Medullary and supramedullary mechanisms regulating sympathetic vasomotor tone.
OBJECTIVE
Neurons in the rostral ventrolateral medulla (RVLM) that project directly to sympathetic preganglionic neurons in the spinal cord play a critical role in maintaining tonic activity in sympathetic vasomotor nerves. Intracellular recordings in vivo from putative RVLM presympathetic neurons have demonstrated that under resting conditions these neurons display an irregular tonic firing rate, and also receive both excitatory and inhibitory synaptic inputs. This paper will briefly review some recent findings on the role of glutamate, GABA and angiotensin II (Ang II) receptors in maintaining the tonic activity of RVLM presympathetic neurons.


RESULTS
Based on these findings, the following hypotheses will be discussed: (1) RVLM neurons receive tonic glutamatergic excitatory inputs, which originate from both medullary and supramedullary sources; (2) at least some neurons that project to and tonically inhibit RVLM presympathetic neurons are themselves tonically inhibited by GABAergic inputs originating from neurons in the caudalmost part of the ventrolateral medulla (caudal pressor area); (3) under normal conditions, Ang II receptors in the RVLM do not contribute significantly to the tonic activity of RVLM presympathetic neurons, but may do so in abnormal conditions such as heart failure or neurogenic hypertension; (4) RVLM presympathetic neurons maintain a significant level of tonic resting activity even when glutamate, GABA and Ang II receptors on the neurons are completely blocked. Under these conditions, the tonic activity is a consequence either of the intrinsic membrane properties of the neurons (autoactivity) or of synaptic inputs mediated by receptors other than glutamate, GABA or Ang II receptors.


CONCLUSIONS
The current evidence indicates that the resting activity of RVLM presympathetic neurons is determined by the balance of powerful tonic excitatory and inhibitory synaptic inputs. Ang II receptors also contribute to the raised resting activity of these neurons in some pathological conditions.
Dampney
R A L
RA
Department of Physiology and Institute for Biomedical Research, University of Sydney, New South Wales, Australia.
Horiuchi
J
J
Tagawa
T
T
Fontes
M A P
MA
Potts
P D
PD
Polson
J W
JW
D000804:Angiotensin II / Q000502:physiology*; D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D001794:Blood Pressure / Q000502:physiology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D007668:Kidney / Q000294:innervation / Q000502:physiology; D007736:Kynurenic Acid / Q000494:pharmacology; D008526:Medulla Oblongata / Q000502:physiology*; D009129:Muscle Tonus / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000502:physiology; D011311:Pressoreceptors / Q000502:physiology; D051381:Rats; D011945:Receptors, Angiotensin / Q000502:physiology*; D018079:Receptors, GABA / Q000187:drug effects / Q000502:physiology*; D017470:Receptors, Glutamate / Q000502:physiology*; D014666:Vasomotor System / Q000502:physiology*
D011945:Receptors, Angiotensin; D018079:Receptors, GABA; D017470:Receptors, Glutamate; D000804:Angiotensin II; D007736:Kynurenic Acid; D001640:Bicuculline