TY - JOUR
T1 - Central control mechanisms in hypertension
AU - Arnolda, Leonard
AU - Wang, Hui H.
AU - Maison, Jane
AU - Llewellyn-Smith, Ida
AU - Suzuki, Satoshi
AU - Pilovosky, Paul
AU - Chalmers, John
PY - 1997
Y1 - 1997
N2 - There is substantial evidence for an activation of the sympathetic nervous system in man as well as in genetic models of hypertension, such as the spontaneously hypertensive rat (SHR), but we are only beginning to understand the central mechanisms that generate changes in sympathetic activity and elevate blood pressure (BP). Significant recent advances have been made in defining the neural pathways involved in BP regulation and in identifying the neurotransmitters these neurones utilise. In this overview, we describe the neural pathways within the medulla oblongata and spinal cord that participate in BP control and examine that role of amino acid neurotransmitters within these pathways. We demonstrate how alterations in these pathways explain the sympathetic activation observed in the SHR and contribute to hypertension in this model. Lastly, we examine the application of modern molecular biological approaches to further our understanding of the neural regulation of the circulation. In these studies, we used the administration of antisense oligonucleotides to interrupt gene expression.
AB - There is substantial evidence for an activation of the sympathetic nervous system in man as well as in genetic models of hypertension, such as the spontaneously hypertensive rat (SHR), but we are only beginning to understand the central mechanisms that generate changes in sympathetic activity and elevate blood pressure (BP). Significant recent advances have been made in defining the neural pathways involved in BP regulation and in identifying the neurotransmitters these neurones utilise. In this overview, we describe the neural pathways within the medulla oblongata and spinal cord that participate in BP control and examine that role of amino acid neurotransmitters within these pathways. We demonstrate how alterations in these pathways explain the sympathetic activation observed in the SHR and contribute to hypertension in this model. Lastly, we examine the application of modern molecular biological approaches to further our understanding of the neural regulation of the circulation. In these studies, we used the administration of antisense oligonucleotides to interrupt gene expression.
KW - Antisense oligonucleotides
KW - Human hypertension
KW - Spontaneously hypertensive rat
KW - Sympathetic nervous system
UR - http://www.scopus.com/inward/record.url?scp=0030826260&partnerID=8YFLogxK
M3 - Article
C2 - 9448900
AN - SCOPUS:0030826260
SN - 0004-8291
VL - 27
SP - 474
EP - 478
JO - Australian and New Zealand Journal of Medicine
JF - Australian and New Zealand Journal of Medicine
IS - 4
ER -