initial peak firing rate; 76+/-2 vs. 77+/-2 vs. 81+/-2%, 10, 20 and 40 Hz, respectively, P=0.187). In contrast, the second population (seven of 43 cells) decreased their firing rate to stimulation. Of the NTS neurons tested for barosensitivity (29/36), none responded to pressure stimulation. These results have identified a population of somatosensitive NTS neurons that exhibit rapid firing rate decay properties during sustained stimulation. However, this population could faithfully encode phasic excitation during rhythmic somatosensory input. These results are discussed in relation to the role of somatosensory input on baroreflex function.

Afferent Pathways↗
PubMed2003

Contraction-sensitive skeletal muscle afferents inhibit arterial baroreceptor signalling in the nucleus of the solitary tract: role of intrinsic GABA interneurons.

Arterial baroreceptor and skeletal muscle receptor afferents relay sensory information to the nucleus of the solitary tract (NTS) during exercise. Previous studies have suggested that skeletal muscle afferent input inhibits baroreflex function; however, detailed information on the role of muscle afferents and GABAergic mechanisms in the NTS is limited. Furthermore, identification of specific afferent modalities that activate GABAergic neurons in the NTS remains unknown. In the present study, we examined the neuroanatomical and physiological interactions between spinal dorsal horn cells that transmit contraction-sensitive input from skeletal muscle and GABAergic interneurons in the NTS. Biotinylated dextran amine (BDA, 10%, 25-100 nL) microinjection into dorsal horn of the cervical spinal cord was combined with glutamate decarboxylase (GAD) immunohistochemistry to visualize the nature of the relationship of BDA-labeled fibers in the NTS with GAD immunoreactivity (GAD-ir). BDA-labeled axons and terminal processes were localized in the medial, commissural, dorsomedial and dorsolateral subdivisions of the caudal NTS. Moreover, BDA-labeled fibers were observed in close proximity to GAD-ir structures throughout these regions of the NTS. The physiological interaction between skeletal muscle receptor and arterial baroreceptor afferents was investigated using an arterially perfused, decerebrate rat preparation. Activation of skeletal muscle afferents by electrically evoked twitch contraction of the forelimb attenuated baroreflex responsiveness (BR, calculated as the ratio of changes in heart rate to systemic pressure) from -1.5+/-0.3 bpm.mm Hg(-1) to -0.1+/-0.1 bpm.mm Hg(-1) (control versus contraction, P<0.05, n=15). However, forelimb contraction failed to inhibit the reflex bradycardia evoked by activation of peripheral chemoreceptor afferents, indicating a reflex-specific action. Bilateral microinjection of bicuculline methiodide (BIC, 10 microM, 40-60 nL) into the caudal NTS restored baroreflex responsiveness during contraction (-1.6+/-0.2 versus -0.1+/-0.1 versus -1.5+/-0.2 bpm.mmHg(-1), control versus contraction versus contraction+BIC P<0.05, n=8). We conclude that activation of ascending spinal neurons from the cervical dorsal horn by contraction-sensitive skeletal muscle afferents selectively inhibits arterial baroreceptor signaling in the NTS via activation of a GABAergic mechanism.

Afferent Pathways↗
PubMed2001

Activation of skeletal muscle afferents evokes release of glutamate in the subretrofacial nucleus (SRF) of cats.

