Interactions of Prostaglandins with the Kallikrein-Kinin and Renin-Angiotensin Systems

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Abstract
1. Prostaglandins together with the kallikrein-kinin system comprise a major vasodepressor system. 2. Prostaglandins can antagonize the actions of pressor hormones and the adrenergic nervous system. They also contribute to the blood pressure-lowering effects of kinins by enhancing the vasodilator and diuretic-natriuretic actions of the peptide. 3. Deficiency of the vasodepressor system may lead to hypertension without any increase in the basal activity of the blood pressure-elevating system. 4. Increased activity of the renin-angiotensin and adrenergic nervous systems evoked by stressful stimuli enhances prostaglandin synthesis, which protects organ function from excessive effects of angiotensins and catecholamines. 5. Several findings preclude unqualified acceptance of prostacyclin as the only important vascular prostaglandin: first, in some blood vessels prostacyclin is not the principal product of enzymic transformation of the cyclic endoperoxides. Secondly, prostaglandin E2, which is also synthesized in the vascular wall, may be the principal modulator prostaglandin. Lastly, prostacyclin may be transformed by some tissues to 6-keto-prostaglandin E1, a more stable product having similar biological potency. 6. Synthesis of prostaglandins by the kidney is important to mechanisms which control renin release and renal vascular resistance.

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