Hypertension management before and under the COVID-19 pandemic: lessons and future directions.

Hypertension is a significant risk factor for cardiovascular diseases. The prevalence of hypertension and its complications is increasing yearly, yet it remains inadequately controlled worldwide. It has already been recognized that self-management, including self-measured blood pressure monitoring at home, is more important than office blood pressure monitoring. The practical application of telemedicine using digital technology was already underway. COVID-19 has promoted the popularization of these management systems in primary care, although the COVID-19 pandemic disrupted lifestyle and healthcare access. At the beginning of the pandemic, we were at the mercy of information on whether certain antihypertensive drugs, for example, might pose a risk of infection in the face of unknown infectious diseases. Over the past three years, however, much knowledge has been accumulated. It has been scientifically proven that there is no serious problem in managing hypertension in the same way as before the pandemic. That is to control blood pressure mainly through home blood pressure monitoring and continuing conventional drug therapy while modifying lifestyle. On the other hand, in the New Normal era, it is necessary to accelerate digital hypertension management and the establishment of new social networks and medical systems to prepare for the re-emergence of future pandemics while continuing to protect against infection. This review will summarize the lessons and future directions we learned from the impact of the COVID-19 pandemic on hypertension management. The COVID-19 pandemic has disrupted our daily life, restricted access to healthcare, and altered some of the conventional management of hypertension.

A pressor dose of angiotensin II has no influence on the angiotensin-converting enzyme 2 and other molecules associated with SARS-CoV-2 infection in mice.

In the early phase of the Coronavirus disease 2019 (COVID-19) pandemic, it was postulated that the renin-angiotensin-system inhibitors (RASi) increase the infection risk. This was primarily based on numerous reports, which stated that the RASi could increase the organ Angiotensin-converting enzyme 2 (ACE2), the receptor of Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), in rodents. RASi can theoretically antagonize the potential influence of angiotensin II (Ang II) on ACE2. However, while Ang II decreases the ACE2 levels in cultured cells, there is little evidence that supports this phenomenon in living animals. In this study, we tested whether Ang II or Ang II combined with its antagonist would alter the ACE2 and other molecules associated with the infection of SARS-CoV-2. Male C57BL6/J mice were administered vehicle, Ang II (400 ng/kg/min), or Ang II with losartan (10 mg/kg/min) for 2 weeks. ACE2 knockout mice were used as a negative control for the ACE2 assay. We found that both Ang II, which elevated blood pressure by 30 mm Hg, and Ang II with losartan, had no effect on the expression or protein activity of ACE2 in the lung, left ventricle, kidney, and ileum. Likewise, these interventions had no effect on the expression of Transmembrane Protease Serine 2 (TMPRSS2) and Furin, proteases that facilitate the virus-cell fusion, and the expression or activity of Tumor Necrosis Factor α-Convertase (TACE) that cleaves cell-surface ACE2. Collectively, physiological concentrations of Ang II do not modulate the molecules associated with SARS-CoV-2 infection. These results support the recent observational studies suggesting that the use of RASi is not a risk factor for COVID-19.