scholarly journals Blood pressure regulation V: in vivo mechanical properties of precapillary vessels as affected by long-term pressure loading and unloading

2013 ◽  
Vol 114 (3) ◽  
pp. 499-509 ◽  
Author(s):  
Ola Eiken ◽  
Igor B. Mekjavic ◽  
Roger Kölegård
2019 ◽  
Vol 316 (5) ◽  
pp. H1113-H1123 ◽  
Author(s):  
Sameed Ahmed ◽  
Rui Hu ◽  
Jessica Leete ◽  
Anita T. Layton

Sex differences in blood pressure and the prevalence of hypertension are found in humans and animal models. Moreover, there has been a recent explosion of data concerning sex differences in nitric oxide, the renin-angiotensin-aldosterone system, inflammation, and kidney function. These data have the potential to reveal the mechanisms underlying male-female differences in blood pressure control. To elucidate the interactions among the multitude of physiological processes involved, one may apply computational models. In this review, we describe published computational models that represent key players in blood pressure regulation, and highlight sex-specific models and their findings.


Physiology ◽  
1989 ◽  
Vol 4 (2) ◽  
pp. 56-59 ◽  
Author(s):  
PB Persson ◽  
H Ehmke ◽  
R Kirchheim Hartmut

Arterial baroreceptors effectively buffer short-term pressure changes. However, their importance for long-term pressure control appears to be minor. In contrast, cardiopulmonary reflexes cannot sense short-term fluctuations in arterial pressure but may be involved in the long-term regulation. Knowledge of the interaction of both receptor areas may enhance our understanding of blood pressure regulation.


1997 ◽  
Vol 272 (4) ◽  
pp. F515-F520 ◽  
Author(s):  
M. I. Oliverio ◽  
C. F. Best ◽  
H. S. Kim ◽  
W. J. Arendshorst ◽  
O. Smithies ◽  
...  

Most of the classic functions of the renin-angiotensin system are mediated by type 1 (AT1) angiotensin receptors, of which two subtypes, AT1A and AT1B, have been identified. However, distinct functions for these two AT1 receptors have been difficult to separate. We examined the pressor effects of angiotensin II in Agtr1A -/- mice, which lack AT1A receptors. In enalapril-pretreated Agtr1A -/- mice, angiotensin II caused significant and dose-proportional increases in mean arterial pressure. This pressor response was not blocked by pretreatment with sympatholytic agents but was completely inhibited by the AT1-receptor antagonists, losartan and candesartan, suggesting that it is directly mediated by AT1B receptors. Chronic treatment of Agtr1A -/- mice with losartan reduced systolic blood pressure from 80 +/- 5 to 72 +/- 4 mmHg (P < 0.04), suggesting a role for AT1B receptors in chronic blood pressure regulation. These studies provide the first demonstration of in vivo pressor effects mediated by AT1B receptors and demonstrate that, when AT1A receptors are absent, the AT1B receptor contributes to the regulation of resting blood pressure.


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