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Biomedical subjects

L B Wilson

Publications and source records attributed to L B Wilson.

At least 19 recordsLinked to original sources
PubMed1998

Segmental effect of NMDA block in the dorsal horn on the pressor reflex.

The purpose of this study was to examine the influence of NMDA receptor blockade in the dorsal horn of adjacent spinal segments as it pertains to the pressor reflex evoked by static contraction and stretch of skeletal muscle. In this preparation, cats were anesthetized and the afferent fibers mediating the pressor reflex entered the spinal cord via the L7 dorsal root. Blockade of dorsal horn NMDA receptors at L6 and L7 attenuated the pressor reflex evoked by static contraction and muscle stretch. However, NMDA block in the L6 dorsal horn alone failed to alter the peak increase in MAP produced by static contraction and muscle stretch, but the initial pressor response evoked by static contraction was attenuated. These data support the hypothesis that the pressor reflex is partially mediated by activation of NMDA receptors in the dorsal horn, and this occurs at multiple spinal segments. Further, these data suggest that activation of NMDA receptors plays an important role in initiating the rise in arterial pressure produced by static contraction of skeletal muscle.

2-Amino-5-phosphonovalerate↗
PubMed1998

Segmental effect of spinal NK-1 receptor blockade on the pressor reflex.

The physiological effects of substance P (SP) are mediated via activation of neurokinin-1 (NK-1) receptors. The purpose of this study was to test the hypothesis that blockade of NK-1 receptors in the dorsal horn, both at the site of entry for the primary afferent neurons and adjacent spinal segments, attenuates the pressor reflex evoked by static contraction and stretch of skeletal muscle. Cats were anesthetized with alpha-chloralose and urethan, and a laminectomy was performed. With the exception of the L7 dorsal root, the dorsal and ventral roots from L5 to S2 were sectioned on one side of the spinal cord. Thus the primary afferent fibers mediating the pressor reflex enter the spinal cord via the L7 dorsal root in these experiments. Based on dose-response data, dialysis of the NK-1 receptor antagonist CP-96,345 (5 mM for 2 h) into the L7 dorsal horn ipsilateral to the contracting muscle attenuated the pressor response to static contraction (75 +/- 15 vs. 46 +/- 7 mmHg; n = 5 cats) but not muscle stretch (60 +/- 12 vs. 50 +/- 8 mmHg). Administration of the inactive enantiomer of CP-96,345, CP-96,344 (5 mM for 2 h), into the L7 dorsal horn failed to alter the cardiovascular changes elicited by contraction (45 +/- 7 vs. 43 +/- 6 mmHg) and stretch (31 +/- 8 vs. 32 +/- 11). Dialysis of 5 mM CP-96, 345 into the dorsal horn at the L6 and S1 segments for 2 h decreased the peak pressor response to static contraction (58 +/- 9 vs. 31 +/- 6 mmHg; n = 7) and muscle stretch (61 +/- 6 vs. 44 +/- 8 mmHg). These data suggest that the activation of NK-1 receptors, both at the site of entry and in regions outside of the entry site for afferent neurons, is involved in the spinal processing that produces the pressor reflex evoked by static contraction of skeletal muscle.

Animals↗
PubMed1997

Static muscle contraction elicits a baroreflex-dependent increase in glutamate concentration in the ventrolateral medulla.

In anesthetized cats, static contraction of the hindlimb reflexly increases mean arterial pressure (MAP). This cardiovascular adjustment is reduced by the arterial baroreflex. Both of these reflex responses are mediated through activation of ventrolateral medullary (VLM) regions. We tested the hypothesis that the concentration of glutamate (Glu) increases in the caudal ventrolateral medulla (cVLM) during static hindlimb contractions in anesthetized cats, and that barodenervation reduces this elevation in Glu levels. Static contractions of the triceps surae muscle of one hindlimb were evoked by electrical stimulation of the peripheral ends of cut L7 and S1 ventral roots. After the insertion of the microdialysis probes and a 3-h recovery period, a 2-min static contraction increased MAP by 47 +/- 7 mmHg. The concentration of Glu increased from 606 +/- 189 to 1042 +/- 228 nM. These results were repeatable in that Glu, as well as MAP, rose by a similar amount in two subsequent contractions. By contrast, in a subset of cats paralyzed prior to the third contraction, neither MAP nor Glu were significantly increased over baseline levels during the third stimulation period. In a third group of cats, hindlimb contraction increased MAP and Glu levels. However, the Glu release was attenuated in subsequent contractions after these cats were barodenervated. During the same periods of stimulation, the denervation accentuated the rise in MAP. These data demonstrate that static contraction of the hindlimb increases the extracellular concentration of Glu in the cVLM. Further, our study implicates this neurotransmitter in the baroreflex mediated reduction of the pressor reflex response to static muscle contraction.

