Showing posts with label chronic SAD. Show all posts
Showing posts with label chronic SAD. Show all posts

Friday, November 15, 2013

Brain stem control of arterial pressure in chronic arterial baroreceptor-denervated rats


Authors: Ann M. Schreihofer, Satoru Ito, and Alan F. Sved

Unlike acute denervation, chronic denervation condition lead  normal sympathetic vasomotor tone. So the authors wanted to examine what is driving sympathetic vasomotor tone. Methods: Sinoaortic denervation (SAD) or NTS lesion was done and the rats were allowed to recovery for one week. Then several microinjecion protocols were done while recording BP responses. Results: BP responses to α adrenergic  injections relieved no differences between control and chronic SAD rats. This data suggests that vascular reactivity is not altered in response to chronic denervation. They also did a spinal transection at the T1 level and BP responses were no different between the control and chronic SAD rats. These results demonstrate that supraspinal regions are still response for control of BP under chronic SAD conditions. In order to investigate the role that RVLM is playing in the control of BP under chronic SAD conditions, they microinjected muscimol into RVLM bilaterally. Results showed that control and NTS lesioned and chronic SAD rats had similar responses. This showed that the RVLM is important to the control of sympathetic vasomotor tone under both intact and chronic SAD conditions. Next they wanted to investigate CVLM GABAergic input to RVLM. After inhibition of CVLM with muscimol they saw no differences between groups. This showed that even after removal of barorecptor inputs to the brain stem, the CVLM is still able to maintain the same level of GABAergic input to RVLM. They saw similar differences for glutamergic input to CVLM between groups. Demonstrating that the same of activation of CVLM neurons is occurring  even in the absence of baroreceptors. 

Conclusion: Under chronic SAD conditions, the CVLM receives baroindependent glutamergic input. This allows for the CVLM to still provide gabaergic input to RVLM in order to maintain BP in chronic denervated rats.

Friday, June 24, 2011

Nucleus tractus solitarius and control of blood pressure in chronic sinoaortic denervated rats

   It has been shown by previous laboratories, that chronic sinoaortic denervated rats blood pressure return to normal ranges. However, initially, they show elevated blood pressure. This article investigated whether the NTS is playing a role in the tonic regulation of blood pressure  in chronic SAD rats because the blood pressure returns to a normal range after a couple weeks. They believed that it could be possible that there are cardiopulmonary afferents traveling to the NTS, in the absence of the barorecptor afferents to the NTS, the cardiopulmonary afferents are then responsible for relaying information about blood pressure to the NTS so that tonic control of blood pressure is still possible.

   The investigators did a couple of interesting things, they microinjected muscimol or lidocaine into the NTS bilateral,  the rats were anesthetized for this experiment. For another experiment,by using electrical current they were able to lesion the NTS  in chronic SAD and control animals. After the NTS lesion was completed the rats were allowed to recovery from  the surgery and the recording of the new AP and HR was done while the animal was conscience animal ( only waited 1 hour after the NTS lesion surgery). In both the control and chronic SAD you would expect an increase in AP and in HR as a response for both procedures if their hypothesis is correct. This was not what they saw in the Chronic SAD , in both of the experiments the chronic SAD had no response, so AP and HR did not change. However, they did see the increase in the AP and in HR in the control rat, along with an increase in the vasopressin concentration in the plasma ( only tested VP before and after applying an electric current to  lesion NTS). In order to make sure that the Chronic SAD  rats were actually able to secrete VP, they tested all the animals to see their response to hypertonic saline. They should release VP in response to hypertonic saline and that is the result they saw. So there was nothing wrong with the chronic SAD rats ability to secrete VP.

  So their findings showed that the NTS is not necessary for tonic control of AP and HR in chronic SAD. There must be another area responsible for this regulation when the barorecptors inputs are abolished or it could be possible that the vessels might have so mechanism that allows for tonic control of AP. They also showed that the chronic SAD  rats still had some cardiopulmonary bararecptor reflexes, however ,this does not contribute to the tonic control of AP that is seen in the chronic SAD rats.