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Decrease in Hypothalamic Gamma Adducin in Rat Models of Hypertension
Author(s) -
Hong Yang,
Phyllis Y. Reaves,
Michael J. Katovich,
Mohan K. Raizada
Publication year - 2004
Publication title -
hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.986
H-Index - 265
eISSN - 1524-4563
pISSN - 0194-911X
DOI - 10.1161/01.hyp.0000113045.12850.cd
Subject(s) - losartan , endocrinology , medicine , blood pressure , angiotensin ii , rat model , hypothalamus , renin–angiotensin system , spontaneously hypertensive rat , in vivo , incubation , chemistry , biology , biochemistry , microbiology and biotechnology
We have previously shown that a decrease in hypothalamic gamma adducin (gamma-adducin) is associated with hypertension in the spontaneously hypertensive rat (SHR). In view of many inherent issues with SHR, our objective in the present study was to provide proof of this concept with the use of 2 nongenetic rat models of hypertension. Subcutaneous angiotensin II (Ang II) infusion for 2 weeks (55 ng/kg per day) resulted in an increase in blood pressure (BP) of 18 mm Hg. This was associated with a 70% decrease in hypothalamic gamma-adducin. Concomitant administration of losartan attenuated the development of hypertension and a decrease in gamma-adducin. Deoxycorticosterone acetate salt-induced hypertension also caused a 70% decrease in hypothalamic gamma-adducin. Finally, neuronal cultures from neonatal rat brains were incubated with 100 nmol/L Ang II for 4 hours to mimic the in vivo Ang II infusion rat model. This chronic incubation with Ang II resulted in a 60% decrease in the neuronal gamma-adducin. Taken together, these observations strengthen our hypothesis that a decrease in hypothalamic gamma-adducin is linked to hypertension.

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