Bie P, Sandgaard N C
Department of Physiology and Pharmacology, University of Southern Denmark, Odense, DK-5000 Odense, Denmark.
Am J Physiol Regul Integr Comp Physiol. 2000 Jan;278(1):R1-R10. doi: 10.1152/ajpregu.2000.278.1.R1.
The relative importance of systemic volume, concentration, and pressure signals in sodium homeostasis was investigated by intravenous infusion of isotonic (IsoLoad) or hypertonic (HyperLoad) saline at a rate (1 micromol Na(+) x kg(-1) x s(-1)), similar to the rate of postprandial sodium absorption. IsoLoad decreased plasma vasopressin (-35%) and plasma ANG II (-77%) and increased renal sodium excretion (95-fold), arterial blood pressure (DeltaBP; +6 mmHg), and heart rate (HR; +36%). HyperLoad caused similar changes in plasma ANG II and sodium excretion, but augmented vasopressin (12-fold) and doubled DeltaBP (+12 mm Hg) without changing HR. IsoLoad during vasopressin clamping (constant vasopressin infusion) caused comparable natriuresis at augmented DeltaBP (+14 mm Hg), but constant HR. Thus vasopressin abolished the Bainbridge reflex. IsoLoad during normotensive angiotensin clamping (enalaprilate plus constant angiotensin infusion) caused marginal natriuresis (9% of unclamped response) despite augmented DeltaBP (+14 mm Hg). Cessation of angiotensin infusion during IsoLoad immediately decreased BP (-13 mm Hg) and increased glomerular filtration rate by 20% and sodium excretion by 45-fold. The results suggest that fading of ANG II is the cause of acute "volume-expansion" natriuresis, that physiological ANG II deviations override the effects of modest systemic blood pressure changes, and that endocrine rather than hemodynamic mechanisms are the pivot of normal sodium homeostasis.
通过以与餐后钠吸收速率相似的速率（1微摩尔钠×千克⁻¹×秒⁻¹）静脉输注等渗（IsoLoad）或高渗（HyperLoad）盐水，研究了全身容量、浓度和压力信号在钠稳态中的相对重要性。IsoLoad降低了血浆血管加压素（-35%）和血浆血管紧张素II（-77%），并增加了肾钠排泄（95倍）、动脉血压（ΔBP；+6 mmHg）和心率（HR；+36%）。HyperLoad在血浆血管紧张素II和钠排泄方面引起了类似的变化，但增加了血管加压素（12倍），使ΔBP加倍（+12 mmHg），而心率不变。血管加压素钳夹期间（持续输注血管加压素）的IsoLoad在ΔBP增加（+14 mmHg）时引起了相当的利钠作用，但心率保持不变。因此，血管加压素消除了 Bainbridge 反射。正常血压的血管紧张素钳夹期间（依那普利拉加持续输注血管紧张素）的IsoLoad尽管ΔBP增加（+14 mmHg），但仅引起轻微的利钠作用（未钳夹反应的9%）。IsoLoad期间停止血管紧张素输注立即降低了血压（-13 mmHg），并使肾小球滤过率增加了20%，钠排泄增加了45倍。结果表明，血管紧张素II的消退是急性“容量扩张”性利钠的原因，生理性血管紧张素II偏差优先于适度全身血压变化的影响，并且内分泌而非血流动力学机制是正常钠稳态的关键。
