Cation excretion and kallikrein secretion by the rat parotid gland in various hypertensive models.

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The major salivary glands are distinguished by a high kallikrein content, localized particularly in regions with intense electrolyte transport (the apical border of striated duct cells and the luminal border of the main excretory ducts). For this reason we used the parotid gland as a test model for investigations on electrolyte (sodium and potassium) and kallikrein transport in various forms of experimental hypertension [spontaneously hypertensive rats, renovascular (two-kidney one-clip) hypertension, and deoxycorticosterone trimethylacetate (DOCA)-salt hypertension]. As compared with values for the controls, the sodium concentration in parotid saliva was decreased in all hypertensive models studied, indicating enhanced sodium reabsorption in the glandular duct system. In DOCA-salt hypertension the flow rate dependency of the sodium concentration was preserved. In contrast, in genetic and renovascular hypertension, the decreased sodium concentration was independent of the salivary flow rate. Salivary potassium concentration showed an inverse relationship to sodium level and was slightly increased in DOCA-salt and renovascular hypertension. In genetic hypertension potassium concentration in saliva was lowered. Salivary kallikrein activity was enhanced in all forms of hypertension studied, with the highest increase in genetic hypertension (factor 3.5), followed by DOCA-salt hypertension (factor 3.0) and finally by renovascular hypertension (factor 2.5). The pathogenesis of the exaggerated kallikrein secretion observed in hypertension is discussed with regard to a counterregulatory mechanism as well as sympathicoadrenergic activation.(ABSTRACT TRUNCATED AT 250 WORDS)