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The biosynthesis of PGE2, PGF2, PGI2 alpha from 14C-arachidonic acid and the catabolism of 3H--PGF1 alpha and 3H--PGE2 were studied in kidney, aorta and lung homogenates of young (1.5 months) and adult (3.5 months) Wistar rats. An increased synthesis of PGE2 was found in aorta and kidneys and PGI2 in lungs and heart of young rats. PGE2 alpha synthesis in kidneys and aorta underwent no alteration with age. The 3H--PGE2 catabolism in lungs and kidneys was more intensive in young rats whereas the 3H--PGF1 alpha degradation did not differ in various age groups but somewhat decreased with age in lungs. Close correlation was found between the biosynthetic coefficients PGF/PPE in kidneys and the AP level in young rats. A reciprocal interrelationship was found between the biosynthetic and the catabolic coefficients PGF/PGE in kidney, aorta and lungs of young and adult rats. This results in a balance of synthesis and catabolism of prostaglandins in kidney and lungs which prevents release of great quantities of prostaglandins from the sites of their synthesis into the systemic circulation. In other words, the processes of biosynthesis and catabolism of prostaglandins in the organism maintain a constant level of these biologically active substances in the systemic circulation.

The biosynthesis of corticoids from exogenic tritated progesteron with and without addition of progstaglandin E2 in incubation medium was studied in rabbits in spring and in summer. C-14 inclusion into aldosteron, cortisone, and 11-dehydrocorticosterone in the spring rabbits was considerably higher than in the summer ones. Prostaglandin E2 suppressed the biosynthesis of the final fraction of corticosteroids in the spring rabbits and did not change the C-14 inclusion into corticosteroids in summer.

The structural component of resistance and vascular reactivity in posterior half of the rat body were studied in intact normotensive animals as well as in rats with hereditary hypertension. Chemical desympathization in the spontaneously hypertensive rats reduced the arterial pressure, cardiac outflow, structural component of the resistance and reactivity to noradrenaline, these parameters remaining, however, higher than in normal intact rats. 2-week hypoxic adaptation of young spontaneously hypertensive rats hinders increasing of the arterial pressure and structural component of resistance. The augmented sympathetic activity along with other factors (genetic, humoral) seem to increase the structural component of resistance and arterial pressure in spontaneously hypertensive rats.

The biosynthesis of PgF2, 6-keto-PgF1 alpha and TxB2 from endogenous precursor in vitro by the rat kidney cortex and medulla in ontogenesis was found to be highest at young age reducing from papillae to kidney cortex. The main product of the biosynthesis in kidney medulla of young and adult rats was PgE.

The hemodynamics was measured under resting conditions in chemically sympathectomized (with guanethidine) and control rats at 2.5, 4.0 and 8.0 months of age. In sympathectomized rats, the cardiac output (CO) was 23, 36 and 53% higher than in control, resp., whereas total peripheral resistance (TPR100) was 22, 27 and 42% lower, resp. The increase in CO was the result of elevation in the stroke volume. In sympathectomized rats, the TPR100 did not significantly change with age in contrast with control rats, and at 1.5 months of age an elevation of vascular resistance at maximal vasodilatation was observed in perfused isolated preparations. This difference diminished with age and disappeared at 4 or 8 months of age. The increase in structurally based resistance of vessels of sympathectomized rats at 1.5 months of age seems to be caused by reduced density of small resistance vessels.