The subretrofacial nucleus (SRF) is a region of the rostral ventrolateral medulla known to play a crucial role in sympathoexcitation. SRF neurons send direct projections to the intermediolateral cell columns of the spinal cord where they form synaptic contact with preganglionic sympathetic motor neurons. Activation of this neural pathway increases sympathetic outflow to the heart and blood vessels affecting cardiac function and vasomotor tone. Previous studies utilizing electrophysiological recording techniques and c-Fos expression have established that the activity of SRF neurons is increased during skeletal muscle contraction. However, the excitatory neurotransmitter mediating this increased activity remains in question. In the present study, static contraction of the triceps surae was induced by electrical stimulation of L7 and S1 ventral roots in anesthetized cats (n=12). Endogenous release of glutamate (Glu) from the SRF was recovered by microdialysis and measured by HPLC. Static muscle contraction for 4 min increased mean arterial pressure (MAP) 38+/-4 mmHg from a control level of 102+/-12 mmHg (P< 0.05). During muscle contraction the extracellular concentration of Glu recovered from the SRF increased from 623+/-117 to 1078+/-187 nM (P<0.05). To determine the effect of muscle contraction on Glu release in the absence of synaptic input from other reflexogenic areas, contraction was repeated following acute sinoaortic denervation and vagotomy. Following this denervation, muscle contraction increased MAP 41+/- 4 mmHg (P < 0.05) and Glu concentration from 635+/-246 to 1106+/-389 nM (P < 0.05). Muscle paralysis prevented the increases in MAP and Glu concentration during ventral root stimulation. These results suggest that: (i) Glu is released in the SRF during activation of contraction-sensitive skeletal muscle afferent fibers in the cat; and (ii) synaptic input from other reflexogenic areas appears to be ineffective in modulating the release of Glu in the SRF during static muscle contraction.

Animals↗
PubMed2001

Naturalistic activation of barosensitive afferents release substance P in the nucleus tractus solitarius of the cat.

The role for substance P (SP) in baroreceptor transmission in the nucleus tractus solitarius (NTS) remains an area of active research. The purpose of the present study was to determine whether naturalistic activation of barosensitive afferent fibers in the glossopharygneal and vagus nerves release SP in the caudal NTS. Experiments were performed on chloralose anesthetized, artificially ventilated and paralyzed cats. A microdialysis probe was stereotaxically positioned unilaterally in the NTS. Dialysate samples were collected and SP-like immunoreactivity (SP-LI) was measured by radioimmunoassay. Barosensitive afferents were mechanically activated by inflation of a balloon catheter positioned in the thoracic aorta at heart level. Graded balloon inflation produced increases in mean arterial pressure (MAP) of 33+/-5 mmHg and 60+/-3 mmHg (P<0.05) and evoked proportional baroreflex decreases in heart rate of 8+/-3 b.p.m. and 19+/-3 b.p.m. (P<0.05). This was accompanied by increases in SP-LI of 16+/-3% and 39+/-8%, respectively (P<0.05). A positive linear relationship was found between changes in MAP and SP-LI (slope=1.73 fmol/microl/mmHg, r(2)=0.62) that was completely abolished following barodenervation. These findings provide evidence that naturalistic activation of pressure-sensitive afferents in the glossopharygneal and vagus nerves release SP in a region of the NTS that receives primary afferent projections from aortic, carotid sinus and cardiac receptors in the cat.

Afferent Pathways↗
PubMed2001

NO formation in nucleus tractus solitarii attenuates pressor response evoked by skeletal muscle afferents.

We have previously shown that static muscle contraction induces the expression of c-Fos protein in neurons of the nucleus tractus solitarii (NTS) and that some of these cells were codistributed with neuronal NADPH-diaphorase [nitric oxide (NO) synthase]-positive fibers. In the present study, we sought to determine the role of NO in the NTS in mediating the cardiovascular responses elicited by skeletal muscle afferent fibers. Static contraction of the triceps surae muscle was induced by electrical stimulation of the L7 and S1 ventral roots in anesthetized cats. Muscle contraction during microdialysis of artificial extracellular fluid increased mean arterial pressure (MAP) and heart rate (HR) 51 +/- 9 mmHg and 18 +/- 3 beats/min, respectively. Microdialysis of L-arginine (10 mM) into the NTS to locally increase NO formation attenuated the increases in MAP (30 +/- 7 mmHg, P < 0.05) and HR (14 +/- 2 beats/min, P > 0.05) during contraction. Microdialysis of D-arginine (10 mM) did not alter the cardiovascular responses evoked by muscle contraction. Microdialysis of N(G)-nitro-L-arginine methyl ester (2 mM) during contraction attenuated the effects of L-arginine on the reflex cardiovascular responses. These findings demonstrate that an increase in NO formation in the NTS attenuates the pressor response to static muscle contraction, indicating that the NO system plays a role in mediating the cardiovascular responses to static muscle contraction in the NTS.

