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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
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↗
PubMed1994

Reflex stimulation of cardiac sympathetic nerve activity during static muscle contraction in cats.

Reflex response of cardiac sympathetic nerve activity (CSNA) during static contraction of the triceps surae muscle was studied using anesthetized cats. A 1-min contraction was evoked by stimulating the peripheral ends of the cut L7 and S1 ventral roots. CSNA increased 48 +/- 13% immediately after the onset of contraction, which was abolished by cutting the L4-S1 dorsal roots. This rapid increase in CSNA preceded rises in heart rate (13 +/- 1 beats/min) and arterial blood pressure (33 +/- 6 mmHg). When tension development was altered by changing the frequency of ventral root stimulation or the initial muscle length, the CSNA increase depended on the tension developed. Passive stretch of the muscle, which primarily activates mechanoreceptors, increased CSNA by 41 +/- 22%. When the contraction was sustained for 5 min, CSNA remained elevated throughout the contraction despite a fall in tension, suggesting that the later increase in CSNA is caused by factors other than a mechanical event of contraction (e.g., metabolic products). Thus it is suggested that cardiac sympathetic outflow is stimulated due to a reflex arising from the contracting muscle. The increase in CSNA at the initiation of contraction is likely to be caused by a reflex from muscle mechanoreceptors, which is followed by a subsequent increase due to a reflex from muscle metaboreceptors.

Animals↗
PubMed1994

Cardiovascular and renal nerve responses to static muscle contraction of decerebrate rabbits.

The purpose of this study was to determine whether the biphasic arterial blood pressure responses elicited by static muscle contraction of decerebrate rabbits are mediated, at least in part, by an initial decrease and a subsequent increase in sympathetic outflow. Renal sympathetic nerve activity (RSNA) was used as an index of sympathetic outflow. Static contraction of the triceps surae muscle (n = 14) initially decreased mean arterial blood pressure (MAP) -20 +/- 3 mmHg and heart rate (HR) -15 +/- 5 beats/min (nadir values). After this initial decrease, MAP increased 12 +/- 2 mmHg (peak increase) above baseline and there was a tendency for HR to be elevated (6 +/- 3 beats/min). The changes in RSNA during muscle contraction (n = 6) mirrored the nadir and peak responses of MAP (-50 +/- 9 and 32 +/- 11%). Muscle stretch (n = 11) also evoked similar nadir and peak responses of MAP (-20 +/- 5 and 9 +/- 1 mmHg), HR (-17 +/- 7 and 3 +/- 3 beats/min), and RSNA (-43 +/- 9 and 46 +/- 15%). These data suggest that the initial depressor and subsequent pressor responses elicited by skeletal muscle contraction and stretch are mediated, at least in part, by biphasic changes in sympathetic outflow.

Animals↗
PubMed1994

Effects of clonidine on the reflex cardiovascular responses and release of substance P during muscle contraction.

The effects of microdialyzing clonidine into the L-7 dorsal horn on the cardiovascular responses, renal sympathetic nerve activity (RSNA), and release of substance P (SP) evoked by static contraction of the triceps surae muscle were studied using anesthetized cats. A microdialysis probe was inserted into the spinal cord ipsilateral to the muscle being contracted or stretched. Contraction, evoked by stimulation of the distal ends of the cut L-7 and S-1 ventral roots for 1 minute, increased mean arterial pressure (MAP), heart rate (HR), and RSNA by 48 +/- 6 mm Hg, 18 +/- 2 beats per minute, and 66 +/- 5%, respectively. Passive stretch of the same muscle for 1 minute also increased MAP, HR, and RSNA by 51 +/- 6 mm Hg, 17 +/- 2 beats per minute, and 50 +/- 3%, respectively. Microdialysis of clonidine (380 mumol/L) blunted the contraction-evoked responses: MAP, HR, and RSNA increased by 19 +/- 4 mm Hg, 7 +/- 1 beats per minute, and 24 +/- 5%, respectively. The increases elicited by passive stretch were also attenuated (MAP, 22 +/- 4 mm Hg; HR, 6 +/- 1 beats per minute; and RSNA, 15 +/- 4%). This attenuation by clonidine was dose dependent (3.8 mumol/L, 38 mumol/L, 380 mumol/L, and 3.8 mmol/L). Preadministration of the alpha 2-adrenergic antagonist yohimbine (3 mmol/L) blocked the effect of clonidine (380 mumol/L) on the cardiovascular and RSNA responses to muscle contraction. Clonidine (380 mumol/L) did not alter the release of SP in the dorsal horn during contraction (before clonidine, 0.380 +/- 0.018 fmol/100 microL; after clonidine, 0.356 +/- 0.012 fmol/100 microL).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1993

