Abstract
Aging results in decreased fluid intake following dehydration and other dipsogenic stimuli; similar reductions in sodium intake have also been observed with aging. Given that cyclooxygenase (COX)-derived prostanoids are elevated in aged rats in the midbrain and proinflammatory prostanoids are known to decrease fluid intake in dehydrated rats, the aim of this study was to determine if the reductions of fluid intake and sodium intake in aging are mediated by proinflammatory eicosanoid signaling. Therefore, we examined the effect of acute COX inhibition in adult (4 months-old) and aged (30 months-old) rats prior to ingestive behavior challenges. COX inhibition, using acetylsalicylic acid (ASA), increased fluid intake in aged, but not adult, rats in response to 24-h dehydration. ASA had no effect on salt intake following sodium depletion and ASA did not change basal fluid or sodium consumption in either age group. Hypothalamic COX-1 and -2, prostaglandin E synthase (PGES) and inducible nitric oxide synthase (iNOS) mRNA expression were all elevated in aged animals, leading to elevated PGE2 levels. COX expression in the hypothalamus was reduced by ASA treatment in rats of both ages resulting in reduced PGE2 levels in aged ASA treated animals. These data indicate that the reduced fluid intake that occurs in aging is due to increased COX-PGE2-mediated inflammation. However, the reduced sodium intake in these animals appears to occur via an alternate mechanism.
Highlights
Aging significantly impairs fluid and sodium balance in mammals (Phillips et al, 1984; Thunhorst and Johnson, 2003); these impairments result from alterations to both behaviorally-mediated intake (Thunhorst et al, 2009) and reduced renal function and renin-angiotensin system (RAS) activity (Ledingham et al, 1987; Antunes-Rodrigues et al, 2004)
All groups had greater sodium intake following depletion than at baseline (p < 0.05), 2-h 0.5 M NaCl solution intake was lower in aged rats than in adult rats (p < 0.05; see Figure 2D)
Aging leads to a significant decline in fluid intake in response to dipsogenic stimuli (Silver et al, 1991; Whyte et al, 2004; McKinley et al, 2006) and sodium intake in response sodium depletion and angiotensin converting-enzyme (ACE) inhibition or sodium depletion (Rowland et al, 1996; Thunhorst and Johnson, 2003)
Summary
Aging significantly impairs fluid and sodium balance in mammals (Phillips et al, 1984; Thunhorst and Johnson, 2003); these impairments result from alterations to both behaviorally-mediated intake (Thunhorst et al, 2009) and reduced renal function and renin-angiotensin system (RAS) activity (Ledingham et al, 1987; Antunes-Rodrigues et al, 2004). Prostaglandins (PG) are produced when cyclooxygenase (COX) enzymes metabolize polyunsaturated long-chain fatty acids to prostaglandin (PG) H; PG synthases metabolize PGH into active PGs. Suppression of fluid intake in response to dehydration occurs following administration of E series prostaglandins (Goldstein et al, 1979; Pérez Guaita and Chiaraviglio, 1980). There are additional changes related to inflammatory signals with aging including an up-regulation of inducible (i) nitric oxide synthase (NOS; Wu et al, 1997; Adachi et al, 2010), a COX activator (Salvemini et al, 1993). Together, these observations may indicate involvement of prostanoids in the reduced fluid intake that occurs with aging
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