Animals↗
PubMed1997

The pressor reflex evoked by static contraction: neurochemistry at the site of the first synapse.

Stimulation of somatic sensory neurons activates the sympathetic nervous system, in turn enhancing cardiovascular function. This has been repeatedly demonstrated when afferent fibers arising from skeletal muscle serve as the sensory neurons. Over the past several years, studies have been performed examining the central nervous system (CNS) mechanisms that cause the reflex increases in arterial blood pressure and heart rate when skeletal muscle contracts. These studies have provided insights into how the CNS alters cardiovascular function, and have helped to enhance our understanding of central sensory transduction processes. Using a variety of techniques, several sites have been identified within the brain and spinal cord that are responsible for producing the reflex pressor response to static contraction. However, the purpose of this manuscript is to review the recent developments concerning only one CNS site: the dorsal horn of the spinal cord. This region serves as the first synapse for afferent fibers from skeletal muscle. The release of neurotransmitters, and possibly neuromodulators, into this region initiates the CNS component of this reflex. In addition, the magnitude of the reflex cardiovascular changes can be modulated at this site. The studies described in this review suggest that the dorsal horn of the spinal cord serves as an important site of integration for sensory signals that influence the cardiovascular system.

Animals↗
PubMed1997

c-Fos expression in the medulla induced by static muscle contraction in cats.

In this study, we examined Fos-like immunoreactivity (FLI) in the medulla after static muscle contraction induced by stimulation of L7 and S1 ventral roots of the spinal cord in anesthetized cats. The results show that FLI increases in the lateral reticular nucleus, nucleus of the solitary tract, lateral tegmental field, vestibular nucleus, subretrofacial nucleus, and A1 region of the medulla in comparison with these same areas in sham-operated animals (P < 0.05 in each region). In the rostral ventrolateral medulla, FLI distribution in neurons containing phenylethanolamine-N-methyltransferase (PNMT, the synthetic enzyme for epinephrine) was also observed utilizing double-labeling methods. The majority of neurons with PNMT also expressed FLI (66 +/- 4%). These data are in contrast to the results from sham-operated animals showing that 24 +/- 3% of the neurons costained with PNMT (P < 0.05). Our findings indicate that expression of FLI can be used to identify neurons activated during static muscle contraction and support previous studies implicating the ventrolateral medulla as a critical region for expression of the exercise pressor reflex. Furthermore, neurons in the rostral ventrolateral medulla containing PNMT were activated during static muscle contraction.

Animals↗
PubMed1997

An acute dystonic reaction with long-term use of ranitidine in an intensive care unit patient.

Dystonic reactions produce twisting and repetitive movements or abnormal posturing; this sign is considered an extrapyramidal sequela that is most typically thought to arise from decreased dopamine activity in the basal ganglia. Severe dystonic reactions have been shown to occur in concert with numerous medications. Although most commonly described with anti-psychotic agents such as haloperidol and phenothiazine, dystonic reactions have been observed in those who have used fluoxetine, erythromycin, crack cocaine, phenobarbital, cisapride, and buspirone. This report details the case of a patient who developed an acute dystonic reaction while taking ranitidine for peptic ulcer prophylaxis, a complication that, to our knowledge, has yet to be described with the use of this agent.

Anti-Ulcer Agents↗
PubMed1996

Divergence of ventilatory responses to isometric contraction in anesthetized cats.

