We describe in gas anesthetized rats an oscillating intratubular pressure response, probably of vascular origin, sensitive to small physiological changes in fluid delivery to the distal tubule. The oscillation apparently indicates that an adjustment of vascular resistance is in operation, but at present it reveals neither the effector site (afferent and/or efferent arteriole) nor the effector mechanism (vasoconstriction and/or dilatation). The renin-angiotensin system seems to be involved in this phenomenon.

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SUMMARY1. The effects of different energy substrates, of low temperature, of urea, and of ouabain and ethacrynic acid were studied on the rate of renin release from viable juxtaglomerular cells during superfusion of isolated rat glomeruli.2. Neither lactate nor glutamate altered renin release rate from that observed using glucose as the sole energy substrate. Succinate 10 mM elevated release transiently but did not influence the release caused by reductions in osmolality through lowering sucrose concentration.3. Peak renin release was more prolonged and returned more slowly to control following reductions in osmolality in phosphate-Ringer than in bicarbonate-Ringer.4. At 370 C, the peak of renin release induced by hypo-osmolality was smaller and delayed, and returned earlier to control than at 300 C.5. Reduction in temperature from 30 to 40 C resulted in a 32-fold increase in basal release rate. At 40 C a 20 m-osmole/kg reduction in tonicity caused an additional 2*5-fold increase in release rate.6. Increasing superfusate osmolality with urea did not affect basal renin release but 100 mm urea suppressed the releasing effect of a 15 mM reduction in NaCl concentration.7. Ouabain (10-4M) caused a small (33+9 %, P < 0.025) transient increase in renin release. Ethacrynic acid (10-3 M) provoked a progressive increase in release reaching 100 + 15 % above control within 50 min. In the presence of both inhibitors the release provoked by hyposmolality was prolonged.8. It is concluded that renin release in vitro is a function of actively regulated cell volume and it is proposed that a similar mechanism could * Visiting scientist, from the University of Melbourne, Australia.

SUMMARY1. The effects of external medium calcium concentration, the ionophore A23187 and lanthanum on the rate of renin release in vitro were studied with particular emphasis on results obtained from isolated superfused glomeruli of rat kidneys.2. The response to reduction in superfusate calcium concentration from 2 mm was a graded and reversible increase in the rate of renin release. An increase in release was detectable at 02 mm calcium; a threefold increase was found 36 mm after a change from 2 mm calcium to calcium-free superfusate. A similar relative increase in release resulted from reductions from 0-1 mm to zero calcium, but the absolute amounts of renin released were greater in this latter series. Renin release from kidney cortical slices similarly increased in response to calcium-free incubation medium.3. The effects of A23,87 on renin release were modest. Changing from 2 mm calcium during control periods to calcium-free Ringer with A23187 added caused an attenuated and more delayed increase in release than the change to calcium-free Ringer without ionophore. This difference in response was abolished when glomeruli were superfused with 0.1 mM calcium during the preceding 1 hr control period. There was no significant difference in renin release from glomeruli exposed to calcium-free EGTARinger with and without A23187 in the 2 mm calcium series; in the 0.1 mm calcium series the increase in release following a shift to calcium-free EGTA-containing superfusate with A23187 added was significantly greater than in the absence of the ionophore.4. Addition of lanthanum (1 or 0 05 mM) to calcium-containing as well as calcium-free superfusate resulted in a significant depression of renin Some of the present data were presented in preliminary form at the VIth Int. Nephrol. Congress, Florence, 1975. Abstracts free communications no. 518. L. BAUMBACH AND P. P. LEYSSAC release. Subsequent removal of the lanthanum did not restore the rate of release unless EGTA was added; in the latter case a massive increase in renin release occurred resulting in a marked depletion of the remaining renin content of the glomeruli.5. It is concluded that calcium influences renin release by a direct action on the juxtaglomerular cells. The data support the previous suggestion that basal renin release is a function of active, calcium-dependent cell volume regulation -swelling causing an increase in the release; and further suggest that membrane-bound calcium has a direct effect on the cell membrane permeability to renin.6. The results exclude that calcium-stimulated exocytosis is responsible for basal renin release from the juxtaglomerular cells adhering to isolated glomeruli.