Vascular reactivity to methoxamine in conscious sinoaortic denervated rats

Moysés, Margareth Ribeiro; Cabral, Antônio M.; Vasquez, Elisardo C.

doi:10.1016/s0031-6989(88)80127-9

Cited by 5 publications

(2 citation statements)

References 7 publications

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“…6,11,18,39). In addition, because adrenergic vascular pressor reactivity is not grossly altered by chronic baroreceptor denervation either by lesions of the NTS or by SAD (5,22,27), comparable evoked changes in systemic AP observed among groups in the present study likely reflect similar functional changes in sympathetic vasomotor tone.…”

Section: Discussionsupporting

confidence: 60%

“…In order for measurements of acute changes in AP to reflect changes in sympathetic vasomotor tone, vascular reactivity to the ␣-adrenergic receptor activation at the blood vessels must not be grossly affected by the experimental condition. Previous studies have demonstrated that rats with chronic SAD do not show altered adrenergic vascular reactivity, as suggested by comparable pressor responses to the ␣1-adrenergic agonists methoxamine or phenylephrine (5,22,27). Because blood volume is not altered by chronic SAD (29), the same doses calculated by weight could be used for intact and denervated rats.…”

Section: Animalsmentioning

confidence: 99%

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Brain stem control of arterial pressure in chronic arterial baroreceptor-denervated rats

Schreihofer¹,

Ito²,

Sved³

2005

American Journal of Physiology-Regulatory, Integrative and Comp

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Interruption of the baroreceptor reflex by transection of afferent nerves (sinoaortic denervation; SAD) or lesions of nucleus tractus solitarius (NTS) elevates sympathetic nerve activity (SNA) and arterial pressure (AP). However, within 1 wk, mean AP returns to normal despite the absence of baroreflexes. In this study, we examine central mechanisms that control AP in chronic baroreceptor-denervated rats. In urethane-anesthetized rats (1.5 g/kg i.v.) after autonomic ganglionic blockade (5 mg/kg i.v. chlorisondamine), alpha1-adrenergic-mediated pressor responses (1-100 microg/kg i.v. phenylephrine) were not altered by chronic lesions of NTS, indicating vascular reactivity to sympathetic stimulation is normal. Transection of the spinal cord at T1 profoundly decreased AP and was not further reduced by chlorisondamine in control or denervated rats. Inhibition of the rostral ventrolateral medulla (RVLM) by microinjections of muscimol (100 pmol/side) decreased AP to levels not further reduced by chlorisondamine in control rats, rats with SAD, and rats with NTS lesions. Blockade of GABA(A) receptors in the RVLM (50 pmol/side bicuculline) increased AP similarly in control rats and denervated rats. In agreement, inhibition of the caudal ventrolateral medulla (CVLM) by microinjections of muscimol or blockade of glutamatergic inputs (2.7 nmol/side kynurenate) produced comparable increases in AP in control and denervated rats. These data suggest the RVLM continues to drive the SNA that regulates AP in the chronic absence of baroreceptor inputs. In addition, despite the absence of a tonic excitatory input from NTS, in chronic baroreceptor-denervated rats glutamatergic inputs drive the CVLM to tonically inhibit the RVLM. Baroreceptor-independent regulation of the ventrolateral medulla may underlie central mechanisms contributing to the long-term control of AP.

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