Animals↗
PubMed2001

Reflex cardiovascular responses evoked by selective activation of skeletal muscle ergoreceptors.

It is well known that the exercise pressor reflex (EPR) is mediated by group III and IV skeletal muscle afferent fibers, which exhibit unique discharge responses to mechanical and chemical stimuli. Based on the difference in discharge patterns of group III and IV muscle afferents, we hypothesized that activation of mechanically sensitive (MS) fibers would evoke a different pattern of cardiovascular responses compared with activation of both MS and chemosensitive (CS) fibers. Experiments were conducted in chloralose-urethane-anesthetized cats (n = 10). Passive muscle stretch was used to activate MS afferents, and electrically evoked contraction of the triceps surae was used to activate both MS and CS muscle afferents. No significant differences were shown in reflex heart rate and mean arterial pressure (MAP) responses between passive muscle stretch and evoked muscle contraction. However, when the reflex responses were matched according to tension-time index (TTI), the peak MAP response (67 +/- 4 vs. 56 +/- 4 mmHg, P < 0.05) was significantly greater at higher TTI (427 +/- 18 vs. 304 +/- 13 kg. s, high vs. low TTI, P < 0.05), despite different modes of afferent fiber activation. When the same mode of afferent fiber activation was compared, the peak MAP response (65 +/- 7 vs. 55 +/- 5 mmHg, P < 0.05) was again predicted by the magnitude of TTI (422 +/- 24 vs. 298 +/- 19 kg. s, high vs. low TTI, P < 0.05). Total sensory input from skeletal muscle ergoreceptors, as predicted by TTI and not the modality of afferent fiber activation (muscle contraction vs. passive stretch), is suggested to be the primary determinant of the magnitude of the EPR-evoked cardiovascular response.

Animals↗
PubMed2001

Selective and nonselective inverse agonists for constitutively active type-1 parathyroid hormone receptors: evidence for altered receptor conformations.

The spontaneous signaling activity of some G protein-coupled receptors and the capacity of certain ligands (inverse agonists) to inhibit such constitutive activity are poorly understood phenomena. We investigated these processes for several analogs of PTH-related peptide (PTHrP) and the constitutively active human PTH/PTHrP receptors (hP1Rcs) hP1Rc-H223R and hP1Rc-T410P. The N-terminally truncated antagonist PTHrP(5-36) functioned as a weak partial/neutral agonist with both mutant receptors but was converted to an inverse agonist for both receptors by the combined substitution of Leu(11) and D-Trp(12). The N-terminally intact analog [Bpa(2)]PTHrP(1-36)-a partial agonist with the wild-type hP1Rc-was a selective inverse agonist, in that it depressed basal cAMP signaling by hP1Rc-H223R but enhanced signaling by hP1Rc-T410P. The ability of [Bpa(2)]PTHrP(1-36) to discriminate between the two receptor mutants suggested that H223R and T410P confer constitutive receptor activity by inducing distinct conformational changes. This hypothesis was confirmed by the observations that: 1) the double mutant receptor hP1Rc-H223R/T410P exhibited basal cAMP levels that were 2-fold higher than those of either single mutant; and 2) hP1Rc-H223R and hP1Rc-T410P internalized (125)I-PTHrP(5-36) to markedly different extents. The overall results thus reveal that two different types of inverse agonists are possible for PTHrP ligands (nonselective and selective) and that constitutively active PTH-1 receptors can access different conformational states.

Animals↗
PubMed2001

Enhanced activity in parathyroid hormone-(1-14) and -(1-11): novel peptides for probing ligand-receptor interactions.

