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Nitric oxide-dependent vasodilation and the regulation of arterial blood pressure

Title: Nitric oxide-dependent vasodilation and the regulation of arterial blood pressure
Authors: FERRARI, ALBERTO; MANCIA, GIUSEPPE; Radaelli, A; Mori, I; Mircoli, L; Perlini, S; Meregalli, P; Fedele, L
Contributors: Ferrari, A; Radaelli, A; Mori, I; Mircoli, L; Perlini, S; Meregalli, P; Fedele, L; Mancia, G
Publisher Information: LIPPINCOTT WILLIAMS & WILKINS; PHILADELPHIA
Publication Year: 2001
Collection: Università degli Studi di Milano-Bicocca: BOA (Bicocca Open Archive)
Subject Terms: nitric oxide; L-nitromonomethyl-L-arginine; sympathectomy; ganglionic blockade; spontaneously hypertensive rat
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
Language: English
Relation: info:eu-repo/semantics/altIdentifier/wos/WOS:000173041600006; volume:38; issue:Suppl. 2; firstpage:S19; lastpage:S22; journal:JOURNAL OF CARDIOVASCULAR PHARMACOLOGY; https://hdl.handle.net/10281/5032
Availability: https://hdl.handle.net/10281/5032
Accession Number: edsbas.EE19CF50
Database: BASE