Gradin K, Persson B
Department of Pharmacology, University of Göteborg, Sweden.
Acta Physiol Scand. 1987 Oct;131(2):273-81. doi: 10.1111/j.1748-1716.1987.tb08237.x.
Spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats were maintained on tap water or 1.5% NaCl for 3 weeks. During the high sodium regime 24-h urinary sodium excretion increased 10-fold and the basal blood pressure increased in the SHR. After 3 weeks the rats received arterial (carotid artery), venous and bladder catheters (suprapubic). Saline was infused continuously and in conscious rats atrial natriuretic peptide (alpha-hANP) was administered as bolus injections (8 and 16 nmol kg-1) and the blood pressure and heart rate and the urinary excretions of sodium, potassium (flame photometry), noradrenaline and dopamine (HPLC) were followed at 5-min intervals. The administration of ANP caused a short-lasting blood pressure reduction, tachycardia, diuresis and increased urinary excretions of sodium, potassium, noradrenaline and dopamine. The blood pressure responses to ANP did not differ between the rat strains, irrespective of the diet. The natriuresis and diuresis to ANP was reduced in animals on a high sodium diet, especially in the SHR. This may be interpreted as a down-regulation of target organ responsiveness to ANP during a high sodium diet and the inappropriately large decrease in the responsiveness that was observed in the SHR may be related to increase in blood pressure during the high sodium diet.
自发性高血压大鼠(SHR)和Wistar-Kyoto(WKY)大鼠分别饮用自来水或1.5%氯化钠溶液3周。在高钠饮食期间,SHR的24小时尿钠排泄量增加了10倍,基础血压升高。3周后,给大鼠插入动脉(颈动脉)、静脉和膀胱导管(耻骨上)。持续输注生理盐水,并对清醒大鼠静脉推注心房利钠肽(α-hANP,剂量为8和16 nmol·kg-1),每隔5分钟记录一次血压、心率以及钠、钾(火焰光度法)、去甲肾上腺素和多巴胺(高效液相色谱法)的尿排泄量。给予ANP可导致血压短暂降低、心动过速、利尿,并增加钠、钾、去甲肾上腺素和多巴胺的尿排泄量。无论饮食如何,大鼠品系之间对ANP的血压反应无差异。高钠饮食组动物对ANP的利钠和利尿作用减弱,尤其是SHR。这可能被解释为高钠饮食期间靶器官对ANP的反应性下调,而在SHR中观察到的反应性过度大幅降低可能与高钠饮食期间血压升高有关。