Substance P release in the spinal cord during the exercise pressor reflex in anaesthetized cats.

1. The purpose of this study was to determine if static skeletal muscle contraction causes the release of substance P(SP) in the L7-dorsal horn region of the spinal cord. A laminectomy was performed to expose the spinal cord of alpha-chloralose anaesthetized cats. The L6 spinal root was cut. A microdialysis probe was inserted into the L7 dorsal horn region ipsilateral to the contracting triceps surae muscle. The probe was perfused with a buffer solution at 3 microliters/min. Substance P-like immunoreactivity (SP-LI) was measured, from the microdialysis samples, by radioimmunoassay. 2. A 5-9 min contraction of the triceps surae muscle was evoked by alternate electrical stimulation of the peripheral ends of the cut L7 and S1 ventral roots. Basal SP-LI release was 0.20 +/- 0.03 fmol/100 microliters and was increased to 0.54 +/- 0.05 fmol/100 microliters (mean +/- S.D.) by static muscle contraction. This increase was greatly attenuated after cutting the L7 and S1 dorsal roots (0.23 +/- 0.03 to 0.39 +/- 0.08 fmol/100 microliters) or completely abolished by muscle paralysis (0.27 +/- 0.03 to 0.31 +/- 0.01 fmol/100 microliters). Muscle contraction also increased mean arterial blood pressure (MAP) 29 +/- 20 mmHg and heart rate (HR) 11 +/- 5 beats/min (mean +/- S.D.). These cardiovascular changes to muscle contraction were abolished by sectioning the dorsal roots or when the ventral roots were electrically stimulated after the cats were paralysed. 3. These results demonstrate that static contraction of skeletal muscle increases the release of SP-LI in the dorsal horn of the spinal cord. Furthermore, these data support the hypothesis that SP plays a role in mediating the cardiovascular responses evoked during static exercise.

Animals↗
PubMed1993

Effects of graded muscle contractions on spinal cord substance P release, arterial blood pressure, and heart rate.

The release of substance P (SP)-like immunoreactivity (SP-LI) in the dorsal horn of the spinal cord and the cardiovascular changes to both high-tension (HT) and low-tension (LT) contractions were determined using alpha-chloralose-anesthetized cats. Over a 10-minute period, seven contractions (HT or LT) were induced. Each contraction was 20 seconds in duration and was followed by an 80-second quiescent period. The tension-time index (TTI) for the HT contractions was 2751 +/- 348 kg.s (mean +/- SD), which was greater than the TTI of 813 +/- 167 kg.s for the LT contractions. The HT contractions caused a greater release of SP-LI than the LT contractions: SP-LI increased from 0.18 +/- 0.02 to 0.32 +/- 0.03 fmol/100 microL and from 0.18 +/- 0.02 to 0.25 +/- 0.04 fmol/100 microL for the two types of contractions, respectively. Concomitant with this greater SP-LI release, HT contractions caused larger increases in mean arterial pressure (34 +/- 16 versus 11 +/- 4 mm Hg) and heart rate (18 +/- 7 versus 8 +/- 4 beats per minute) than did the LT contractions. These changes in SP-LI, mean arterial pressure, and heart rate were virtually abolished when the contractions were repeated after sectioning the L-5-S-2 dorsal and ventral roots or when the electrical stimulation of the ventral roots was repeated after muscle paralysis with gallamine triethiodide. These results demonstrate that contraction-evoked SP-LI release in the dorsal horn is related to the developed tension. Furthermore, these data provide additional support for the hypothesis that the release of SP from the central terminations of muscle afferents plays a role in mediating the cardiovascular responses to static contraction of skeletal muscle.

