1. The role of the renal sympathetic nerves in the urinary sodium excretion response to ‘mental stress’ in spontaneously hypertensive rats (SHR) and in Wistar-Kyoto normotensive (WKY) rats was examined. Urinary sodium excretion was measured during ‘rest’ and during a 20 min period of ‘mental stress’ in intact rats and in renal denervated rats. Under similar conditions renal sympathetic activity was also measured in a separate group of rats.
2. Urinary sodium excretion fell more during the stress period in SHR (-64 ± 5%) than in WKY rats (-34 ± 7%), despite a greater arterial pressure increase in SHR. This greater decrease in sodium excretion appeared to result from both a more pronounced reduction in GFR and a greater increase in tubular sodium reabsorbtion.
3. Renal sympathetic nerve activity, which was higher at rest in SHR than in WKY rats, increased much more in SHR than in WKY rats during stress. This may explain the greater reduction in sodium excretion in SHR during stress, because renal denervation almost abolished this latter response.
4. The neurogenically elicited renal response might contribute in an important way to the early development of SHR hypertension. Renal denervation, as well as attenuating sodium retention, also delays the pressure rise in the young SHR.
5. The initial tachycardia after mental stress gradually subsided towards the end of the stress period in SHR, whereas renal sympathetic activity remained elevated. This indicates that the increase in heart rate, if anything, may underestimate the true extent of sympathetic activation in for example the renal and splanchnic regions during arousal.