The purpose of this study was to determine if the initial ventilatory and phrenic nerve responses to isometric contraction of the triceps surae muscle of anesthetized cats are influenced by the pattern of the contraction. To address this, three different types of muscle contraction were evoked: (1) a high tension, continuous tetanic (HT-CT) contraction; (2) a moderate tension, continuous tetanic (MT-CT) contraction; and (3) high tension, intermittent tetanic (HT-IT) contractions. The duration of each contraction period was 60 sec. The MT-CT and HT-IT contractions increased minute volume (VE; 19 +/- 4% and 15 +/- 5%, respectively) within the first 15 sec. These increases were the result of rises in breathing frequency and tidal volume. However, only the MT-CT contraction increased phrenic activity (pVE) in the first 15 sec. By contrast, ventilation and phrenic nerve activity failed to increase within the first 15 sec of the HT-CT contraction. If fact, 'tidal' phrenic activity (pVT; -14 +/- 5%) decreased during the first 5 sec, and there was a tendency for tidal volume (VT; -8 +/- 5%), VE (-8 +/- 6%), and pVE (-16 +/- 8%) to fall. These data suggest that stimulation of muscle afferent fibers by static contraction can initially inhibit phrenic nerve activity, provided the activation is sustained and of sufficient intensity.

Anesthesia, General↗
PubMed1996

Microdialysis of a non-NMDA receptor antagonist into the L7 dorsal horn attenuates the pressor response to static muscle contraction but not passive stretch in cats.

Mean arterial pressure (MAP) and heart rate (HR) were measured during static contraction or passive stretch of the triceps surae muscle of chloralose-anaesthetized cats. MAP and HR increased by 46 +/- 5 mmHg and 17 +/- 3 beats min-1, respectively, during a 1 min contraction. Passive stretch of the same muscle for 1 min reflexly increased MAP and HR by 40 +/- 7 mmHg and 14 +/- 3 beats min-1, respectively. Microdialysis of 2 mM 6-cyano-7-nitroquinoxaline-2,3-dione (CNX), a non-NMDA receptor antagonist, into the dorsal horn at the L7 spinal level attenuated the reflex pressor response to static contraction (2 h of dialysis: delta MAP = 23 +/- 5 mmHg, delta HR = 8 +/- 2 beats min-1). By contrast, there was no attenuation of the pressor response to passive stretch at 2 h of CNQX perfusion. However, the simultaneous microdialysis of 2 mM CNQX into the L6 and S1 levels blunted the pressor and tachycardic responses to contraction and stretch. These data show that the reflex pressor response to static muscle contraction is partly mediated by activation of non-NMDA receptors at the level of afferent fibre entry into the dorsal horn and through collateral pathways. Further, it appears that the afferent pathways within the dorsal horn for the signal transduction arising from static muscle contraction and passive stretch of the hindlimb are dissimilar.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1996

NMDA receptor blockade in cat dorsal horn blunts reflex pressor response to muscle contraction and stretch.

The role of N-methyl-D-aspartate (NMDA) receptors in the reflex pressor response to static muscle contraction and passive stretch was examined by microdialyzing the NMDA receptor antagonist DL-2-amino-5-phosphonovalerate (AP-5) into the L7 or L6 and S1 levels of the dorsal horn of anesthetized cats. Contraction, elicited by electrical stimulation of the cut L7 and S1 ventral roots, increased mean arterial pressure (MAP) and heart rate (HR). Passive stretch at tensions similar to those generated by contraction also increased these variables. These cardiovascular changes were unaffected by dialyzing AP-5 (10 mM) into the dorsal horn at L7. Increasing the syringe concentration of AP-5 to 100 mM attenuated the pressor and HR responses from 62 +/- 8 to 31 +/- 6 mmHg and 18 +/- 4 to 12 +/- 4 beats/min, respectively. AP-5 blunted the increase in MAP (59 +/- 10 vs. 41 +/- 10 mmHg) evoked by muscle stretch. Simultaneously microdialyzing AP-5 (10 or 100 mM) into the dorsal horn at the L6 and S1 spinal levels also blunted the MAP and HR responses to contraction and stretch. These results suggest that NMDA receptors play a role in mediating the MAP and HR responses to static muscle contraction at the spinal level of the central nervous system. Furthermore, these data demonstrate that collaterals from muscle afferents partially mediate the reflex cardiovascular responses evoked by muscle contraction and stretch.

2-Amino-5-phosphonovalerate↗
PubMed1996

Excitatory amino acid concentrations in the spinal dorsal horn of cats during muscle contraction.

