| Title: |
Nitric oxide-dependent vasodilatation and the regulation of arterial blood pressure. |
| Authors: |
Ferrari A. U.; Radaelli A.; Mori I.; Mircoli L.; Meregalli P.; Fedele L.; Mancia G.; PERLINI, STEFANO |
| Contributors: |
Ferrari, A. U.; Radaelli, A.; Mori, I.; Mircoli, L.; Perlini, Stefano; Meregalli, P.; Fedele, L.; Mancia, G. |
| Publisher Information: |
Lippincott, Williams & Wilkins:530 Walnut Street:Philadelphia, PA 19106:(800)638-3030, (301)223-2300, EMAIL: orders@lww.com, INTERNET: http://www.lww.com, Fax: (301)223-2320, (301)223-2320 |
| Publication Year: |
2001 |
| Collection: |
IRIS UNIPV (Università degli studi di Pavia) |
| Subject Terms: |
Animal Model; Aorta; Innervation; Blood Pressure; Drug Effect; Chronic Disease; Denervation; Ganglionic Blocker; Pharmacology; Hexamethonium; Nitric Oxide; Rat; Sympathectomy; Vasodilation; Vasodilator Agent; Omega-N-Methylarginine |
| Description: |
Conflicting evidence has been reported on the hypothesis that vascular nitric oxide (NO) release is modulated by autonomic influences. Another controversial question is whether an insufficient degree of NO-dependent vasodilation may play a contributory role in the genesis of arterial hypertension. To address these questions we evaluated NO-dependent vasodilation in conscious rats subjected to various experimental manipulations that interfere with autonomic function: chronic chemical sympathectomy (CCSx), acute ganglionic blockade (AGx) and chronic sinoaortic denervation (CSAD). Experiments were also carried out on 6- and 12-week-old spontaneously hypertensive rats (SHR) (i.e. during the pre-hypertensive and the early established hypertensive stage) and in age-matched Wistar-Kyoto (WKY) rats. Nitric oxide-dependent vasodilation was quantified from the extent of blood pressure (BP) elevation in response to acute inhibition of NO synthesis by L-nitromonomethyl-L-arginine (L-NMMA). Chronic chemical sympathectomy was produced by repeated 6-hydroxydopamine injections; AGx was induced by hexamethonium infusion; and CSAD was obtained by aortic nerve section and carotid sinus wall stripping. Nitric oxide synthesis inhibition by L-NMMA was followed by a marked BP elevation in all groups. Rats with CCSx, Agx or CSAD never showed reduced BP responses to L-NMMA compared to intact, control rats. Neither 6- nor 12-week-old SHR had attenuated pressor responses to L-NMMA compared to age-matched WKY rats. In conclusion, the data indicate that (i) in unanaesthetized quietly-behaving rats there is no significant modulation of NO release by autonomic influences and (ii) young SHR have unimpaired NO-dependent vasodilation so it is unlikely that a deficit of vascular NO release plays any etiologic role in the BP elevation of this experimental model. |
| Document Type: |
article in journal/newspaper |
| File Description: |
STAMPA |
| Language: |
English |
| Relation: |
info:eu-repo/semantics/altIdentifier/pmid/11811370; info:eu-repo/semantics/altIdentifier/wos/000173041600006; volume:38; issue:Suppl 2; firstpage:19; lastpage:22; numberofpages:4; journal:JOURNAL OF CARDIOVASCULAR PHARMACOLOGY; http://hdl.handle.net/11571/112208; http://www.ncbi.nlm.nih.gov/pubmed/11811370 |
| Availability: |
http://hdl.handle.net/11571/112208; http://www.ncbi.nlm.nih.gov/pubmed/11811370 |
| Accession Number: |
edsbas.20C2ED07 |
| Database: |
BASE |