Beal A M
School of Biological Science, University of New South Wales, Sydney, Australia.
Arch Oral Biol. 1997 Oct-Nov;42(10-11):705-16. doi: 10.1016/s0003-9969(97)00074-5.
Mechanisms of primary fluid formation by macropodine mandibular glands were investigated in anaesthetized red kangaroos using ion-transport and carbonic anhydrase inhibitors. Bumetanide at carotid plasma concentrations of 0.005-0.1 mmol/l progressively reduced a stable, acetylcholine-evoked flow rate of 1.02 +/- 0.024 ml/min to 0.16 +/- 0.016 ml/min (mean +/- SEM). Concurrently, saliva [Na], [Cl] and osmolality decreased, [K] and [HCO3] increased and HCO3 excretion was unaffected. High-rate cholinergic stimulation was unable to increase salivary flow above 12 +/- 1.5% of that for equivalent pre-bumetanide stimulation. Furosemide (1.0 mmol/l) and ethacrynate (0.5 mmol/l) caused depression of salivary flow and qualitatively similar effects on ion concentrations to those of bumetanide. Amiloride (up to 0.5 mmol/l) caused no reduction in salivary flow rates or [Na] but decreased [K] and [Cl] and increased [HCO3]. When compared with bumetanide alone, amiloride combined with bumetanide further augmented [K] and [HCO3] and lowered [Cl], but had no additional effects on Na or flow. At the higher level, 4-acetamido-4'- isothiocyanatostilbene-2,2'disulphonic acid (SITS) (0.05 and 0.5 mmol/l) stimulated fluid output, increased [HCO3] and [protein], and depressed [Na], [K] and [Cl]. Relative to bumetanide alone, SITS given with bumetanide had no additional effects on salivary flow or electrolytes. Methazolamide (0.5 mmol/l) in combination with bumetanide curtailed the decrease in [Cl] and the increases in [K] and [HCO3] associated with bumetanide. The residual methazolamide-resistant HCO3 excretion was sufficient to support 2-6% of primary fluid secretion. It was concluded that secretion of primary fluid by the kangaroo mandibular gland is initiated mainly (> 90%) by Cl transport resulting from Na-K-2Cl symport activity. A small proportion of the fluid secretion (up to 6%) appears to be supported by HCO3 secretion. No evidence was found for fluid secretion being dependent on Cl transport involving Na/H and Cl/HCO3 antiports or on HCO3 synthesis involving carbonic anhydrase.
利用离子转运和碳酸酐酶抑制剂，在麻醉的红袋鼠身上研究了大袋鼠下颌腺产生原发性唾液的机制。当颈动脉血浆中布美他尼浓度为0.005 - 0.1 mmol/l时，能使由乙酰胆碱诱发的稳定唾液流速从1.02±0.024 ml/min逐渐降至0.16±0.016 ml/min（平均值±标准误）。同时，唾液中的[Na]、[Cl]和渗透压降低，[K]和[HCO₃]升高，而HCO₃排泄不受影响。高频率胆碱能刺激无法使唾液流速增加至超过布美他尼给药前同等刺激流速的12±1.5%。呋塞米（1.0 mmol/l）和依他尼酸（0.5 mmol/l）可使唾液流速降低，且对离子浓度的影响与布美他尼定性相似。氨氯地平（浓度高达0.5 mmol/l）不会使唾液流速或[Na]降低，但会降低[K]和[Cl]并增加[HCO₃]。与单独使用布美他尼相比，氨氯地平与布美他尼联合使用会进一步增加[K]和[HCO₃]并降低[Cl]，但对Na或流速没有额外影响。在较高浓度水平，4 - 乙酰氨基 - 4'-异硫氰酸基芪 - 2,2'-二磺酸（SITS）（0.05和0.5 mmol/l）可刺激液体分泌，增加[HCO₃]和[蛋白质]，并降低[Na]、[K]和[Cl]。相对于单独使用布美他尼，SITS与布美他尼联合使用对唾液流速或电解质没有额外影响。甲醋唑胺（0.5 mmol/l）与布美他尼联合使用可减少与布美他尼相关的[Cl]降低以及[K]和[HCO₃]升高。甲醋唑胺耐药的残余HCO₃排泄足以支持2 - 6%的原发性唾液分泌。研究得出结论，袋鼠下颌腺原发性唾液的分泌主要（>90%）由Na - K - 2Cl协同转运活性导致的Cl转运启动。一小部分（高达6%）的唾液分泌似乎由HCO₃分泌支持。未发现唾液分泌依赖于涉及Na/H和Cl/HCO₃反向转运的Cl转运或涉及碳酸酐酶的HCO₃合成的证据。
