Several sources of evidence have shown that the renal kallikrein-kinin system is altered in various forms of hypertension. The impact of these results is limited by the possible dependence of urinary kallikrein excretion on the effective renal mass which might be reduced in hypertension due to nephrosclerosis and/or the underlying inflammatory kidney disease. Therefore, investigations of the kallikrein-kinin system in other kallikrein-containing tissues might be of interest. In normal subjects, the kallikrein excretion of parotid saliva is inversely related to flow rate and sodium concentration. An increased salivary kallikrein concentration is found in human essential, adrenomedullary and renoparenchymal hypertension associated with impaired kidney function. In contrast to the kallikrein secretion, the flow-dependent sodium concentration of parotid saliva is reduced in human essential and renoparenchymal hypertension which indicates an enhanced sodium reabsorption in the glandular duct system. Furthermore, in most forms of hypertension, there is a tendency of higher potassium levels in the saliva. The pathogenesis of the enhanced glandular kallikrein secretion in hypertension is discussed with regard to a counter-regulatory mechanism in hypertension as well as a sympathicoadrenergic activation. The enhanced sodium reabsorption in the duct system during various forms of hypertension could be the cause as well as the consequence of the high blood pressure.