Animals↗
PubMed1992

Neurally mediated renal vasoconstriction during isometric muscle contraction in cats.

The aim of this study was to determine if the reflex increase in renal sympathetic nerve activity (RSNA) during static (isometric) muscle contraction evokes renal vasoconstriction and decreases renal blood flow. RSNA, renal blood flow velocity, and arterial pressure were measured simultaneously during isometric contraction of the hindlimb triceps surae muscle in eight chloralose-anesthetized cats. A 1-min contraction was evoked by stimulating the peripheral ends of the cut L7 and S1 ventral roots. RSNA and mean arterial pressure (MAP) increased 41 +/- 14% (SE) and 50 +/- 10 mmHg during static contraction, whereas mean renal blood flow velocity (MRBV) decreased 14 +/- 5%. Calculated renal vascular resistance increased 73 +/- 20% during the contraction. The increase in RSNA preceded the decrease in MRBV by 20 s. Passive mechanical stretch of the muscle increased RSNA 21 +/- 12% but did not alter MRBV. Renal denervation abolished the decrease in MRBV during isometric contraction but only attenuated the rise in MAP. Cutting the L4-S1 dorsal roots or muscle paralysis abolished the MRBV and MAP responses. Thus reflex stimulation of RSNA from the contracting muscle can induce renal vasoconstriction and decrease renal blood flow.

Animals↗
PubMed1992

Effect of spinal microinjections of an antagonist to substance P or somatostatin on the exercise pressor reflex.

The purpose of this study was to determine the heart rate and arterial blood pressure changes to isometric skeletal muscle contraction and muscle stretch before and after microinjecting an antagonist to substance P (SP) or somatostatin (SOM) into the L-7 dorsal horn region of the spinal cord of anesthetized cats. Anesthesia was induced by administering an anesthetic gas mixture and was subsequently maintained with alpha-chloralose. Triceps surae contraction was induced by electrically stimulating the L-7 ventral root. Three muscle manipulations (all 1 minute in duration) were performed: 1) continuous tetanic contraction, 2) intermittent tetanic contractions (1 second of contraction, 1 second of relaxation), and 3) passive muscle stretch. Saline microinjections had no effect on the cardiovascular responses to these muscle manipulations. However, both peptide antagonists blunted the pressor response to a continuous tetanic contraction as mean arterial pressure increased 47 +/- 4 and 44 +/- 4 mm Hg before and 28 +/- 3 and 28 +/- 4 mm Hg after microinjecting the SP or SOM antagonist, respectively. In contrast, neither antagonist influenced the increase in mean arterial pressure produced by passive stretch; values were 43 +/- 6 versus 41 +/- 6 mm Hg (SP antagonist) and 39 +/- 7 versus 42 +/- 7 mm Hg (SOM antagonist) before and after injections, respectively. Microinjecting the SOM antagonist attenuated the pressor response to intermittent tetanic contractions (44 +/- 4 mm Hg before SOM antagonist versus 26 +/- 4 mm Hg after SOM antagonist), whereas the SP antagonist had no effect (35 +/- 3 mm Hg before SP antagonist versus 32 +/- 4 mm Hg after SP antagonist).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Multiplicity of the afferent pathways mediating the exercise pressor reflex.

