  Tropical climates provoke adaptations in skin pigmentation and in mechanisms
controlling the volume, salt-content and pressure of body fluids. For many
whose distant ancestors moved to temperate climes, these adaptations proved
harmful: pigmentation decreased by natural selection and susceptibility to
hypertension emerged. Now an added risk is lung inflammation from coronavirus
that may be furthered by innate immune differences. Hypertension and
coronavirus have in common angiotensin converting enzyme 2 (ACE2), which
decreases blood pressure and mediates virus entry. In keeping with less
detailed studies, a long-term case-report shows that decreased blood pressure
induced by blocking a primary angiotensin receptor is supplemented, above
critical blocker dosage, by a further temperature-dependent fall, likely
mediated by ACE2 and secondary angiotensin receptors. Temperature-dependence
suggests a linkage with tropical heritage and an influence of blockers on the
progress of coronavirus infections. Positive therapeutic results should result
from negation of host pro-inflammatory effects mediated by the primary
angiotensin receptor and concomitant promotion of countervailing
anti-inflammatory effects mediated by ACE2 through other receptors. These
effects may involve innate immune system components (lectin complement pathway,
NAD metabolome). Black vulnerability - more likely based on physiological than
on socioeconomic differences - provides an important clue that may guide
treatments.
