Responsiveness of the Parotid Salivary Gland of Red Kangaroos (Macropus Rufus) to Mineralocorticoids

During both acute and chronic mineralocorticoid administration, parotid saliva was obtained by acetylcholine stimulation at rates of 1·0–1·5 ml min⁻¹ from anaesthetized red kangaroos. The Na/K ratio of saliva from chronically Na-replete kangaroos was virtually unaltered by ipsilateral intracarotid infusion of aldosterone at rates of 8, 40 or 80μgh⁻¹ for 4h, the ratio falling from 20·1 ± 1·09 to 17·5 ± 0·53 (t₆ = 2·07; NS) at 80μgh⁻¹. Kangaroos given intramuscular injection of the mineralocorticoid, deoxycorticosterone (DOCA), at rates of 0· 25 or 0· 30mgkg⁻¹ 12h⁻¹ showed a progressive fall in salivary Na/K ratio from 19· 1 ±0· 47 to 1· 76 ± 0· 41 (t₅ = 27· 4; P<0· 001) over the 21-day period of injection. The DOCA treatment caused hypertrophy of the ducts, particularly the intralobular ducts of the parotid gland. Aldosterone acetate given intramuscularly at 0· 03 mg kg⁻¹ 12h⁻¹ for 10 days also reduced the Na/K ratio of the saliva. As soon as the salivary Na/K ratio had returned to replete values, some 3– 4 days after cessation of the DOCA injections, the kangaroos were given a 5-h infusion of aldosterone. Intracarotid infusion of aldosterone at 8 μgh⁻¹ produced a near maximal fall in salivary Na/K ratio after 3 h of infusion, and increasing the infusion to 80μgh⁻¹ had little additional effect. The minimum Na/K ratio obtained at this time was 5· 7 ± 1· 04 (t₅ = 14· 21 ; P< 0· 001), which was equivalent to the ratio obtained at 3– 6 days of DOCA injection. Significant regression of the intralobular ducts occurred during the 3 days following cessation of DOCA administration; 24 days after the end of DOCA treatment duct development was approaching that of Na-replete, untreated kangaroos.

The results demonstrate that the parotid glands of kangaroos from a sodium-rich environment are almost unable to respond to acute fluctuations in endogenous aldosterone levels; that chronically high levels of mineralocorticoids cause hypertrophy of the sodium-transporting ducts of the parotid gland, which results in an increasing ability to reduce the Na/K ratio of the saliva; and that responsiveness to mineralocorticoids declines rapidly in the absence of high mineralocorticoid levels due to regression of the ducts.