Sex-specific long-term blood pressure regulation: Modeling and analysis
Hypertension is a global health challenge: it affects one billion people worldwide and is estimated to account for >60% of all cases or types of cardiovascular disease. In part because sex differences in blood pressure regulation mechanisms are not sufficiently well understood, fewer hypertensive...
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Published in | Computers in biology and medicine Vol. 104; pp. 139 - 148 |
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Language | English |
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01.01.2019
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Abstract | Hypertension is a global health challenge: it affects one billion people worldwide and is estimated to account for >60% of all cases or types of cardiovascular disease. In part because sex differences in blood pressure regulation mechanisms are not sufficiently well understood, fewer hypertensive women achieve blood pressure control compared to men, even though compliance and treatment rates are generally higher in women. Thus, the objective of this study is to identify which factors contribute to the sexual dimorphism in response to anti-hypertensive therapies targeting the renin angiotensin system (RAS). To accomplish that goal, we develop sex-specific blood pressure regulation models. Sex differences in the RAS, baseline adosterone level, and the reactivity of renal sympathetic nervous activity (RSNA) are represented. A novel aspect of the model is the representation of sex-specific vasodilatory effect of the bound angiotensin II type two receptor (AT2R-bound Ang II) on renal vascular resistance. Model simulations suggest that sex differences in RSNA are the largest cause of female resistance to developing hypertension due to the direct influence of RSNA on afferent arteriole resistance. Furthermore, the model predicts that the sex-specific vasodilatory effects of AT2R-bound Ang II on renal vascular resistance may explain the higher effectiveness of angiotensin receptor blockers in treating hypertensive women (but not men), compared to angiotensin converting enzyme inhibitors.
•Sex specific computational models of long-term blood pressure regulation introduced.•Different enzymatic activity is key to male sensitivity to angiotensin II infusion.•Renal sympathetic nervous activity is key to female resistance to renal hypertension.•Angiotensin type 2 receptor key to female strength of ARB over ACEI treatment. |
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AbstractList | Hypertension is a global health challenge: it affects one billion people worldwide and is estimated to account for
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60% of all cases or types of cardiovascular disease. In part because sex differences in blood pressure regulation mechanisms are not sufficiently well understood, fewer hypertensive women achieve blood pressure control compared to men, even though compliance and treatment rates are generally higher in women. Thus, the objective of this study is to identify which factors contribute to the sexual dimorphism in response to anti-hypertensive therapies targeting the renin angiotensin system (RAS). To accomplish that goal, we develop sex-specific blood pressure regulation models. Sex differences in the RAS, baseline adosterone level, and the reactivity of renal sympathetic nervous activity (RSNA) are represented. A novel aspect of the model is the representation of sex-specific vasodilatory effect of the bound angiotensin II type two receptor (AT2R-bound Ang II) on renal vascular resistance. Model simulations suggest that sex differences in RSNA are the largest cause of female resistance to developing hypertension due to the direct influence of RSNA on afferent arteriole resistance. Furthermore, the model predicts that the sex-specific vasodilatory effects of AT2R-bound Ang II on renal vascular resistance may explain the higher effectiveness of angiotensin receptor blockers in treating hypertensive women (but not men), compared to angiotensin converting enzyme inhibitors. Hypertension is a global health challenge: it affects one billion people worldwide and is estimated to account for >60% of all cases or types of cardiovascular disease. In part because sex differences in blood pressure regulation mechanisms are not sufficiently well understood, fewer hypertensive women achieve blood pressure control compared to men, even though compliance and treatment rates are generally higher in women. Thus, the objective of this study is to identify which factors contribute to the sexual dimorphism in response to anti-hypertensive therapies targeting the renin angiotensin system (RAS). To accomplish that goal, we develop sex-specific blood pressure regulation models. Sex differences in the RAS, baseline adosterone level, and the reactivity of renal sympathetic