Skeletal muscle vasodilation during electrical stimulation of the preoptic recess

Kenneth G Proctor, S. L. Bealer

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Abstract

Transverse (3rd-order) arterioles (diam 12 ± 2 μm, n = 6) in rat spinotrapezius muscle were observed with video microscopy during electrical stimulation of preoptic recess in periventricular region of hypothalamus (AV3V region) to test whether active skeletal muscle vasodilation was mediated by a β-adrenergic mechanism. Bipolar wire electrodes were implanted in AV3V 3-7 days before an experiment. Continuous superfusion of propranolol (10-5 M) caused steady-state reduction (3 ± 1 μm) in arteriolar diameter and reduced steady-state vasodilation (26 ± 2 vs. 11 ± 2 μm) caused by a continuous superfusion of isoproterenol (10-6 M). Six arterioles were observed with and without propranolol during four frequencies of AV3V stimulation (8-15 V, 0.2-0.5 ms pulse duration; 10, 15, 20, and 25 Hz; 1 min stimulus duration). Stimulation caused frequency-related reductions in arterial blood pressure (10-20 mmHg), which were sustained and not altered by propranolol. Transient peak diameters were observed after 30 ± 7 s; the time was not related to stimulus frequency or affected by propranolol. Peak diameters averaged 14-17 μm during vehicle and 11-12 μm during propranolol (maximum diam 32 ± 3). Peak vasodilations were significant but identical with vehicle or propranolol (avg 3 ± 1 μm) and not related to stimulus frequency. Diameters stabilized at steady-state values above base line only during 15 and 20 Hz with vehicle and only during 20 Hz with propranolol. We conclude that AV3V stimulation causes transient vasodilation in spinotrapezius muscle that is probably not mediated by β-adrenergic receptors. If these responses can be generalized to other skeletal muscles, it is unlikely that skeletal muscle vasodilation accounts for the sustained decrease in arterial pressure accompanying AV3V stimulation.

Original languageEnglish
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume250
Issue number2
StatePublished - Jan 1 1986
Externally publishedYes

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Vasodilation
Propranolol
Electric Stimulation
Skeletal Muscle
Arterioles
Arterial Pressure
Video Microscopy
Muscles
Implanted Electrodes
Isoproterenol
Adrenergic Agents
Adrenergic Receptors
Hypothalamus

ASJC Scopus subject areas

  • Physiology

Cite this

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title = "Skeletal muscle vasodilation during electrical stimulation of the preoptic recess",
abstract = "Transverse (3rd-order) arterioles (diam 12 ± 2 μm, n = 6) in rat spinotrapezius muscle were observed with video microscopy during electrical stimulation of preoptic recess in periventricular region of hypothalamus (AV3V region) to test whether active skeletal muscle vasodilation was mediated by a β-adrenergic mechanism. Bipolar wire electrodes were implanted in AV3V 3-7 days before an experiment. Continuous superfusion of propranolol (10-5 M) caused steady-state reduction (3 ± 1 μm) in arteriolar diameter and reduced steady-state vasodilation (26 ± 2 vs. 11 ± 2 μm) caused by a continuous superfusion of isoproterenol (10-6 M). Six arterioles were observed with and without propranolol during four frequencies of AV3V stimulation (8-15 V, 0.2-0.5 ms pulse duration; 10, 15, 20, and 25 Hz; 1 min stimulus duration). Stimulation caused frequency-related reductions in arterial blood pressure (10-20 mmHg), which were sustained and not altered by propranolol. Transient peak diameters were observed after 30 ± 7 s; the time was not related to stimulus frequency or affected by propranolol. Peak diameters averaged 14-17 μm during vehicle and 11-12 μm during propranolol (maximum diam 32 ± 3). Peak vasodilations were significant but identical with vehicle or propranolol (avg 3 ± 1 μm) and not related to stimulus frequency. Diameters stabilized at steady-state values above base line only during 15 and 20 Hz with vehicle and only during 20 Hz with propranolol. We conclude that AV3V stimulation causes transient vasodilation in spinotrapezius muscle that is probably not mediated by β-adrenergic receptors. If these responses can be generalized to other skeletal muscles, it is unlikely that skeletal muscle vasodilation accounts for the sustained decrease in arterial pressure accompanying AV3V stimulation.",
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N2 - Transverse (3rd-order) arterioles (diam 12 ± 2 μm, n = 6) in rat spinotrapezius muscle were observed with video microscopy during electrical stimulation of preoptic recess in periventricular region of hypothalamus (AV3V region) to test whether active skeletal muscle vasodilation was mediated by a β-adrenergic mechanism. Bipolar wire electrodes were implanted in AV3V 3-7 days before an experiment. Continuous superfusion of propranolol (10-5 M) caused steady-state reduction (3 ± 1 μm) in arteriolar diameter and reduced steady-state vasodilation (26 ± 2 vs. 11 ± 2 μm) caused by a continuous superfusion of isoproterenol (10-6 M). Six arterioles were observed with and without propranolol during four frequencies of AV3V stimulation (8-15 V, 0.2-0.5 ms pulse duration; 10, 15, 20, and 25 Hz; 1 min stimulus duration). Stimulation caused frequency-related reductions in arterial blood pressure (10-20 mmHg), which were sustained and not altered by propranolol. Transient peak diameters were observed after 30 ± 7 s; the time was not related to stimulus frequency or affected by propranolol. Peak diameters averaged 14-17 μm during vehicle and 11-12 μm during propranolol (maximum diam 32 ± 3). Peak vasodilations were significant but identical with vehicle or propranolol (avg 3 ± 1 μm) and not related to stimulus frequency. Diameters stabilized at steady-state values above base line only during 15 and 20 Hz with vehicle and only during 20 Hz with propranolol. We conclude that AV3V stimulation causes transient vasodilation in spinotrapezius muscle that is probably not mediated by β-adrenergic receptors. If these responses can be generalized to other skeletal muscles, it is unlikely that skeletal muscle vasodilation accounts for the sustained decrease in arterial pressure accompanying AV3V stimulation.

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