In anesthetized cats, static hindlimb muscle contraction reflexly increases mean arterial pressure (MAP) and heart rate (HR). Pharmacological and immunohistochemical evidence suggests that excitatory amino acids are involved in the spinal transmission of this reflex. Using microdialysis and high-performance liquid chromatography technology, we tested the hypothesis that static contraction of the triceps surae muscle increases the extracellular concentration of glutamate (Glu) and aspartate (Asp) at the L7 level of the dorsal horn of the spinal cord. With the exception of the L7 dorsal root, the L5-S2 dorsal and ventral roots were cut ipsilateral to the contracting muscle. After the insertion of microdialysis probes and a 3-h recovery period, a 2-min static contraction was electrically evoked. MAP and HR increased by 53 +/- 8 mmHg and 20 +/- 4 beats/min. The concentration of Glu increased from 324 +/- 59 to 857 +/- 80 nM, whereas Asp increased from 199 +/- 57 to 499 +/- 113 nM. These results were repeatable, in that Glu and Asp rose by similar amounts in two subsequent contractions. In both of these latter contractions, MAP and HR were also significantly increased. By contrast, in a subset of cats whose L7 dorsal roots were cut after the first contraction, neither MAP, HR, Glu, nor Asp was significantly increased over baseline levels. These data demonstrate that static contraction of the hindlimb increases the extracellular concentration of Glu and Asp in the dorsal horn. In summary, the results from this study are in agreement with previous findings suggesting that excitatory amino acids are involved in the spinal transmission of sensory information from the hindlimb muscle.

Animals↗
PubMed1995

Cardiovascular effects elicited by central administration of physostigmine via M2 muscarinic receptors in conscious cats.

The cardiovascular effects of an intracerebroventricular (i.c.v.) injection of physostigmine were studied using conscious cats. Physostigmine (5-25 micrograms: 5 microliters) caused a dose-dependent increase in mean arterial pressure (MAP) and heart rate (HR). The highest dose (25 micrograms) increased MAP and HR by 32 +/- 3 mmHg and 45 +/- 5 beats/min, respectively (n = 5). Pre-administration of the muscarinic receptor antagonist, atropine (25 micrograms; i.c.v.) blocked the effects of physostigmine (25 micrograms; i.c.v.). Also, the pre-administration of the M2 muscarinic antagonist, methoctramine (25 micrograms; i.c.v.), antagonized the cardiovascular effects of physostigmine without altering the baseline variables. However, the M1 muscarinic antagonist, pirenzepine (100 micrograms; i.c.v.) did not alter baseline MAP or HR, and also failed to inhibit the cardiovascular responses to physostigmine. Similarly, the M3 muscarinic blocker, 4-diphenyl-acetoxy-N-methylpiperidine methiodide (50 micrograms; i.c.v.), neither changed baseline cardiovascular variables nor blocked the effects of physostigmine. When the same cats were anesthetized with intravenous injection of sodium pentobarbital (25-30 mg/kg), physostigmine (25 micrograms; i.c.v.) evoked a decrease in MAP and HR of 13 +/- 6 mmHg and 15 +/- 6 bpm, respectively (n = 5). These results demonstrate that the increases in MAP and HR to the i.c.v. administration of physostigmine in conscious cats are possibly mediated through stimulation of central M2 muscarinic receptors. In addition, anesthesia reverses the effects elicited by the central administration of physostigmine to a decrease in MAP and HR.

Animals↗
PubMed1995

Differential effects of clonidine on renal sympathetic nerve activity and heart rate at onset of static exercise.

The effects of the alpha 2-adrenergic agonist clonidine on the increase in renal sympathetic nerve activity (RSNA) and heart rate (HR) at the onset of voluntary static exercise were studied using conscious cats. Five cats were trained to press a bar with one forelimb. A total of 60 exercise trials were performed before and after injection of clonidine (5-10 micrograms/kg i.v.). Before clonidine, RSNA and HR increased immediately before or at the onset of exercise, which was followed by a rise in arterial blood pressure (AP). The initial increases in RSNA and HR are likely to be caused by descending input from higher brain centers. After clonidine, baseline RSNA was decreased to 21 +/- 5% of the control before clonidine, probably due to a central action of clonidine. HR and AP were decreased from 221 +/- 4 to 178 +/- 5 bpm and from 108 +/- 2 to 82 +/- 4 mmHg, respectively. The increase in RSNA at the onset of exercise and the rise in AP during exercise were blunted to 56-57% of the responses before clonidine injection. In contrast, the increase in HR at the onset of exercise was not altered by clonidine. Thus, it is suggested that clonidine, administered intravenously, attenuates the centrally-induced increase in RSNA at the onset of static exercise but does not affect the increase in HR.

