ABSTRACT
Despite its Earth-like size and source material1,2, Venus is extremely dry3,4, indicating near-total water loss to space by means of hydrogen outflow from an ancient, steam-dominated atmosphere5,6. Such hydrodynamic escape likely removed most of an initial Earth-like 3-km global equivalent layer (GEL) of water but cannot deplete the atmosphere to the observed 3-cm GEL because it shuts down below about 10-100 m GEL5,7. To complete Venus water loss, and to produce the observed bulk atmospheric enrichment in deuterium of about 120 times Earth8,9, nonthermal H escape mechanisms still operating today are required10,11. Early studies identified these as resonant charge exchange12-14, hot oxygen impact15,16 and ion outflow17,18, establishing a consensus view of H escape10,19 that has since received only minimal updates20. Here we show that this consensus omits the most important present-day H loss process, HCO+ dissociative recombination. This process nearly doubles the Venus H escape rate and, consequently, doubles the amount of present-day volcanic water outgassing and/or impactor infall required to maintain a steady-state atmospheric water abundance. These higher loss rates resolve long-standing difficulties in simultaneously explaining the measured abundance and isotope ratio of Venusian water21,22 and would enable faster desiccation in the wake of speculative late ocean scenarios23. Design limitations prevented past Venus missions from measuring both HCO+ and the escaping hydrogen produced by its recombination; future spacecraft measurements are imperative.
ABSTRACT
RATIONALE: Tetrahydrobiopterin (BH4) is an essential cofactor of nitric oxide synthases (NOS). Oral BH4 supplementation preserves cardiac function in animal models of cardiac disease; however, the mechanisms underlying these findings are not completely understood. OBJECTIVE: To study the effect of myocardial transgenic overexpression of the rate-limiting enzyme in BH4 biosynthesis, GTP cyclohydrolase 1 (GCH1), on NOS activity, myocardial function, and Ca2+ handling. METHODS AND RESULTS: GCH1overexpression significantly increased the biopterins level in left ventricular (LV) myocytes but not in the nonmyocyte component of the LV myocardium or in plasma. The ratio between BH4 and its oxidized products was lower in mGCH1-Tg, indicating that a large proportion of the myocardial biopterin pool was oxidized; nevertheless, myocardial NOS1 activity was increased in mGCH1-Tg, and superoxide release was significantly reduced. Isolated hearts and field-stimulated LV myocytes (3 Hz, 35°C) overexpressing GCH1 showed a faster relaxation and a PKA-mediated increase in the PLB Ser16 phosphorylated fraction and in the rate of decay of the [Ca2+]i transient. RyR2 S-nitrosylation and diastolic Ca2+ leak were larger in mGCH1-Tg and ICa density was lower; nevertheless the amplitude of the [Ca2+]i transient and contraction did not differ between genotypes, because of an increase in the SR fractional release of Ca2+ in mGCH1-Tg myocytes. Xanthine oxidoreductase inhibition abolished the difference in superoxide production but did not affect myocardial function in either group. By contrast, NOS1 inhibition abolished the differences in ICa density, Ser16 PLB phosphorylation, [Ca2+]i decay, and myocardial relaxation between genotypes. CONCLUSIONS: Myocardial GCH1 activity and intracellular BH4 are a limiting factor for constitutive NOS1 and SERCA2A activity in the healthy myocardium. Our findings suggest that GCH1 may be a valuable target for the treatment of LV diastolic dysfunction.