The cardiovascular responses to isometric contraction of the triceps surae muscle of one leg were determined before and after transecting the ipsilateral L7 or L6 and S1 spinal roots. Sectioning only the L7 spinal root slightly attenuated the pressor, but not the heart rate response induced by skeletal muscle contraction, while cutting the L6 and S1 spinal roots (L7 intact) had no effect on the cardiovascular changes. This indicates that there is multiplicity in neural afferent pathways that mediate the exercise pressor reflex.

Animals↗
PubMed1991

The effect of static exercise on renal sympathetic nerve activity in conscious cats.

1. Renal sympathetic nerve activity (RNA), heart rate (HR), arterial blood pressure (AP), and force development were measured simultaneously during voluntary static (isometric) exercise performed by conscious cats. The cats were operantly trained to press a bar with one forelimb. When the force applied to the bar exceeded a predetermined value (threshold), a sound was emitted by a buzzer for audio-feedback. If the cat continued to produce the appropriate force for a period of 26-55 s, food was given as a reward. 2. A total of eighty-nine exercise trials were performed by seven cats. The peak force applied to the bar was 468 +/- 28 g (mean +/- S.E.M.). RNA, HR, and AP increased significantly from the control value during static exercise by 102 +/- 14%, 23 +/- 2 beats/min, and 11 +/- 1 mmHg, respectively. 3. The increase in RNA had both an initial and a late component. The initial component occurred at or immediately before the onset of force development and lasted for 10 s, while the late component gradually increased 14 s after the onset of static exercise and was sustained until the exercise was terminated. 4. HR also increased at the beginning of static exercise with a similar time course as RNA. Then, HR returned to the control value and remained at that level during the remainder of exercise. The increase in AP was delayed by 10 s from the initial increase in RNA and then continued to rise throughout the period of exercise. 5. The sound of the buzzer was emitted during rest to determine any influence of anticipation or conditioning on the response. RNA and AP increased slightly, but HR did not change. The increases in RNA and AP were much smaller than the increases obtained during static exercise. Thus, the increases in RNA, HR and AP during static exercise appeared to be associated with the exercise itself and not due to anticipation and/or conditioning. 6. When AP was elevated by a bolus injection of noradrenaline, RNA during rest was almost abolished and the increase of RNA during static exercise was markedly inhibited. Thus the arterial baroreflex significantly influences RNA both during rest and during static exercise. 7. This study suggests that the initial increases in RNA and HR at the beginning of static exercise in conscious cats are caused by descending input from higher brain centres and not by afferent feedback signals from muscle receptors or by arterial baroreceptors.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Static muscle contraction reflexly increases adrenal sympathetic nerve activity in rats.

Little is known about the mechanisms responsible for activation of sympathoadrenal function during exercise. We hypothesized that sympathoadrenal discharge is activated at the onset of exercise by a reflex arising in the contracting muscle. Adrenal sympathetic nerve activity (SNA) was recorded during 1 min stimulation of the tibial nerve at two times motor threshold, before and during neuromuscular blockade, in 12 alpha-chloralose-anesthetized rats. Static muscle contractions, induced by stimulation before neuromuscular blockade, were repeated during ganglionic blockade (n = 6) to specifically test reflex activation of preganglionic activity to the adrenal gland. During static contraction, adrenal SNA rapidly increased (P less than 0.05) to a maximum of 89 +/- 12% above basal and then declined, reaching basal levels after 30 s of muscle contraction. Tibial nerve stimulation during neuromuscular blockade had no effect on adrenal SNA. In most rats, adrenal SNA decreased with ganglionic blockade, indicating postganglionic as well as preganglionic innervation of the adrenal gland. During ganglionic blockade, static muscle contractions elicited a 140 +/- 21% increase in adrenal preganglionic SNA. In conclusion, static muscle contraction reflexly increases SNA to the adrenal gland, providing a mechanism for sympathoadrenal activation at the onset of exercise.

Adrenal Glands↗