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Central nNOS neuron functions to compensate salt‐sensitive hypertension in Dahl rats.
Author(s) -
Nishida Yasuhiro,
Tandai-Hiruma Megumi,
Kemuriyama Takehito,
Maruyama Satoshi,
Ohta Hiroyuki,
Tashiro Akimasa,
Takashi Iwakawa,
Tamura Risa,
Hagisawa Kohsuke
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.872.25
Subject(s) - blood pressure , medicine , endocrinology , neuron , chemistry , salt (chemistry) , psychiatry
Salt‐sensitive hypertension produces central nNOS neurons enhanced markedly in the number of neurons and enzymatic activity. Which of salt‐load, high blood pressure or rat line causes enchancement has not been clarified. To determine the cause of the enhancement, high blood pressure was suppressed by nifedipie in Dahl salt‐sensitive (DSS) hypertensive rats fed 8% salt food, resulting in no enhacement was found in central nNOS neurons. The result indicates that high blood pressure per se may induce central nNOS enhancement. Central nNOS neurons are known to suppress blood pressure‐controlling sympathetic activity in acute phase. Then next, to determine if its sympathoinhibitory effect works in long‐term, a selective inhibitor, S‐methiy‐L‐thiocitrulline (SMTC), was intracerebroventricularly (icv) infused for 2 weeks, and arterial pressure was measured by a radiotelemetry method in DSS hypertensive rats fed 8% NaCl food, resulting in that chronic icv SMTC enhanced more hypertension. These results suggested that central nNOS neurons may function to suppress sympathetic activity to compensate high arterial pressure for lowering in salt‐sensitive hypertension.