Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/17702
Title: Pathophysiological Links Between Diabetes and Blood Pressure.
Austin Authors: Libianto, Renata;Batu, Duygu ;MacIsaac, Richard J;Cooper, Mark E;Ekinci, Elif I 
Affiliation: Department of Medicine, The University of Melbourne, Melbourne, Australia
Department of Endocrinology, Austin Health, Heidelberg, Victoria, Australia
Department of Endocrinology and Diabetes, St Vincent's Hospital Melbourne, Melbourne, Australia
Department of Medicine, Monash University, Melbourne, Australia
Issue Date: May-2018
metadata.dc.date: 2018-01-31
Publication information: The Canadian journal of cardiology 2018; 34(5): 585-594
Abstract: Hypertension is highly prevalent among people with diabetes, and the presence of diabetes among those with hypertension portends an increase in cardiovascular risk. In this review we aim to explore the pathophysiological links between diabetes and hypertension. Renal sodium handling differs in diabetes because there is an upregulation of sodium transporters in the kidneys. The renin-angiotensin-aldosterone system may be upregulated in diabetes, leading to hypertension through a direct effect mediated by angiotensin II, as well as indirectly through upregulation of sympathetic activity. Renin-angiotensin-aldosterone system blockade is a mainstay therapy for hypertension, and evidence suggests that it might also reduce the incidence of diabetes. People with diabetes frequently have autonomic dysfunction, which could contribute to hypertension through increased sympathetic tone and through stimulation of renin production in the juxtaglomerular apparatus. Furthermore, people with diabetes also frequently show an abnormality in their circadian blood pressure pattern. Another important link between hypertension and diabetes is the development as well as progression of diabetic kidney disease, the pathophysiology of which is mediated through several pathways including endothelial dysfunction and advanced glycation end products. Finally, obesity and the metabolic syndrome, through their effects on various hormones and inflammation, might also contribute to the pathogenesis of hypertension and diabetes.
URI: http://ahro.austin.org.au/austinjspui/handle/1/17702
DOI: 10.1016/j.cjca.2018.01.010
ORCID: 0000-0003-2372-395X
PubMed URL: 29731021
Type: Journal Article
Appears in Collections:Journal articles

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