The amino-terminal portion of PTH is critical for PTH-1 receptor (P1Rc) activation. In exploring this component of the ligand receptor interaction, we recently showed that the agonist potency of the weakly active PTH-(1-14)NH(2) peptide can be enhanced by natural amino acid substitutions at several positions, including position 11 (normally leucine). Here we show that the potency of PTH-(1-14)NH(2) can be enhanced by using nonnatural amino acids that increase the length and polarizability of the position 11 side-chain. Thus, in LLC-PK(1) cells stably expressing high levels of the human P1Rc, [homoarginine([Har)(11)]PTH-(1-14)NH(2) was 30-fold more potent for cAMP production than was native PTH-(1-14)NH(2). Combining the homoarginine-11 substitution with other recently identified activity-enhancing substitutions yielded [Ala(3,12),Gln(10),Har(11),Trp(14)]PTH-(1-14)NH(2), which was 1500-fold more potent than PTH-(1-14)NH(2) (EC(50) = 0.12 +/- 0.04 and 190 +/- 20 microM, respectively) and only 63-fold less potent than PTH-(1-34) (EC(50) = 1.9 +/- 0.5 nM). The even shorter analog [Ala(3),Gln(10),Har(11)]PTH-(1-11)NH(2) was also a full cAMP agonist (EC(50) = 3.1 +/- 1.5 microM). Receptor mutations at Phe(184) and Leu(187) located near the boundary of the amino-terminal domain and transmembrane domain-1 severely impaired responsiveness to the PTH-(1-11) analog. Overall, these studies demonstrate that PTH analogs of only 11 amino acids are sufficient for activation of the PTH-1 receptor through interaction with its juxtamembrane region.

Amino Acid Sequence↗
PubMed2001

Exercise and sensory integration. Role of the nucleus tractus solitarius.

Since NTS neurons receive synaptic input from many sensory modalities, it is crucial to understand the neuronal mechanisms involved in synaptic processing. We have proposed that GABA-containing neurons in the NTS are the primary target for somatic afferent fibers activated by skeletal muscle contraction. In our model, local inhibition of baroreceptor signaling is necessary to counteract the increase in baroreceptor input such that NTS output is normalized and baroreflex sensitivity is maintained during exercise. This GABAergic mechanism, in conjunction with sympathoexcitation evoked by somatic afferents, preserves reflex sensitivity and resets the baroreflex, respectively. Unfortunately, there is insufficient data to date to support or refute the proposed role for GABA on baroreflex function during exercise. However, we feel that this model will be useful in formulating future experiments to explore these synaptic interactions.

Animals↗
PubMed2000

Somatosympathetic reflex in a working heart-brainstem preparation of the rat.

The purpose of the present study was to examine the cardiorespiratory responses (CR) evoked by a somatosympathetic reflex (SSR) in the working heart-brainstem preparation (WHBP). Sprague-Dawley rats (75-100 g) were anesthetized with halothane, bisected sub-diaphramatically and decerebrated pre-collicularly (n = 15). The preparation was transferred to a recording chamber and perfused via the thoracic aorta with Ringer's solution containing an oncotic agent (Ficoll, 1.25%). SSR was activated by electrical stimulation (5 s) of the brachial nerve (0.5-40 Hz, 1-20 V, 0.1 ms) or the forelimb (0.5-40 Hz, 5-60 V, 2 ms). Stimulation at 40 Hz significantly increased heart rate (HR, 366 +/- 10 to 374 +/- 9 beats/min), systemic perfusion pressure (PP, 83 +/- 5 to 89 +/- 6 mmHg) and phrenic nerve discharge (PND, 0.4 +/- 0.1 to 1.4 +/- 0.3 Hz). Ganglionic blockade with hexamethonium (300 microM) eliminated the tachycardia and pressor response but did not alter the tachypnea to forelimb stimulation (n = 3). Transection of the brachial nerve plexus abolished the increase in PP and PND (n = 4). This indicates that a neural reflex mediated these responses. Spinal transection (C1-C2) completely abolished all responses indicating that they were mediated via a supraspinal pathway (n = 2). Based upon these findings, we conclude that activation of somatosensory afferent fibers in the WHBP evokes a programmed pattern of autonomic responses altering the activity-state of both the cardiovascular and respiratory systems. The WHBP provides a unique opportunity to investigate the medullary circuits and neuronal mechanisms that may be involved in coupling cardiorespiratory and somatomotor activity during locomotion/exercise.

Afferent Pathways↗
PubMed2000

Minimization of parathyroid hormone. Novel amino-terminal parathyroid hormone fragments with enhanced potency in activating the type-1 parathyroid hormone receptor.

