LITMIR.BIZ

CHAPTER 15 Water and electrolyte balances in ageing

       Stewart G. Albert1 and Alexis M. McKee2

      ¹ Division of Endocrinology, Diabetes & Metabolism, Department of Internal Medicine, Saint Louis University School of Medicine, St Louis, Missouri, USA

      ² Division of Endocrinology, Metabolism & Lipid Research, Washington University School of Medicine, Saint Louis MO , USA

Introduction

      Water and volume homeostasis is under meticulous control through a complex interrelationship of the hypothalamus‐posterior pituitary and the renin‐angiotensin‐adrenal axis.^1,2 The elderly, however, are at increased risk for syndromes of both hyponatremia and hypernatremia, and these disorders are associated with further clinical complications.^3–5 Therefore, it is important to understand the physiology involved in normal water homeostasis, the potential problems associated with ageing, and the possible therapeutic modalities to correct these disorders.

Normal physiology

There is dual control of water and serum osmolality.^1,2 The hypothalamus and posterior pituitary are involved in water retention, and the renin‐angiotensin‐aldosterone axis is involved in sodium retention. The supraoptic and paraventricular nuclei of the hypothalamus respond primarily to increases in serum osmolality with the release of arginine vasopressin (AVP), also known as antidiuretic hormone (ADH) (see Figure 15.1). The release of ADH is mediated through changes in an electrochemical gradient in these magnocellular neurons to maintain serum osmolality at 285±2 mOsm/kg. These neurons are also under the influence of neurotransmitters such as acetylcholine (i.e. through the vagus nerve, as described below), catecholamines, opioids, and angiotensin. Small changes in osmolality allow for acute adjustment in serum ADH levels with resulting water retention or free water clearance by the kidney.^1,2

There is also parallel autonomic nervous system regulation of water retention in which vascular receptors respond to decreases in total body water and changes in organ perfusion. There are high‐pressure (blood pressure) baroreceptors in the carotid sinus and aortic arch and low‐pressure stretch receptors in the cardiac atria and pulmonary venous systems. Both types of receptors transmit regulatory impulses via the vagus nerve to the hypothalamic neurons to stimulate ADH in the event of low effective arterial blood volume (EABV).^1,2 Pathophysiological states of diminished EABV stimulate the release of ADH above that due to osmolality. Thus, ADH may be ‘appropriate’ for the diminished EABV but appears inappropriate for serum osmolality. Conditions that may increase ADH release are shown in Figure 15.2. The baroreceptors may respond to changes in blood pressure associated with volume loss (gastrointestinal losses or diuretic‐induced volume loss), decreased intravascular volume in hypoalbuminemic oedema‐forming states (ascites or nephrotic syndrome), orthostatic hypotension (due to adrenal cortical insufficiency, mineralocorticoid insufficiency, or autonomic neuropathy), and decreased arterial perfusion (due to reduced cardiac output such as cardiac tamponade, cardiomyopathy, or severe hypothyroidism). Decreased stretch of the volume receptors in the cardiac left atrium may occur in states of low EABV as described above. Diminished stretch in these receptors may also ‘appear’ as low pressure due to restrictions in pulmonary vascular return to the heart, as a result of increased intra‐thoracic pulmonary pressure in severe reactive airway disease, or with mechanical ventilation.^1,2

Vasopressin activates V2 receptors in the distal collecting tubules of the kidney (Figure 15.3). In the absence of ADH, the tubule is impermeable to water transport. As shown in Figure 15.3, 15 to 30 litres/day of free water may reach the distal collecting tubules. The entire volume may be potentially lost through the urine in central diabetes insipidus (lack of renal concentration ability due to partial or complete ADH deficiency). In the presence of ADH, water is transported from the intraluminal collecting duct through aquaphorin‐2 channels, across a concentration gradient to the intra‐renal capillaries to reabsorb free water. The concentration gradient is derived at the loop of Henle through the medullary urea countercurrent system. The urea is freely permeable into the collecting duct. In the presence of ADH, the kidney may concentrate the urine to a volume of 0.7 litres per day with an osmolality of 600–1200 mOsm/kg, made up primarily of the secreted urea.

Thirst, the conscious desire to drink, is another active component of water retention.^6,7 Thirst is under the control of a closely located series of hypothalamic neurons in the organum vasculosum of the lamina terminalis (OVLT).^1,2 This area is independent of the blood‐brain barrier. These neurons, like ADH‐secreting neurons, are under similar influence of serum osmolality, neurotransmitters, and angiotensin. Normally, thirst lags behind ADH release in response to increases in serum osmolality. The threshold of thirst, as measured on a visual analogue scale or the volume of water ingested, is approximately 10 mOsm/kg greater than the ADH threshold.^5,6 There are pathological conditions in which thirst may be independent of ADH release. Thirst is inappropriately diminished in response to serum osmolality in central nervous system conditions characterized by a reset or diminished thirst response to serum osmolality (essential hypernatremia) or in complete lack of thirst response to severe hypernatremia (adipsia) (Figure 15.4).⁶