Rostral ventrolateral medulla : A source of sympathetic activation in rats subjected to long-term treatment with L-NAME.

@article{Bergamaschi1999RostralVM,
  title={Rostral ventrolateral medulla : A source of sympathetic activation in rats subjected to long-term treatment with L-NAME.},
  author={Cassia T Bergamaschi and Ruy R. Campos and Oswaldo Ubr{\'i}aco Lopes},
  journal={Hypertension},
  year={1999},
  volume={34 4 Pt 2},
  pages={
          744-7
        }
}
The major aim of the present study was to evaluate the role of the rostral ventrolateral medulla (RVLM) in the maintenance of hypertension in rats subjected to long-term treatment with N(G)-nitro-L-arginine methyl ester (L-NAME) (70 mg/kg orally for 1 week). We inhibited or stimulated RVLM neurons with the use of drugs such as glycine, L-glutamate, or kynurenic acid in urethane-anesthetized rats (1.2 to 1.4 g/kg IV). Bilateral microinjection of glycine (50 nmol, 100 nL) into the RVLM of… 
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Effects of angiotensin blockade in the rostral ventrolateral medulla on maintenance of hypertension induced by chronic l-NAME treatment
Cardiovascular responses to glutamate and angiotensin II in ventrolateral medulla of hypertension induced by chronic inhibition of nitric oxide.
TLDR
No may have an inhibitory influence on the actions of L-glutamate and angiotensin II in the RVLM of rats treated with an NO synthase inhibitor, NG-nitro-L-arginine methyl ester.
Selective Sensitization by Nitric Oxide of Sympathetic Baroreflex in Rostral Ventrolateral Medulla of Conscious Rabbits
TLDR
It is suggested that nNOS-derived NO facilitates sympathetic baroreflex transmission in the RVLM at least in part via a sGC-dependent, superoxide-independent mechanism.
Blockade of Rostral Ventrolateral Medulla (RVLM) Bombesin Receptor Type 1 Decreases Blood Pressure and Sympathetic Activity in Anesthetized Spontaneously Hypertensive Rats
TLDR
Results show that BBS can evoke sympathoexcitatory and pressor responses by activating RVLM BB1 receptors, which might be involved in the maintenance of high levels of arterial blood pressure in SHR.
Discharge of RVLM vasomotor neurons is not increased in anesthetized angiotensin II-salt hypertensive rats.
TLDR
It is concluded that heightened resting discharge of sympathoexcitatory RVLM neurons is not required for maintenance of neurogenic ANG II-salt hypertension.
Sympathetic activation in rats with L-NAME-induced hypertension.
TLDR
The present study shows that the vasoconstriction in response to L-NAME was mediated by the sympathetic drive, and the sympathetic tone plays an important role in the initiation and maintenance of hypertension.
Downregulation of Basal iNOS at the Rostral Ventrolateral Medulla Is Innate in SHR
TLDR
It is concluded that a predisposed reduction in molecular synthesis and functional expression of basal iNOS in the RVLM is associated with the sympathetic vasomotor overactivity during hypertension.
Neurochemistry within ventrolateral medulla and cardiovascular effects during static exercise following eNOS antagonism
Angiotensin in the nucleus tractus solitarii contributes to neurogenic hypertension caused by chronic nitric oxide synthase inhibition.
TLDR
The results suggest that increased sympathetic nerve activity plays a role in hypertension caused by chronic nitric oxide synthase inhibition and that activation of the renin-angiotensin system in the NTS is involved at least in part in this increased sympathetic nerves activity via AT(1) receptors.
The asymmetric dimethylarginine-mediated inhibition of nitric oxide in the rostral ventrolateral medulla contributes to regulation of blood pressure in hypertensive rats.
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References

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TLDR
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TLDR
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