Angiotensin II (AngII) can reach the brain through circumventricular organs (CVOs), such as the subfornical organ (SFO) and the organum vasculosum of the lamina terminalis, to control blood pressure (OVLT). We wanted to see if elevated amounts of superoxide in the OVLT play a role in AngII's hypertensive effects. To allow superoxide dismutase overexpression, adenoviral vectors carrying human copper/zinc superoxide dismutase (CuZnSOD) or control adenovirus (AdEmpty) were injected directly into the OVLT of rats. Rats were administered AngII (10 ng/kg/min) intravenously for ten days after three days of saline infusion. After 10 days, AdEmpty rats (n = 6) had a blood pressure rise of 33 8 mmHg, whereas rats overexpressing CuZnSOD (n = 8) in the OVLT had a blood pressure increase of just 18 5 mmHg Infusion of AngII. These findings back up the idea that excessive OVLT production plays a role in the development of persistent AngII-dependent hypertension. The brain is thought to perceive circulating angiotensin II (AngII) levels through circumventricular organs like the subfornical organ (SFO) and adjust sympathetic nervous system output accordingly. However, the cellular signalling pathways involved in these interactions remain unclear. We investigated if an underlying mechanism in the long-term hypertensive consequences of chronic AngII is overproduction of intracellular superoxide in the median preoptic nucleus (MnPO). Adenoviral vectors carrying human CuZnSOD (AdCuZnSOD) or a control vector (AdEmpty) were directly injected into the MnPO of rats equipped with aorta telemetric transmitters for arterial pressure measurement. Rats were administered AngII (10 ng/kg/min) intravenously for ten days after a three-day saline infusion control period. In the MnPO, rats overexpressing CuZnSOD (n = 7) had after ten days of AngII infusion, blood pressure increased only 6 2 mmHg, but blood pressure increased 21 4 mmHg in AdEmpty-infected rats (n = 9). These results support the idea that MnPO production contributes to the development of chronic AngII-dependent hypertension.
Author(S) Details
John P. Collister
Department of Veterinary and Biomedical Sciences, College of Veterinary Medicine, University of Minnesota, St. Paul, MN 55108, USA.
Mitch Bellrichard
Department of Veterinary and Biomedical Sciences, College of Veterinary Medicine, University of Minnesota, St. Paul, MN 55108, USA.
Donna Drebes
Department of Veterinary and Biomedical Sciences, College of Veterinary Medicine, University of Minnesota, St. Paul, MN 55108, USA.
David Nahey
Department of Veterinary and Biomedical Sciences, College of Veterinary Medicine, University of Minnesota, St. Paul, MN 55108, USA.
Jun Tian
Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Matthew C. Zimmerman
Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
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