Nitric oxide and salt resistance in Dahl rats: no role of inducible NO synthase
Jazyk angličtina Země Česko Médium print-electronic
Typ dokumentu časopisecké články
PubMed
36545880
PubMed Central
PMC10069813
DOI
10.33549/physiolres.935047
PII: 935047
Knihovny.cz E-zdroje
- MeSH
- chlorid sodný MeSH
- hypertenze * chemicky indukované MeSH
- krevní tlak fyziologie MeSH
- krysa rodu Rattus MeSH
- kuchyňská sůl * MeSH
- oxid dusnatý MeSH
- potkani inbrední Dahl MeSH
- potkani Wistar MeSH
- synthasa oxidu dusnatého, typ II MeSH
- synthasa oxidu dusnatého MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- chlorid sodný MeSH
- kuchyňská sůl * MeSH
- oxid dusnatý MeSH
- pimagedine MeSH Prohlížeč
- synthasa oxidu dusnatého, typ II MeSH
- synthasa oxidu dusnatého MeSH
Inducible NO synthase (NOS II) was proposed to play an important role in salt resistance of Dahl salt-resistant (SR/Jr) rats. Its chronic inhibition by specific inhibitors was accompanied by blood pressure (BP) elevation in animals subjected to high salt intake. The aim of our study was to evaluate 1) whether such inhibitors affect BP and/or its particular components (sympathetic tone and NO-dependent vasodilation) only under the conditions of high salt intake, and 2) whether similar BP effects are elicited after systemic or intracerebroventricular (icv) application of these inhibitors. Wistar rats fed Altromin diet (0.45 % NaCl) and SR/Jr rats fed either a low-salt (LS, 0.3 % NaCl) or a high-salt (HS, 4 % NaCl) diet were studied. Aminoguanidine (AMG) and 2-amino-5,6-dihydro-6-methyl-4H-1,3-thiazine (AMT) were used as NOS II inhibitors. BP and its responses to acute blockade of renin-angiotensin system (captopril), sympathetic nervous system (pentolinium) and NO synthase (L-NAME) were measured in conscious cannulated rats. There were no significant changes of BP or its components in either Wistar rats or SR/Jr rats subjected to chronic inhibition of NOS II by peroral aminoguanidine administration (50 mg/kg/day for 4 weeks). This was true for SR/Jr rats fed either LS or HS diets. Furthermore, we have studied BP effects of chronic icv administration of both NOS II inhibitors in SR/Jr rats fed HS diet, but we failed to find any BP changes elicited by such treatment. In conclusion, inducible NO synthase does not participate in the resistance of SR/Jr rats to hypertensive effects of excess salt intake.
Zobrazit více v PubMed
Chen PY, Sanders PW. Role of nitric oxide synthesis in salt-sensitive hypertension in Dahl/Rapp rats. Hypertension. 1993;22:812–818. doi: 10.1161/01.HYP.22.6.812. PubMed DOI
Zicha J, Dobešová Z, Kuneš J. Relative deficiency of nitric oxide-dependent vasodilation in salt-hypertensive Dahl rats: the possible role of superoxide anions. J Hypertens. 2001;19:247–254. doi: 10.1097/00004872-200102000-00011. PubMed DOI
Deng AY, Rapp JP. Locus for the inducible, but not a constitutive, nitric oxide synthase cosegregates with blood pressure in the Dahl salt-sensitive rat. J Clin Invest. 1995;95:2170–2177. doi: 10.1172/JCI117906. PubMed DOI PMC
Dukhanina OI, Dene H, Deng AY, Choi CR, Hoebee B, Rapp JP. Linkage map and congenic strains to localize blood pressure QTL on rat chromosome 10. Mamm Genome. 1997;8:229–235. doi: 10.1007/s003359900399. PubMed DOI
Hojná S, Kadlecová M, Zicha J, Kuneš J. Polymorphism in Nos2 gene is absent in Prague colony of Dahl/Rapp salt-sensitive and salt-resistant rats. Physiol Res. 2005;54:201–206. doi: 10.33549/physiolres.930000.54.201. PubMed DOI
Rudd MA, Trolliet M, Hope S, Scribner AW, Daumerie G, Toolan G, Cloutier T, Loscalzo J. Salt-induced hypertension in Dahl salt-resistant and salt-sensitive rats with NOS II inhibition. Am J Physiol. 1999;277:H732–H739. doi: 10.1152/ajpheart.1999.277.2.H732. PubMed DOI
Tan DY, Meng S, Cason GW, Manning RD. Mechanisms of salt-sensitive hypertension: role of inducible nitricoxide synthase. Am J Physiol. 2000;279:R2297–R2303. doi: 10.1152/ajpregu.2000.279.6.R2297. PubMed DOI
Řezáčová L, Hojná S, Kopkan L, Rauchová H, Kadlecová M, Zicha J, Vaněčková I. Role of angiotensin II in chronic blood pressure control of heterozygous Ren-2 transgenic rats: Peripheral vasoconstriction versus central sympathoexcitation. Biomed Pharmacother. 2019;116:108996. doi: 10.1016/j.biopha.2019.108996. PubMed DOI
Paxinos G, Watson C. The Rat Brain in Stereotaxic Coordinates. Elsevier Academic Press; Burlington, MA: 2005.
Minami N, Imai Y, Hashimoto J, Abe K. Contribution of vascular nitric oxide to basal blood pressure in conscious spontaneously hypertensive rats and normotensive Wistar Kyoto rats. Clin Sci (Lond) 1995;89:177–182. doi: 10.1042/cs0890177. PubMed DOI
Dobešová Z, Kuneš J, Zicha J. The altered balance between sympathetic nervous system and nitric oxide in salt hypertensive Dahl rats: ontogenetic and F2 hybrid studies. J Hypertens. 2002;20:945–955. doi: 10.1097/00004872-200205000-00030. PubMed DOI
Mark AL. Sympathetic neural contribution to salt-induced hypertension in Dahl rats. Hypertension. 1991;17(Suppl I):I86–I90. doi: 10.1161/01.HYP.17.1_Suppl.I86. PubMed DOI
Sander M, Hansen J, Victor RG. The sympathetic nervous system is involved in the maintenance but not initiation of the hypertension induced by Nω-nitro-L-arginine methyl ester. Hypertension. 1997;30:64–70. doi: 10.1161/01.HYP.30.1.64. PubMed DOI
Pecháňová O, Dobešová Z, Čejka J, Kuneš J, Zicha J. Vasoactive systems in L-NAME hypertension: the role of inducible nitric oxide synthase. J Hypertens. 2004;22:167–173. doi: 10.1097/00004872-200401000-00026. PubMed DOI