Inhibition of Nitric Oxide Synthase 1 Induces Salt-Sensitive Hypertension in Nitric Oxide Synthase 1α Knockout and Wild-Type Mice.

摘要: We recently showed that α, β, and γ splice variants of neuronal nitric oxide synthase (NOS1) expressed in the macula densa NOS1β accounts for most NO generation. have also demonstrated mice with deletion NOS1 specifically from developed salt-sensitive hypertension. However, global knockout (NOS1KO) strain is neither hypertensive nor salt sensitive. This NOS1KO actually an NOS1αKO model. Consequently, we hypothesized inhibition induces C57BL/6 wild-type (WT) were implanted telemetry transmitters divided into 7-nitroindazole (10 mg/kg/d)-treated nontreated groups. All fed a normal (0.4% NaCl) diet 5 days, followed by high-salt (4% NaCl). generation was inhibited >90% WT treated 7-nitroindazole. Glomerular filtration rate conscious increased ≈ 40% after both mice. In response to acute volume expansion, glomerular rate, diuretic natriuretic significantly blunted Mean arterial pressure had no significant changes diet, but 15 mm Hg similarly conclude NOS1β, not NOS1α, plays important role control sodium excretion hemodynamics either or chronic loading.