Abstract
In pentobarbital-anesthetized rats, pretreatment with yohimbine (10 μg), which was microinjected into the bilateral nucleus reticularis gigantocellularis (NRGC), significantly antagonized the reduction in arterial pressure, and the force and rate of heart contraction normally promoted by systemic administration of guanabenz (10 μg/kg, i.v.). At the same time, the vasodepressive as well as negative inotropic and chronotropic effects of direct application of guanabenz (500 ng) into the NRGC were attenuated by bilateral cervical vagotomy or atropine sulfate (1 mg/kg, i.v.). We conclude that guanabenz may promote antihypertension by activating the α2-adrenoceptors in the NRGC, which in turn elicits cardiovascular suppression by at least facilitating the vagal outflows to the heart.
| Original language | English |
|---|---|
| Pages (from-to) | 45-50 |
| Number of pages | 6 |
| Journal | Neuroscience Letters |
| Volume | 63 |
| Issue number | 1 |
| DOIs | |
| State | Published - 02 01 1986 |
| Externally published | Yes |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- bradycardia
- guanabenz
- heart contractility reduction
- nucleus reticularis gigantocellularis
- rat
- vagal mechanism hypotension
- α-adrenoceptor
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