Effects of chronic dietary salt loading on the renin angiotensin and adrenergic systems of rainbow trout (Oncorhynchus mykiss)

Abstract

NJ, Montpetit C. Effects of chronic dietary salt loading on the renin angiotensin and adrenergic systems of rainbow trout (Oncorhynchus mykiss). Am J Physiol Regul Integr Comp Physiol 301: R811-R821, 2011. First published June 22, 2011 doi:10.1152/ajpregu.00244.2011.-Previous studies have demonstrated that chronic dietary salt loading causes hypertension and a decreased sensitivity of the systemic vasculature to ␣-adrenergic stimulation and other hypertensive stimuli (e.g. hypercapnia) in rainbow trout (Oncorhynchus mykiss). This reduced sensitivity to hypertensive stimuli is consistent with a possible blunting of homeostatic responses normally aimed at raising blood pressure. To test this idea, we examined the consequences of long-term salt feeding and the associated hypertension on the interactive capacities of the renin angiotensin system (RAS) and adrenergic systems to elevate blood pressure in trout. Secretion of catecholamines in response to a range of doses of homologous ANG II in vivo and in situ (using a perfused posterior cardinal vein preparation) was reduced in the salt-fed fish. The reduced sensitivity to ANG II could not be explained by alterations in stored catecholamine (adrenaline or noradrenaline) levels or the general responsiveness of the chromaffin cells to depolarizing stimuli (60 mmol/l KCl). Despite the decreased responsiveness of the chromaffin cells to ANG II, plasma catecholamines were increased to a greater extent in the salt-fed fish during acute hypoxia (a condition that activates the RAS). Interestingly, the pressor effects of ANG II in vivo were actually heightened in the salt-fed fish. The increased pressor response to exogenous ANG II was likely attributable to its direct interaction with vascular ANG II receptors because the effect persisted even after blockade of ␣-adrenergic receptors. Treating fish with the vascular smooth muscle relaxant papaverine caused similar reductions in blood pressure and increases in plasma ANG II levels regardless of diet. Similarly, inhibition of angiotensin converting enzyme with lisinopril reduced blood pressure equally in control and salt-fed fish. These results indicate that, while long-term dietary salt loading blunts the response of trout chromaffin cells to ANG II, the RAS itself appears to be unaffected. Indeed, the capacity of ANG II to elevate blood pressure is not compromised nor do fish exhibit a reduced capacity to mount an acute humoral adrenergic stress response during acute hypoxia. high dietary salt; hypertension; catecholamines; chromaffin cells; angiotensin II; hypoxia; control of blood pressure ALTHOUGH EPIDEMIOLOGICAL studies (21) have revealed a significant correlation between dietary salt intake and blood pressure in humans, the underlying mechanisms have not been clearly identified (for reviews see Refs. 6 and 30). In most individuals, the vascular volume expansion associated with moderately increased levels of ingested salt is restored rapidly by increased urine production, and thus the related increases in blood pressur...

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“…It is wellknown that a variety of cardiovascular risk factors are closely associated with Ang II (21)(22)(23). The ability of Ang II to elevate blood pressure is 10∼40 times powerful than adrenaline (24). Ang II raises blood pressure through multiple factors, mainly through stimulating zona glomerulosa of the adrenal gland, promoting aldosterone secretion and sodium-water retention (20,(25)(26)(27).…”

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“…In teleost fish, catecholamine secretion is stimulated via acetylcholine release at the terminal end of nerve fibres of chromaffin cells located in the posterior cardinal vein and the head kidney (Nilsson et al, 1976; Porteus et al, 2012). Hypoxia (Porteus et al, 2012), hypotension (Perry et al, 2011; Sandblom et al, 2010), air exposure (Lennox et al, 2016; Sopinka et al, 2016), metabolic acidosis (Wood, 1991, 1994), and changes in water temperature (Currie et al, 2013) can lead to increased levels of circulating catecholamines. While sustained aerobic exercise is not correlated with changes in circulating catecholamine levels (Butler et al, 1986), increases have been observed following burst swimming exercise of fish (Primmett et al, 1986).…”

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“…In teleost fish, catecholamine secretion is stimulated via acetylcholine (ACh) release at the terminal end of nerve fibres of chromaffin cells located in the posterior cardinal vein and the head kidney (Nilsson et al 1976;Porteus et al 2012). Hypoxia (Porteus et al 2012), hypotension (Sandblom et al 2010;Perry et al 2011), air exposure (Lennox et al 2016;Sopinka et al 2016), metabolic acidosis (Wood 1991(Wood , 1994 and changes in water temperature (Currie et al 2013) can lead to increased levels of circulating catecholamines. While sustained aerobic exercise is not correlated with changes in circulating catecholamine levels (Butler et al 1986), increases have been observed following burst swimming exercise in fish (Primmett et al 1986).…”