Adrenergic Fibers↗
PubMed1995

Modulation of reflex pressor response to contraction and effect on substance P release by spinal 5-HT1A receptors.

This study investigated whether activation of serotonin1A [5-hydroxytryptamine (5-HT)1A] receptors in the dorsal horn of the spinal cord attenuates the reflex pressor response to static contraction and passive muscle stretch. In addition, we determined if the attenuation of the response to contraction is mediated by inhibiting substance P (SP) release in the dorsal horn. Static contractions of the triceps surae muscle of chloralose-anesthetized cats were induced by stimulating the cut L7 and S1 ventral roots. Microdialysis (10 mM) of a selective 5-HT1A agonist [8-hydroxy-2-(di-N-propylamino)tetralin (8-OH-DPAT)] into the L7 dorsal horn region produced a reversible attenuation of the reflex pressor response to a 1-min contraction (in mmHg: control = 36 +/- 3; 8-OH-DPAT = 17 +/- 3; recovery = 31 +/- 8; P = 0.013; n = 6) or passive stretch (in mmHg: control = 36 +/- 6; 8-OH-DPAT = 15 +/- 2; recovery = 32 +/- 6; P = 0.002; n = 6). However, a 5-HT1B agonist, 1-[3-(trifluoromethyl)-phenyl]piperazine, had no effect on the reflex pressor response. During 5-min contractions (n = 8), 8-OH-DPAT (10 mM) also blunted the pressor response but had no effect on the levels of SP-like immunoreactivity (in fmol/100 microliters: control = 0.492 +/- 0.026; 8-OH-DPAT = 0.501 +/- 0.034). These results suggest that activation of 5-HT1A receptors in the dorsal horn attenuates the reflex pressor response to contraction through a mechanism other than inhibition of SP release.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1995

Effect of skeletal muscle fiber type on the pressor response evoked by static contraction in rabbits.

The purpose of this study was to determine whether the reflex hemodynamic responses to static contraction of predominately glycolytic muscle are greater than the changes elicited by primarily oxidative muscle. Low-frequency electrical stimulation (continuous 21 days) of the tibial nerve of one hindlimb of adult rabbits converted the metabolic characteristics of the predominately glycolytic gastrocnemius to a muscle that was primarily oxidative. After 21 days of stimulation, the rabbits were decerebrated, and static contraction of the glycolytic muscle (unstimulated gastrocnemius) initially decreased heart rate (HR; -16 +/- 3 beats/min) and mean arterial pressure (MAP; -17 +/- 3 mmHg). Thereafter, MAP increased 13 +/- 3 mmHg above baseline. Static contraction of the oxidative muscle (stimulated gastrocnemius) produced similar decreases in HR and MAP (-12 +/- 4 beats/min and -12 +/- 3 mmHg, respectively). However, the subsequent increase in MAP (8 +/- 3 mmHg; above baseline) was less than that evoked by contraction of the glycolytic muscle. The responses evoked by stretch of each muscle and high-intensity electrical stimulation were the same, indicating that the afferents from the muscle were not destroyed by the chronic-stimulation technique. These results support the hypothesis that metabolic by-products play a role in the pressor response to static contraction of skeletal muscle. In addition, these data confirm that contraction of predominately oxidative muscle can evoke a reflex pressor response, albeit smaller than the change elicited from primarily glycolytic muscle.

Analysis of Variance↗
PubMed1995

Attenuation of the exercise pressor reflex. Effect of opioid agonist on substance P release in L-7 dorsal horn of cats.

Using alpha-chloralose-anesthetized cats, we studied blood pressure and heart rate responses to static contraction and passive stretch of the triceps surae muscle before and after microdialyzing the mu-opioid agonist [D-Ala2]-methionine enkephalinamide (DAME, 200 mumol/L) into the L-7 dorsal horn of the spinal cord. In addition, we measured contraction-induced substance P release in the dorsal horn before and after drug delivery. After 92 +/- 3 minutes of dialyzing the opioid agonist, contraction-induced increases in mean arterial pressure and heart rate were attenuated from control values of 58 +/- 7 mm Hg and 17 +/- 3 beats per minute to postdrug values of 27 +/- 7 mm Hg and 10 +/- 2 beats per minute, respectively. A similar attenuation was observed for the passive muscle stretches after 97 +/- 5 minutes of dialysis (control, 38 +/- 4 mm Hg and 8 +/- 2 beats per minute; after drug, 23 +/- 4 mm Hg and 5 +/- 1 beats per minute). Prior microdialysis of naloxone (300 mumol/L), a mu-antagonist, blocked this effect, suggesting that the opioid agonist has a specific receptor action. Naloxone alone had no effect on the pressor or tachycardiac responses. The contraction-induced increase in substance P-like immunoreactivity was reduced from a control value of 0.119 +/- 0.024 to 0.047 +/- 0.010 fmol/100 microL by DAME. Time-control experiments revealed no decrease in the release of substance P-like immunoreactivity. Thus, activation of opioid receptors modulates the transmission of group III and IV muscle afferent nerve activity through the L-7 dorsal horn.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1995

