Showing posts with label BP. Show all posts
Showing posts with label BP. Show all posts

Friday, November 15, 2013

Dependence of sympathetic vasomotor tone on bilateral input from the rostral ventrolateral medulla in the rabbit: role of baroreceptor reflexes

J. Horiuchi and R.A.L. Dampney

It has been observed that bilateral but not unilateral inactivation of RVLM leads to profound decreases in BP. However, the mechanism that allows for one RVLM under intact baroreceptor conditions to be able to maintain bp is unknown. The current study investigated both unilateral and bilateral inhibition of RVLM on blood pressure and sympathetic output. Method: Following removal of aortic and carotid baroreceptors along with bilateral vagii removal muscimol was injected in the right RVLM and then the left rvlm. MAP, rSNA were recorded along with HR.Results: The response to unilateral blockade of rvlm in SAD rabbits drop MAP to that of spinal levels. It also caused a dramatic fall in rSNA in SAD rabbits when compared to intact rabbits.

Conclusion: Data suggests that the baroreflex is important for maintaining BP and SNA when the activity of RVLM neurons is impaired.

Friday, August 12, 2011

The ventrolateral medulla and sympathetic regulation of arterial pressure.

ANN M. SCHREIHOFER AND ALAN F. SVED.  The ventrolateral medulla and sympathetic regulation of arterial pressure. In: Central regulation of autonomic functions.  2nd Edition. Eds: I.J. Llewellyn-Smith and A.J. Verberne Oxford University Press, Inc. New York, 2011.

So in honor of our guest from Australia I thought it was timely to provide a posting on one of the chapters from Ida's recent book that will likely be considered the bible on neural control for at least the next 5-10 years.  The particular chapter I chose is of course most relevant to our studies on the RVLM, although other chapters in this book are also important in terms of our understanding of brainstem control of arterial pressure.  In this chapter Ann Schreihofer and Alan Sved provide a nice overview of the history and development of what the current knowledge is on brainstem control of sympathetic outflow.  They do a great job in discussing the number of techniques used to examine the ventrolateral medulla in term of it's anatomy and physiology.  Several nice figures combine immunohistochemistry, histology, BP and SNA responses etc. to illustrate the relationship between the CVLM and the RVLM.  There is also some clarification on the confusion caused by the original nomenclature of the C1 cells and that while serving as a useful marker for barosensitive, bulbospinal neurons controlling SNA, use glutamate not epinephrine serves as the primary neurotransmitters of RVLM neurons.  A thorough discussion of the roles of the RVLM and CVLM is provided.   There is a section of the caudal pressor area which while interesting, seems to pale in comparison to the importance of the CVLM and RVLM.  Finally, the last two sections are devoted to differential control and the role of the VLM in hypertension.  Both nice summaries but also highlight the number of unaswered questions that remain to be answered, some of which are being addressed in our laboratory.  Overall this is a chapter that every student, postdoc and faculty working in the field needs to be well-versed in so if you haven't done so recently or already, I would suggest giving it a look soon.

Posted by Pat

Friday, July 1, 2011

Exercise Training Restores Baroreflex Sensitivity in Never-Treated Hypertensive Patients

Laterza MC, de Matos LD, Trombetta IC, Braga AM, Roveda F, Alves MJ, Krieger EM, Negrão CE, Rondon MU. Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil.Hypertension. 2007 Jun;49(6):1298-306. Epub 2007 Apr 16.


As we have already established, the baroreflex is an important mechanism in cardiovascular control, and exercise is a good way to deal with the hypertension. There is a possibility that arterial baroreflex sensitivity is decreased in individuals who suffer from some cardiovascular diseases, such as hypertension. Based on this possibility, the researchers in this study wanted to find if there was a decreased baroreflex response upon muscle sympathetic nerve activity (MSNA) and blood pressure (BP) and whether these two parameters were related in their changes in response to the exercise.


Using 20 hypertensive individuals who have never been treated for that condition before, as well as 10 normotensive individuals as a control, they made two subgroups of exercise-trained and non-exercised trained individuals. The MSNA was monitored by microneurography, and the BP was monitored both by sphygmomanometer and by a finger photoplethysmography device. Arterial baroreflex responsiveness was measured by infusion of either phenylephrine or sodium nitroprusside into the antecubital vein while monitoring drug effects upon mean BP, MSNA, and heart rate.


In the hypertensive individuals, their BP was significantly higher than in the normotensive individuals, and their MSNA had a higher burst frequency and burst incidence than the normotensive individuals. Baroreflex control of the BP was significantly lower in the hypertensive individuals. At the conclusion of the experiment, the baroreflex control of the exercise trained individuals was more on par with the baroreflex control of the normotensive individuals. Also, the changes in MSNA and changes in BP were significantly correlated in the exercise-trained and non-trained individuals.


Therefore, baroreflex control of MSNA was shown, by this study, to be decreased in hypertensive individuals, and that exercise would produce control that is similar to the level found in normotensive individuals. Also, the study showed a relationship between MSNA activity and BP, but does not establish how they are related.