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Perceived stress, sex and occupational status interact to increase the risk of future high blood pressure: the IPC cohort study.

ABSTRACT: Contrary to lay beliefs, current perceived stress is not consistently associated with the incidence of high blood pressure (BP) in prospective studies, possibly because of moderating factors. The present prospective study examined this association and explored the potential moderating effects of sex or occupational status.The 4-item Perceived Stress Scale was filled at baseline by 19 766 normotensive adults (13 652 men, mean age ± SD: 46.8 ± 9.3 years), without history of cardiovascular and renal disease, and not on either psychotropic or antihypertensive drugs.After a mean follow-up of 5.8 ± 2.1 years, 3774 participants (19.1%) had high BP, defined as having a SBP at least 140 mmHg or a DBP at least 90 mmHg, or using antihypertensive drugs. There was a significant interaction between baseline-perceived stress and sex (P = 0.02) in relation to high BP at follow-up. After adjustment for potential confounders, baseline perceived stress was associated with high BP at follow-up in women [odds ratio 1.20, 95% confidence interval 1.03-1.38, P = 0.016). In addition, the interaction between perceived stress and occupational status was significant among women (P = 0.02). Baseline-perceived stress was positively associated with high BP at follow-up among women of medium or low occupational status, with odds ratio suggesting a linear increase of the risk (P = 0.005).Perceived stress may be considered as a risk factor for hypertension in women of lower occupational status. Research addressing the relationships between stress and high BP should systematically look for possible interactions with sex and occupational status.

SUBMITTER: Wiernik E

PROVIDER: S-EPMC5397536 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Cytomegalovirus (CMV) infection is a common infection in adults (seropositive 60-99% globally), and is associated with cardiovascular diseases, in line with risk factors such as hypertension and atherosclerosis. Several viral infections are linked to hypertension, including human herpes virus 8 (HHV-8) and HIV-1. The mechanisms of how viral infection contributes to hypertension or increased blood pressure are not defined. In this report, the role of CMV infection as a cause of increased blood pressure and in forming aortic atherosclerotic plaques is examined. Using in vivo mouse model and in vitro molecular biology analyses, we find that CMV infection alone caused a significant increase in arterial blood pressure (ABp) (p<0.01 approximately 0.05), measured by microtip catheter technique. This increase in blood pressure by mouse CMV (MCMV) was independent of atherosclerotic plaque formation in the aorta, defined by histological analyses. MCMV DNA was detected in blood vessel samples of viral infected mice but not in the control mice by nested PCR assay. MCMV significantly increased expression of pro-inflammatory cytokines IL-6, TNF-alpha, and MCP-1 in mouse serum by enzyme-linked immunosorbent assay (ELISA). Using quantitative real time reverse transcriptase PCR (Q-RT-PCR) and Western blot, we find that CMV stimulated expression of renin in mouse and human cells in an infectious dose-dependent manner. Co-staining and immunofluorescent microscopy analyses showed that MCMV infection stimulated renin expression at a single cell level. Further examination of angiotensin-II (Ang II) in mouse serum and arterial tissues with ELISA showed an increased expression of Ang II by MCMV infection. Consistent with the findings of the mouse trial, human CMV (HCMV) infection of blood vessel endothelial cells (EC) induced renin expression in a non-lytic infection manner. Viral replication kinetics and plaque formation assay showed that an active, CMV persistent infection in EC and expression of viral genes might underpin the molecular mechanism. These results show that CMV infection is a risk factor for increased arterial blood pressure, and is a co-factor in aortic atherosclerosis. Viral persistent infection of EC may underlie the mechanism. Control of CMV infection can be developed to restrict hypertension and atherosclerosis in the cardiovascular system.

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Perceived stress, sex and occupational status interact to increase the risk of future high blood pressure: the IPC cohort study.

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