Fitzsimons J T
Proc R Soc Lond B Biol Sci. 1980 Oct 29;210(1178):165-82. doi: 10.1098/rspb.1980.0126.
Several neuroactive peptides have been implicated in thirst and sodium appetite in different species; three peptides are considered here. The best established of these is the octapeptide angiotensin II, which when administered systemically or intracranially causes completely normal drinking behaviour in all vertebrates tested, including many mammals, four or five birds, one reptile and one bony fish. In the rat, in which the original experiments were carried out, injection of a few femtomoles of angiotensin II caused a brisk drinking response within a minute or so of injection at a time of day when the animal would usually be resting. The response is usually completed within 10 min and after the larger doses the amounts of water taken may approach what the animal would normally drink in the course of 24 h. Another response to intracranial angiotensin, seen so far only in the rat, is an increase in sodium appetite. This is slower in onset than thirst, lasts for many hours and the response tends to become greater with repeated injections of hormone. Naturally occurring increases in sodium appetite may be caused by angiotensin generated by the action of cerebral isorenin. A second neuroactive peptide that affects thirst is the undecapeptide eledoisin, which is found in the salivary glands of certain Mediterranean cephalopods. Eledoisin and, to a lesser extent, substance P, with which it is related, are potent intracranial dipsogens in the pigeon, producing behaviour that is indistinguishable from that produced by angiotensin. However, in contrast to the stimulatory action of angiotensin on drinking behaviour in all other vertebrate species tested, these substances specifically depress drinking in the rat. A third peptide that has been implicated in thirst is antidiuretic hormone (ADH). This hormone has a profound but indirect effect on water intake in diabetes insipidus. In the dog, however, ADH in physiological amounts may influence thirst mechanisms by direct action on the central nervous system. In this species, but not in the rat, ADH lowers the threshold of thirst in response to osmotic stimulation and also to infusion of angiotensin. Of these three peptides, and others not mentioned here, angiotensin II has the best claim to be regarded as a neuroactive peptide. It alone is always dipsogenic when injected into the brain and it also stimulates sodium appetite. Whether the effects of angiotensin, on thirst and sodium appetite should be regarded as manifestations of the activity of a classical endocrine system, of a paracrine system, of a neurotransmitter system, or of all of these, cannot be decided at present. But these actions of angiotensin, when considered with its other actions on the distribution and conservation of body fluid, show that the hormone is intimately concerned in extracellular fluid volume control.
几种神经活性肽与不同物种的口渴及钠食欲有关；这里讨论三种肽。其中最知名的是八肽血管紧张素II，当全身给药或颅内给药时，它能使所有受试脊椎动物（包括许多哺乳动物、四五种鸟类、一种爬行动物和一种硬骨鱼）产生完全正常的饮水行为。在最初进行实验的大鼠中，注射几飞摩尔的血管紧张素II会在动物通常休息的一天中的某个时间点注射后一分钟左右引发快速的饮水反应。反应通常在10分钟内完成，大剂量注射后摄入的水量可能接近动物在24小时内正常的饮水量。对颅内血管紧张素的另一种反应，目前仅在大鼠中观察到，是钠食欲增加。这种反应的起效比口渴慢，持续数小时，并且随着激素的反复注射反应往往会增强。钠食欲的自然增加可能由脑内异肾素作用产生的血管紧张素引起。第二种影响口渴的神经活性肽是十一肽eledoisin，它存在于某些地中海头足类动物的唾液腺中。Eledoisin以及与其相关程度较低的P物质，在鸽子中是有效的颅内致渴剂，产生与血管紧张素引起的行为无法区分的行为。然而，与血管紧张素对所有其他受试脊椎动物物种饮水行为的刺激作用相反，这些物质在大鼠中会特异性地抑制饮水。第三种与口渴有关的肽是抗利尿激素（ADH）。这种激素对尿崩症患者的水摄入有深远但间接的影响。然而，在狗中，生理量的ADH可能通过直接作用于中枢神经系统来影响口渴机制。在这个物种中，但在大鼠中不是这样，ADH会降低对渗透压刺激以及血管紧张素输注的口渴阈值。在这三种肽以及这里未提及的其他肽中，血管紧张素II最有资格被视为神经活性肽。单独注射到脑内时，它总是具有致渴作用，并且还能刺激钠食欲。血管紧张素对口渴和钠食欲的影响应被视为经典内分泌系统、旁分泌系统、神经递质系统或所有这些系统活性的表现，目前尚无法确定。但是，当将血管紧张素的这些作用与其对体液分布和保存的其他作用一起考虑时，表明该激素与细胞外液量的控制密切相关。