The amino-terminal and carboxyl-terminal portions of the 1-34 fragment of parathyroid hormone (PTH) contain the major determinants of receptor activation and receptor binding, respectively. We investigated how the amino-terminal signaling portion of PTH interacts with the receptor by utilizing analogs of the weakly active fragment, rat (r) PTH(1-14)NH(2), and cells transfected with the wild-type human PTH-1 receptor (hP1R-WT) or a truncated PTH-1 receptor which lacked most of the amino-terminal extracellular domain (hP1R-delNt). Of 132 mono-substituted PTH(1-14) analogs, most having substitutions in the (1-9) region were inactive in assays of cAMP formation in LLC-PK1 cells stably expressing hP1R-WT, whereas most having substitutions in the (10-14) region were active. Several substitutions (e.g. Ser(3) --> Ala, Asn(10) --> Ala or Gln, Leu(11) --> Arg, Gly(12) --> Ala, His(14) --> Trp) enhanced activity 2-10-fold. These effects were additive, as [Ala(3),(10,12),Arg(11), Trp(14)] rPTH(1-14)NH(2) was 220-fold more potent than rPTH(1-14)NH(2) (EC(50) = 0.6 +/- 0.1 and 133 +/- 16 micrometer, respectively). Native rPTH(1-11) was inactive, but [Ala(3,10), Arg(11)]rPTH(1-11)NH(2) achieved maximal cAMP stimulation (EC(50) = 17 micrometer). The modified PTH fragments induced cAMP formation with hP1R-delNt in COS-7 cells as potently as they did with hP1R-WT; PTH(1-34) was 6,000-fold weaker with hP1R-delNt than with hP1R-WT. The most potent analog, [Ala(3,10,12),Arg(11), Trp(14)]rPTH(1-14)NH(2), stimulated inositol phosphate production with hP1R-WT. The results show that short NH(2)-terminal peptides of PTH can be optimized for considerable gains in signaling potency through modification of interactions involving the regions of the receptor containing the transmembrane domains and extracellular loops.

Animals↗
PubMed1999

Amino-terminal modifications of human parathyroid hormone (PTH) selectively alter phospholipase C signaling via the type 1 PTH receptor: implications for design of signal-specific PTH ligands.

Parathyroid hormone (PTH) and PTH-related peptide (PTHrP) activate the PTH/PTHrP receptor to trigger parallel increases in adenylyl cyclase (AC) and phospholipase C (PLC). The amino (N)-terminal region of PTH-(1-34) is essential for AC activation. Ligand domains required for activation of PLC, PKC, and other effectors have been less well-defined, although some studies in rodent systems have identified a core region [hPTH-(29-32)] involved in PKC activation. To determine the critical ligand domain(s) for PLC activation, a series of truncated hPTH-(1-34) analogues were assessed using LLC-PK1 cells that stably express abundant transfected human or rat PTH/PTHrP receptors. Phospholipase C signaling and ligand-binding affinity were reduced by carboxyl (C)-terminal truncation of hPTH-(1-34) but were coordinately restored when a binding-enhancing substitution (Glu(19) --> Arg(19)) was placed within hPTH-(1-28), the shortest hPTH peptide that could fully activate both AC and PLC. Phospholipase C, but not AC, activity was reduced by substituting Gly(1) for Ser(1) in hPTH-(1-34) and was eliminated entirely by removing either residue 1 or the alpha-amino group alone. These changes did not alter binding affinity. These findings led to design of an analogue, [Gly(1),Arg(19)]hPTH-(1-28), that was markedly signal-selective, with full AC but no PLC activity. Thus, the extreme N-terminus of hPTH constitutes a critical activation domain for coupling to PLC. The C-terminal region, especially hPTH-(28-31), contributes to PLC activation through effects upon receptor binding but is not required for full PLC activation. The N-terminal determinants of AC and PLC activation in hPTH-(1-34) overlap but are not identical, as subtle modifications in this region may dissociate activation of these two effectors. The [Gly(1),Arg(19)]hPTH-(1-28) analogue, in particular, should prove useful in dissociating AC- from PLC-dependent actions of PTH.

Adenylyl Cyclases↗
PubMed1999

Skeletal muscle afferent fibres release substance P in the nucleus tractus solitarii of anaesthetized cats.