Attenuation of the reflex responses to muscle contraction by the coadministration of antagonists to substance P and somatostatin into the dorsal horn.

OBJECTIVE: The aim was to determine if the coadministration of antagonists to substance P and somatostatin into the L7 dorsal horn blunts the reflex cardiovascular responses to static contraction to a greater extent than each antagonist alone. The possibility that this attenuation is mediated by blunting the contraction evoked increases in sympathetic outflow was also tested. METHODS: Using alpha chloralose anaesthetised cats (n = 8), static contraction and stretch of the triceps surae muscle were performed before and after microinjecting (1 microliter) 250 ng of the substance P antagonist, D-Pro2-D-Phe7-D-Trp9-substance P, and the somatostatin antagonist, cyclo(7-amino-heptanoyl-phenylalanyl-D-tryptophyl-lysyl-threonyl-[ benzyl]). The muscle was contracted by electrically stimulating the peripheral end of the cut L7 ventral root. RESULTS: Before injecting the antagonists, static muscle contraction increased mean arterial blood pressure by 40(SEM 6) mm Hg, heart rate by 13(2) beats.min-1, and renal sympathetic nerve activity (RSNA) by 41(7)%. These changes were blunted by the antagonists since the increases in blood pressure, heart rate, and RSNA were reduced to 21(3) mm Hg, 8(1) beats.min-1, and 23(5)%, respectively. In contrast, antagonist administration did not affect the pressor [33(5) v 31(5) mm Hg], heart rate [9(2) v 10(2) beats.min-1], or RSNA [23(4)% v 25(5)%] responses to muscle stretch. Microinjection of 2% lignocaine into the dorsal horn virtually abolished the reflex changes elicited by muscle stretch. CONCLUSIONS: The release of substance P and somatostatin in the spinal cord plays a role in mediating the cardiovascular changes caused by static contraction, but the release of other neurotransmitters/neuromodulators is also involved. The attenuation produced by these antagonists is mediated, at least in part, by reducing sympathetic outflow.

Animals↗
PubMed1994

Central cholinergic modulation of the exercise pressor reflex in anesthetized cats.

Effects of central administration of a cholinesterase inhibitor, physostigmine, on cardiovascular responses to static contraction and passive stretch of the triceps surae were studied using anesthetized cats. Contraction increased mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) by 44 +/- 5 mmHg, 18 +/- 1 beats/min, and 86 +/- 6%, respectively. MAP, HR, and RSNA increased during stretch by 44 +/- 5 mmHg, 15 +/- 1 beats/min, and 61 +/- 4%, respectively. Administration of physostigmine (100 micrograms; 5 microliters) into the third ventricle decreased resting MAP by 22 +/- 3 mmHg and RSNA by 32 +/- 4%, with no effect on HR. Physostigmine attenuated the contraction-evoked responses as MAP, HR, and RSNA increased by 17 +/- 2 mmHg, 3 +/- 1 beats/min, and 31 +/- 6%, respectively. Also, physostigmine blunted MAP, HR, and RSNA responses to stretch (16 +/- 2 mmHg, 4 +/- 1 beats/min, and 9 +/- 6%, respectively). Posterior hypothalamic stimulation increased MAP by 39 +/- 3 mmHg, which was unaffected by physostigmine, despite a lower baseline. Cardiovascular and RSNA responses to contraction and stretch returned to control 90-120 min after physostigmine. Preadministration of the muscarinic antagonist, atropine sulfate (100 micrograms; 5 microliters), blocked the effects of physostigmine. Results suggest central cholinergic stimulation can inhibit the exercise pressor reflex in anesthetized cats.

Anesthesia↗