nervous activity (RSNA) are represented. A novel aspect of the model is the representation of sex-specific vasodilatory effect of the bound angiotensin II type two receptor (AT2R-bound Ang II) on renal vascular resistance. Model simulations suggest that sex differences in RSNA are the largest cause of female resistance to developing hypertension due to the direct influence of RSNA on afferent arteriole resistance. Furthermore, the model predicts that the sex-specific vasodilatory effects of AT2R-bound Ang II on renal vascular resistance may explain the higher effectiveness of angiotensin receptor blockers in treating hypertensive women (but not men), compared to angiotensin converting enzyme inhibitors. Hypertension is a global health challenge: it affects one billion people worldwide and is estimated to account for >60% of all cases or types of cardiovascular disease. In part because sex differences in blood pressure regulation mechanisms are not sufficiently well understood, fewer hypertensive women achieve blood pressure control compared to men, even though compliance and treatment rates are generally higher in women. Thus, the objective of this study is to identify which factors contribute to the sexual dimorphism in response to anti-hypertensive therapies targeting the renin angiotensin system (RAS). To accomplish that goal, we develop sex-specific blood pressure regulation models. Sex differences in the RAS, baseline adosterone level, and the reactivity of renal sympathetic nervous activity (RSNA) are represented. A novel aspect of the model is the representation of sex-specific vasodilatory effect of the bound angiotensin II type two receptor (AT2R-bound Ang II) on renal vascular resistance. Model simulations suggest that sex differences in RSNA are the largest cause of female resistance to developing hypertension due to the direct influence of RSNA on afferent arteriole resistance. Furthermore, the model predicts that the sex-specific vasodilatory effects of AT2R-bound Ang II on renal vascular resistance may explain the higher effectiveness of angiotensin receptor blockers in treating hypertensive women (but not men), compared to angiotensin converting enzyme inhibitors. •Sex specific computational models of long-term blood pressure regulation introduced.•Different enzymatic activity is key to male sensitivity to angiotensin II infusion.•Renal sympathetic nervous activity is key to female resistance to renal hypertension.•Angiotensin type 2 receptor key to female strength of ARB over ACEI treatment. |
Author | Leete, Jessica Layton, Anita T. |
AuthorAffiliation | 1 Computational Biology & Bioinformatics Program, Duke University, Durham, North Carolina, U.S.A 2 Departments of Mathematics, Biomedical Engineering, and Medicine, Duke University, Durham, North Carolina, U.S.A 3 Department of Applied Mathematics and School of Pharmacy, University of Waterloo, Waterloo, Ontario, Canada, N2L 3G1 |
AuthorAffiliation_xml | – name: 3 Department of Applied Mathematics and School of Pharmacy, University of Waterloo, Waterloo, Ontario, Canada, N2L 3G1 – name: 2 Departments of Mathematics, Biomedical Engineering, and Medicine, Duke University, Durham, North Carolina, U.S.A – name: 1 Computational Biology & Bioinformatics Program, Duke University, Durham, North Carolina, U.S.A |
Author_xml | – sequence: 1 givenname: Jessica surname: Leete fullname: Leete, Jessica email: jessica.leete@duke.edu organization: Computational Biology & Bioinformatics Program, Duke University, Durham, NC, USA – sequence: 2 givenname: Anita T. surname: Layton fullname: Layton, Anita T. organization: Departments of Mathematics, Biomedical Engineering, and Medicine, Duke University, Durham, NC, USA |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30472496$$D View this record in MEDLINE/PubMed |
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Keywords | Hypertension Blood pressure renin angiotensin system ACE inhibitors Angiotensin receptor blockers |
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SubjectTerms | ACE inhibitors Angiotensin Angiotensin II Angiotensin receptor blockers Angiotensin-Converting Enzyme Inhibitors - pharmacology Antihypertensives Blood Pressure Cardiovascular diseases Computer simulation Enzyme inhibitors Enzymes Female Females Gender aspects Gender differences Global health Humans Hypertension Hypertension - drug therapy Hypertension - physiopathology Kidney - innervation Kidney - physiopathology Kidneys Male Males Models, Cardiovascular Peptides Peptidyl-dipeptidase A Physiology Ratios Renin renin angiotensin system Renin-Angiotensin System - drug effects Sensory neurons Sex Sex Characteristics Sex differences Sexual dimorphism Sympathetic Nervous System Womens health |
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Title | Sex-specific long-term blood pressure regulation: Modeling and analysis |
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