Lack of the serotonin transporter does not prevent mineralocorticoid hypertension in rat and mouse

We hypothesized that lack of a functional serotonin transporter (SERT) would increase basal blood pressure and enhance the development of deoxycorticosterone acetate (DOCA)-salt hypertension compared to wild type (WT) controls. Mean arterial blood pressure was measured in WT and SERT knockout (KO) m...

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Bibliographic Details
Published in:European journal of pharmacology 2008-07, Vol.589 (1-3), p.225-227
Main Authors: Ni, Wei, Zhou, Huawei, Diaz, Jessica, Murphy, Dennis L., Haywood, Joseph R., Watts, Stephanie W.
Format: Article
Language:English
Subjects:
5-HT
Animals
Arterial hypertension. Arterial hypotension
Biological and medical sciences
Blood and lymphatic vessels
Blood Pressure - genetics
Blood Pressure Monitoring, Ambulatory - methods
Cardiology. Vascular system
Desoxycorticosterone
Disease Models, Animal
Hypertension - chemically induced
Hypertension - genetics
Hypertension - metabolism
Hypertension - physiopathology
Hypertension - prevention & control
Male
Medical sciences
Mice
Mice, Inbred C57BL
Mice, Knockout
Mineralocorticoids
Pharmacology. Drug treatments
Rats
Rats, Wistar
Serotonin Plasma Membrane Transport Proteins - deficiency
Serotonin Plasma Membrane Transport Proteins - genetics
Serotonin transporter
Systemic hypertension
Telemetry
Time Factors
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Summary:We hypothesized that lack of a functional serotonin transporter (SERT) would increase basal blood pressure and enhance the development of deoxycorticosterone acetate (DOCA)-salt hypertension compared to wild type (WT) controls. Mean arterial blood pressure was measured in WT and SERT knockout (KO) mice and rat models through radiotelemetry. Basal blood pressures were not different between respective WT and KO. Moreover, blood pressure elevated similarly (∼50 mm Hg) in all strains given DOCA and salt. Thus, the lack of functional SERT did not prevent development of DOCA-salt induced hypertension or modify basal blood pressure significantly.
ISSN:0014-2999
1879-0712
DOI:10.1016/j.ejphar.2008.06.012