Open AccessAlterations of NO synthase isoforms in brain and kidney of rats with genetic and salt hypertension
Author(s) -
Silvie Hojná,
Jaroslav Kuneš,
Josef Zicha
Publication year - 2010
Publication title -
physiological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.647
H-Index - 70
eISSN - 1802-9973
pISSN - 0862-8408
DOI - 10.33549/physiolres.932064
Subject(s) - endocrinology , diencephalon , medicine , enos , brainstem , blood pressure , nitric oxide synthase , kidney , forebrain , endothelial nos , renin–angiotensin system , nitric oxide , hypothalamus , central nervous system
Both brain and peripheral nitric oxide (NO) play a role in thecontrol of blood pressure and circulatory homeostasis. Central NOproduction seems to counteract angiotensin II-inducedenhancement of sympathetic tone. The aim of our study was toevaluate NO synthase (NOS) activity and protein expression of itsthree isoforms – neuronal (nNOS), endothelial NOS (eNOS) andinducible (iNOS) – in two brain regions involved in blood pressurecontrol (diencephalon and brainstem) as well as in the kidney ofyoung adult rats with either genetic (12-week-old SHR) or saltinduced hypertension (8-week-old Dahl rats). We have demonstrated reduced nNOS and iNOS expression in brainstem of both hypertensive models. In SHR this abnormality wasaccompanied by attenuated NOS activity and was corrected bychronic captopril treatment which prevented the development ofgenetic hypertension. In salt hypertensive Dahl rats nNOS andiNOS expression was also decreased in the diencephalon whereneural structures important for salt hypertension developmentare located. As far as peripheral NOS activity and expression isconcerned, renal eNOS expression was considerably reduced inboth genetic and salt-induced hypertension. In conclusions, wedisclosed similar changes of NO system in the brainstem (but notin the diencephalon) of rats with genetic and salt-inducedhypertension. Decreased nNOS expression was associated withincreased blood pressure due to enhanced sympathetic tone.