1. The tachykinin substance P was recovered from the commissural subdivision of the nucleus tractus solitarii (cNTS) using in vivo microdialysis during activation of cardiorespiratory and skeletal muscle receptors in thirteen chloralose-anaesthetized cats. 2. Tetanic muscle contraction was evoked by stimulating L7-S1 ventral roots (n = 7). Electrically induced muscle contraction increased mean arterial pressure (MAP) by 55 +/- 10 mmHg and heart rate by 29 +/- 6 beats min-1. During contraction the dialysate concentration increased 154 % above resting control levels (from 0.217 +/- 0.009 to 0.546 +/- 0.023 fmol (100 microl)-1, control vs. contraction, P < 0.05). 3. Loss of cardiorespiratory input following disruption of the carotid sinus and vagus nerves significantly blunted, but did not abolish, the increase in substance P during muscle contraction (from 0.247 +/- 0.022 to 0.351 +/- 0.021 fmol (100 microl)-1, control vs. contraction, P < 0.05). Approximately 44 % of the substance P release during contraction was independent of cardiorespiratory input transmitted by carotid sinus and vagus nerves. 4. To determine the contribution of cardiorespiratory related neural input on substance P release, an intravascular balloon positioned in the thoracic aorta was inflated to increase arterial pressure (n = 6). Balloon inflation increased MAP by 50 +/- 5 mmHg and substance P increased from 0.251 +/- 0.025 to 0.343 +/- 0. 028 fmol (100 microl)-1 (control vs. balloon inflation, P < 0.05). This increase was completely abolished following interruption of vagal and carotid sinus nerves (from 0.301 +/- 0.012 to 0.311 +/- 0. 014 fmol (100 microl)-1, control vs. balloon inflation). This finding shows that neural input from cardiorespiratory receptors (primarily arterial baroreceptors) accounted for 37 % of the total substance P release during muscle contraction. 5. The findings from this study demonstrate that activation of skeletal muscle receptors and cardiorespiratory receptors (predominantly arterial baroreceptors) increases the extraneuronal concentration of substance P in the cNTS. Because substance P release was not completely abolished during muscle contraction following disruption of carotid sinus and vagus nerves it is proposed that: (1) afferent projections from contraction-sensitive skeletal muscle receptors may release substance P in the NTS; (2) neural input from muscle receptors activates substance P-containing neurones within the NTS; and (3) convergence of afferent input from skeletal muscle receptors and arterial baroreceptors onto substance P-containing neurones in the cNTS facilitates the release of substance P. The role of tachykininergic modulation of cardiorespiratory input is discussed.

Anesthesia↗
PubMed1998

Respiratory sinus arrhythmia during exercise in aerobically trained and untrained men.

Respiratory sinus arrhythmia (RSA) was examined in aerobically trained (AT) and untrained (NT) college-aged males during 12 periods consisting of a 3-min sitting baseline, six common 3-min absolute exercise stages, and five 3-min recovery stages that followed voluntary exhaustion to determine the relationship of work and training status to parasympathetic influence upon the heart. RSA systematically decreased during absolute exercise, was observed at heart rates (HR) above 100 beats x min(-1), and progressively increased during recovery. Additionally, independent of work stages, comparative regression analyses were conducted for both the exercise and recovery phases, separately, in which HR was regressed on RSA, as well as RSA on % VO2max, to contrast the obtained relationships for the AT and NT. No differences were revealed as a function of endurance training status as the slopes and intercepts obtained for the two groups from each of these analyses were similar. The within-subject correlations between RSA and % VO2max, calculated for each of the individuals across all 12 periods, were consistently negative. Between-subjects correlations of RSA with RR and tidal volume were predominantly nonsignificant, indicating that RSA, as measured here, is independent of individual differences in ventilatory activity and, as such, can be compared between groups during exercise. The findings demonstrate that RSA is detectable during both exercise and recovery, even at HR beyond 100 beats x min(-1), and reveals a similar relationship to HR and metabolic state in both aerobically trained and untrained populations.

