Abstract
We evaluated the transmembrane signaling mechanism that may underlie the facilitatory action of somatostatin (SOM) on baroreceptor reflex (BRR), using adult, male, Sprague-Dawley rats anesthetized with pentobarbital sodium (40 mg/kg, i.p.). Intracerebroventricular (i.c.v.) application of SOM (2 nmol) promoted a significant elevation in BRR response, induced by phenylephrine (5 micrograms/kg, i.v.). This potentiatory action of the tetradecapeptide was significantly reversed after pretreating animals with bilateral microinjection of pertussis toxin (25 ng) or N-ethylmaleimide (2 nmol) into the nucleus tractus solitarius (NTS), the terminal site for baroreceptor afferents. These results suggest that a pertussis toxin-sensitive GTP-binding regulatory protein, possibly Gi, may be involved in the modulation of the BRR by SOM at the NTS.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Afferent Pathways / drug effects
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Afferent Pathways / physiology
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Animals
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Blood Pressure / drug effects*
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Cerebral Ventricles / drug effects
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Cerebral Ventricles / physiology*
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Ethylmaleimide / administration & dosage
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Ethylmaleimide / pharmacology*
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Heart Rate / drug effects*
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Injections, Intravenous
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Injections, Intraventricular
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Male
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Medulla Oblongata / drug effects
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Medulla Oblongata / physiology*
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Microinjections
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Pertussis Toxin*
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Phenylephrine / administration & dosage
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Phenylephrine / pharmacology
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Pressoreceptors / drug effects
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Pressoreceptors / physiology*
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Rats
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Rats, Inbred Strains
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Reflex / drug effects
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Somatostatin / administration & dosage
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Somatostatin / antagonists & inhibitors
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Somatostatin / pharmacology*
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Time Factors
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Virulence Factors, Bordetella / administration & dosage
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Virulence Factors, Bordetella / pharmacology*
Substances
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Virulence Factors, Bordetella
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Phenylephrine
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Somatostatin
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Pertussis Toxin
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Ethylmaleimide