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Non-technical summary Humans have the tendency to damage the natural environment in many ways. Deforestation and conversion of forests for residential, industrial development, and expansion of agricultural crops, as well as the burning of fossil fuels, are some activities that disrupt natural ecosystems and wildlife and contribute to climate change. As a result, the life cycles of pathogens and intermediate hosts (insects, rodents, mammals) as well as biodiversity are affected. Through these activities, humans meet wild animals that transmit pathogens, resulting in their infection by zoonoses and causing epidemics–pandemics, the effects of which have as their final recipient himself and his activities. Technical summary This article aims to highlight the two-way relationship between those human activities and the occurrence of epidemics–pandemics. We will try to elaborate this two-way relationship, through the overview of the current pandemic (origin of SARS-CoV-2, modes of transmission, clinical picture of the disease of COVID-19, influence of weather and air pollution on prevalence and mortality, pandemic effects, and treatments). They are used as primary sources, scientific articles, literature, websites, and databases (Supplementary appendix) to analyze factors involved in the occurrence and transmission of zoonotic diseases in humans (Ebola, influenza, Lyme disease, dengue fever, cholera, AIDS/HIV, SARS-CoV, MERS-CoV). The present paper concluded that humanity today faces two major challenges: controlling the COVID-19 pandemic and minimizing the risk of a new global health crisis occurring in the future. The first can be achieved through equitable access to vaccines and treatments for all people. The second needs the global community to make a great change and start protecting the natural environment and its ecosystems through the adoption of prevention policies. Summary of social media Two-way relationship between human activities and epidemics highlighted, through review of the COVID-19 pandemic.

Nifedipine is a widely used anti-anginal and anti-hypertensive agent. It is associated with significant gingival changes attributed more to collagen hyperplasia than to enhancement of protein synthesis. We investigated the influence of nifedipine on morphological changes in the parotid glands of rats in a model of hypertension. Twenty-eight male Wistar rats (8–10 weeks; 200 ± 15 g) were divided into four groups (A–D). Hypertension was induced by surgical means in groups C and D. Animals in groups B and D were treated with nifedipine (0.85 mg/kg) via a gastroesophageal catheter the day after surgery (experimental day-1) for 2 weeks. A significant difference was observed between the control group and nifedipine group and between the control group and hypertension group with regard to the weight of the parotid gland and its surface area. Histological findings demonstrated changes in the parotid glands of hypertensive animals with mild vessel dilatation and infiltration of inflammatory cells. These histological findings seemed to be due more to changes in venous function than to alterations in gland architecture.