Adult↗
PubMed1998

Effect of barodenervation on c-Fos expression in the medulla induced by static muscle contraction in cats.

A previous study has shown increased Fos-like immunoreactivity (FLI), a marker of neural activation, in the nucleus of the solitary tract (NTS) and the ventrolateral medulla (VLM) after static muscle contraction elicited by electrical stimulation of L7 and S1 ventral roots of the spinal cord in anesthetized, baroreceptor-intact cats. Because the electrically induced static muscle contraction reflexly increased arterial blood pressure, the concomitant activation of the arterial baroreceptor reflex during static muscle contraction may have resulted in some of the FLI labeling that was observed in the medulla. The purpose of this study was to determine regions in the medulla that are activated by muscle contraction in the absence of arterial baroreceptor input. Electrical stimulation of L7 and S1 ventral roots of the spinal cord was used to elicit static muscle contraction, and FLI in the medulla was determined in barointact and barodenervated cats. In barointact contraction cats, FLI was observed in the lateral reticular nucleus (LRN), NTS, lateral tegmental field (FTL), subretrofacial nucleus (SRF), and A1 region of the medulla. In barodenervated contraction cats, FLI increased in the same regions; however, the number of FLI-labeled cells in the NTS, FTL, and A1 region was significantly less than in barointact contraction animals. No significant difference in the number of FLI-labeled cells was found in the LRN and SRF between the two groups. These results clearly demonstrate that cardiovascular regions in the medulla are activated by input from afferent activity originating in skeletal muscle independently of concomitant arterial baroreceptor reflex activation.

Afferent Pathways↗
PubMed1998

Reduction in arterial compliance alters carotid baroreflex control of cardiac output in a model of hypertension.

Baroreflex regulation of cardiac output is determined by the performance of the heart as well as the available blood flow returning to the heart (i.e., venous return). We hypothesized that a decrease in arterial compliance (C(a)) would affect carotid baroreflex control of cardiac output by altering the slope of the venous return curve (VR curve). Baroreflex control of systemic arterial pressure (Pa), central venous pressure (Pv), heart rate, cardiac output (CO), and peripheral vascular resistance (R) were determined during bilateral carotid occlusion (BCO) in spontaneously hypertensive (hypertensive, HT) and Sprague-Dawley (normotensive, NT) rats. C(a) was determined from the rate of arterial pressure decay when CO was transiently stopped, and the VR curve was obtained during graded inflation of a vascular balloon positioned in the right atrium. The inverse slope of the VR curve was used as an index of the resistance to venous return (RVR). The baseline slope of the VR curve was -50.5 +/- 3.3 vs. -35.5 +/- 2.6 ml.kg-1.min-1.mmHg-1 in NT vs. HT, respectively (P < 0.05). Control values of Pa (96 +/- 5 vs. 124 +/- 8 mmHg) and R [0.43 +/- 0.04 vs. 0.80 +/- 0.07 peripheral resistance units (PRU)] were reduced in NT, whereas Ca (0.062 +/- 0010 vs. 0.036 +/- 0.003 ml.kg-1.mmHg-1) was elevated in NT vs. HT, respectively (P < 0.05). Analysis of the pressure dependence of C(a) demonstrated that C(a) was a nonlinear function of Pa, and the exponential decay constant for the C(a)-Pa relationship was reduced in HT (0.0055 +/- 0.0012 vs. 0.0012 +/- 0.0002 min, NT vs. HT, P < 0.05). Baroreflex activation by BCO significantly increased Pa (delta Pa, 20 +/- 4 vs. 28 +/- 3 mmHg) and R (delta R, 0.16 +/- 0.04 vs. 0.24 +/- 0.06 PRU) in NT vs. HT, respectively. However, BCO significantly decreased CO in NT but not HT (delta CO, -24 +/- 5 vs. -4 +/- 6 ml.kg-1.min-1, P < 0.05). In NT, RVR was increased 39 +/- 9% during BCO (P < 0.05), whereas RVR increased 8 +/- 3% in HT (P = NS). From these findings, we conclude that the difference in baroreflex control of CO is mediated, in part, by the reduction in C(a), which minimized the baroreflex-evoked increase in RVR.

Animals↗