Central cholinergic modulation of the exercise pressor reflex in anesthetized cats

Q: What is the clinical evidence from this study?

Intervention: Physostigmine vs. Baseline/control. Primary outcome: Cardiovascular responses (MAP, HR, RSNA) to static contraction and passive stretch.

Q: What does this research mean for the field?

Central cholinergic stimulation inhibits the exercise pressor reflex through muscarinic receptor activation in anesthetized cats. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

Ahmmed Ally; A. F. Meintjes; J. H. Mitchell; L. B. Wilson

doi:10.1152/ajpheart.1994.267.1.h109

July 1, 1994AJP Heart and Circulatory Physiology

Central cholinergic modulation of the exercise pressor reflex in anesthetized cats

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Key result

Central physostigmine reduces contraction-evoked MAP increases by ~61%, inhibiting the exercise pressor reflex.

Key Points

To determine whether central cholinergic activation via third-ventricle administration of physostigmine modulates cardiovascular and sympathetic responses evoked by static muscle contraction and passive stretch.
Monitored mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) during static contraction and passive stretch of the triceps surae in anesthetized cats.
Administered the cholinesterase inhibitor physostigmine (100 µg; 5 µL) into the third cerebral ventricle, both alone and following preadministration of the muscarinic antagonist atropine sulfate (100 µg; 5 µL).
Tested electrical stimulation of the posterior hypothalamus before and after physostigmine to assess central autonomic response specificity.
Physostigmine injection into the third ventricle reduced baseline resting MAP by 22 ± 3 mmHg and RSNA by 32 ± 4% without affecting baseline HR.
Physostigmine significantly attenuated contraction-evoked increases in MAP (17 ± 2 vs. 44 ± 5 mmHg), HR (3 ± 1 vs. 18 ± 1 beats/min), and RSNA (31 ± 6% vs. 86 ± 6%), with similar marked reductions observed during passive stretch.
Cardiovascular and RSNA responses recovered to baseline within 90–120 minutes, and muscarinic blockade with atropine sulfate completely prevented all inhibitory actions of physostigmine.

Structured PICO

P

Population

Anesthetized cats studied for cardiovascular responses to static contraction and passive stretch.

I

Intervention

Central administration of physostigmine (100 micrograms; 5 microliters) into the third ventricle

C

Comparator

Control responses (baseline and 90-120 min post-physostigmine) and preadministration of muscarinic antagonist atropine sulfate (100 micrograms; 5 microliters)

O

Outcome

Mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) responses to static contraction and passive stretch of the triceps suraesurrogate

Central cholinergic stimulation with physostigmine inhibits the exercise pressor reflex in anesthetized cats.

Implication

Hypothesis-generating for central cholinergic modulation of exercise pressor reflex; leaves open translation to human cardiovascular control.

Abstract

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.

Discussion

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Cite This Study

Ally et al. (1994) studied this question. Physostigmine vs. Baseline/control was evaluated on Cardiovascular responses (MAP, HR, RSNA) to static contraction and passive stretch. Central administration of physostigmine attenuated contraction-evoked increases in MAP (17 vs 44 mmHg), HR, and RSNA, suggesting central cholinergic stimulation inhibits the exercise pressor reflex.

synapsesocial.com/papers/6aa61bf7d3d41ccc68922bb6 https://doi.org/10.1152/ajpheart.1994.267.1.h109

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Central cholinergic modulation of the exercise pressor reflex in anesthetized cats

Key Points

Structured PICO

Implication

Abstract

Discussion

Cite This Study

Central cholinergic modulation of the exercise pressor reflex in anesthetized cats

Key Points

Structured PICO

Implication

Abstract

Discussion

Cite This Study

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