Role of kinins and prostacyclin in blood pressure regulation

The main vasodepressor hormone systems are the kallikrein-kinin systems and the vascular prostacyclin. Kallikreins release kinins which are the biological active compounds of the kallikrein-kinin systems. Kinins are one of the most potent vasodilators reducing systemic blood pressure by diminution of vascular resistance. The reduction in blood pressure is strongly dose related. Prostacyclin develops similar effects on blood pressure as kinins. There is a close relationship between kinins and prostacyclin since kinins stimulate prostacyclin synthesis very effectively. In arterial hypertension there is a lack in kallikrein-kinin and prostacyclin activity. This could also be shown under experimental conditions in spontaneously hypertensive and in Dahl salt-sensitive rats. In clinical studies these experimental results were confirmed in primary hypertension. The blood pressure response to exogenous vasodepressor hormones is increased in hypertensives suffering from reduced endogenous vasodilator activity. In the knowledge of reduced vasodilator activities in primary hypertension the stimulation of kinins by prostacyclin will be of major interest in the management of primary hypertension. In the last years some drugs have been investigated with regard to their kinin prostacyclin stimulating effect, but only angiotensin converting enzyme inhibitors, linolenic acid and cicletanin seemed to induce therapeutic prostacyclin stimulation. However, it remains unclear whether these drugs develop their blood pressure lowering effect by stimulation of the discussed vasodilators or by some other effect.