Hemodynamic effects of L-glutamate in NTS of conscious rats: a possible role of vascular nitrosyl factors
- PMID: 9575908
- DOI: 10.1152/ajpheart.1998.274.4.H1066
Hemodynamic effects of L-glutamate in NTS of conscious rats: a possible role of vascular nitrosyl factors
Abstract
This study examined peripheral mechanisms responsible for changes in mean arterial blood pressure, heart rate, and renal, mesenteric, and hindquarter vascular resistances produced by microinjections of L-glutamate (L-Glu) into the nucleus tractus solitarii (NTS) of conscious rats. Microinjection of L-Glu produced an initial pressor response, bradycardia, and vasoconstriction in each vascular bed. Subsequent hindquarter vasodilation was observed. After prazosin was administered, L-Glu produced initial hypotension that was probably due to reduced cardiac output. This hypotension was followed by hindquarter vasodilation. Inhibition of nitric oxide synthesis did not affect the initial hypotension or bradycardia in rats treated with prazosin, but the first microinjection of L-Glu after administration of prazosin and NG-nitro-L-arginine methyl ester (L-NAME) produced significantly greater hindquarter vasodilation than after administration of prazosin alone. Second and third microinjections of L-Glu produced significantly smaller hindquarter vasodilation. We conclude that 1) hemodynamic effects produced by microinjection of L-Glu into the NTS of conscious rats involves activation of the sympathetic nervous system and 2) release of preformed nitrosyl factors may mediate vasodilation in the hindquarter vascular bed.
Similar articles
-
Use-dependent loss of active sympathetic neurogenic vasodilation after nitric oxide synthase inhibition in conscious rats. Evidence for the presence of preformed stores of nitric oxide-containing factors.Hypertension. 1996 Sep;28(3):347-53. doi: 10.1161/01.hyp.28.3.347. Hypertension. 1996. PMID: 8794815
-
Nitrosyl factors mediate active neurogenic hindquarter vasodilation in the conscious rat.Hypertension. 1994 Jun;23(6 Pt 2):962-6. doi: 10.1161/01.hyp.23.6.962. Hypertension. 1994. PMID: 8206636
-
Central nitric oxide modulates hindquarter vasodilation elicited by AMPA receptor stimulation in the NTS of conscious rats.Am J Physiol Regul Integr Comp Physiol. 2006 May;290(5):R1330-6. doi: 10.1152/ajpregu.00150.2005. Epub 2005 Dec 29. Am J Physiol Regul Integr Comp Physiol. 2006. PMID: 16384860
-
Stimulation of lumbar sympathetic nerves may produce hindlimb vasodilation via the release of pre-formed stores of nitrosyl factors.Neuroscience. 1996 Jun;72(4):881-7. doi: 10.1016/0306-4522(96)00090-5. Neuroscience. 1996. PMID: 8735216
-
Beta-adrenoceptor dysfunction after inhibition of NO synthesis.Hypertension. 2000 Sep;36(3):376-82. doi: 10.1161/01.hyp.36.3.376. Hypertension. 2000. PMID: 10988268
Cited by
-
Central blockade of nitric oxide synthesis reduces moxonidine-induced hypotension.Br J Pharmacol. 2004 Jun;142(4):765-71. doi: 10.1038/sj.bjp.0705853. Epub 2004 Jun 1. Br J Pharmacol. 2004. PMID: 15172964 Free PMC article.
-
NADPH diaphorase detects S-nitrosylated proteins in aldehyde-treated biological tissues.Sci Rep. 2020 Dec 3;10(1):21088. doi: 10.1038/s41598-020-78107-6. Sci Rep. 2020. PMID: 33273578 Free PMC article.
-
L-NAME-resistant bradykinin-induced relaxation in porcine coronary arteries is NO-dependent: effect of ACE inhibition.Br J Pharmacol. 2000 Sep;131(2):195-202. doi: 10.1038/sj.bjp.0703555. Br J Pharmacol. 2000. PMID: 10991911 Free PMC article.
-
Rostral ventrolateral medulla: an integrative site for muscle vasodilation during defense-alerting reactions.Cell Mol Neurobiol. 2003 Oct;23(4-5):579-95. doi: 10.1023/a:1025076130854. Cell Mol Neurobiol. 2003. PMID: 14514017 Free PMC article. Review.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources