Neuroendocrine changes and natriuresis in response to social stress in rats.

Sympathetic activation is detected by the tachycardic, hypertensive and hyperthermic responses during social conflicts in rodents and primates. Sympathetic nervous system activation promoting sodium retention has long been recognized to play a significant role in the development and maintenance of salt-sensitive hypertension. The objective was to investigate neuroendocrine activation and renal sodium excretion in response to chronic social stress. Male Wistar rats were subjected to social stress in accordance with the resident-intruder paradigm. Intruder rats were subjected to social confrontation once daily for 6 days. After the last confrontation, plasma corticosterone and urinary catecholamines were determined to assess the neuroendocrine activation. Plasma aldosterone, plasma and urinary creatinine, Na(+) , K(+) and urinary volume were also measured. Chronic social stress increased the urinary norepinephrine, dopamine and plasma corticosterone levels, with no changes in epinephrine levels. On the other hand, high plasma aldosterone levels and low urinary sodium excretion without differences in creatinine clearance were observed. In conclusion, social stress had a strong antinatriuretic effect, which is coincident with noradrenergic and corticoadrenal activation and an increase in plasma aldosterone levels. Activation of these factors may promote sodium retention, which has long been recognized to play a significant role in the development and maintenance of hypertension.

Renal mechanisms involved in stress-induced antinatriuresis and antidiuresis in rats.

The present study was conducted to investigate if changes in sodium and water excretion in stressed animals were due to modifications in the glomerular filtration rate (GFR) and to determine the participation of angiotensin II (Ang II) and alpha and beta-adrenoceptors on sodium and water renal excretion in rats subjected to immobilization stress (IMO). Male Wistar rats (250-300 g) were randomly separated into five different groups and vehicle (0.9% NaCl) via intraperitoneal (i.p.) or propanolol (3 mg/kg i.p.) or captopril (6 mg/kg i.p.) or yohimbine (3 mg/kg i.p.) or prazosin (1 mg/kg i.p.) were injected respectively. During experimental measurements, the animals were kept in metabolic cages for 6 h and sodium, potassium and water renal excretion and saline (1.5% NaCl) and water intake were determined at day 1 (drug effect) and day 7 (drug + IMO effects). GFR was measured by creatinine clearance in control and IMO rats. A stress-induced antinatriuresis and antidiuresis was reversed by alpha 1 and alpha 2-adrenoceptor antagonists, while captopril inhibited only the antidiuresis and propranolol had no effect on either parameter. No differences were observed in creatinine clearance in the studied groups. Since yohimbine blocks alpha 2-adrenoceptors and prazosin blocks alpha 1-adrenoceptors and alpha 2B-adrenoceptors, the stress-induced renal sodium reabsorption mainly could be attributed to alpha 2B-adrenoceptors. The present results indicate that beta-adrenoceptors do not participate in this response and, Ang II only reverses the antidiuresis and shows a slight participation in antinatriuresis. The increment in sodium and water reabsorption caused by IMO occurred without changes in the glomerular filtration rate.

Renal excretion and saline intake during post-stress immobilization period in rats.

An experiment in which the rats access either to 0.5% or 1.5% saline was designed in order to further characterise the relationship between sodium intake and renal excretion after acute immobilization stress. A saline solution for 3 days was provided to the rats previous to the experimental day. On that day, after finishing acute immobilization stress, all variables under observation were measured every 6 h for 24 h. These periods were denominated as follows: T1 (12.00 to 18.00 h), T2 (18.00 to 24.00 h), T3 (24.00 to 06.00 h) and T4 (06.00 to 12.00 h). Acute immobilization stress reduced sodium renal excretion in both T1 and T2. Sodium intake in acute immobilization stress rats was lower than in control rats during all observed periods, while the urine volume was only reduced in the stressed animals in T1. These results were similar in both saline solution concentrations. A good correlation was observed between sodium intake and sodium excretion in control rats having access to either 0.5% or 1.5% saline as well as in stressed rats having access to 0.5% saline, this correlation was not observed in stressed rats with 1.5% saline. This suggests that stress impaired the renal capability of rats to handle high sodium but not a slight sodium overload. The inability of the kidney to excrete sodium may be critical to reduce sodium intake after acute immobilization stress.