A Release of Renin From Dog Kidney Cortex Slices

Abstract

A release of renin from kidney cortex slices in vitro was first reported by the present authors (1). Recently, the renin release from kidney slices of rats, pretreated with de oxycorticosterone acetate, clipping of renal artery, bleeding or decapitation, was shown by Jong (2) ' and BoCovic et al. (3). In their experiments, the fundamental process of renin release has not been made clear. In our previous paper, it was pointed out that renin is released from dog kidney slices into an incubation medium depending on the temperature and pH of the medium and about 10% of renin contained in the original slices is released within 60 minutes of incubation.Presently, the effects of metal ions in the incubation medium and atmosphere on renin release were studied. From the present findings, it is assumed that renin is re leased, partialy included in the renin granule, into the incubation medium. Further study was made on the release of several enzymes found in other cell particles to compare the releasing pattern of renin from slices. MATERIALS AND METHODS Preparation of the kidney cortex slicesMongrel dogs weighing 10 to 20 kg were used. Their kidneys were removed under pentobarbital anesthesia and immediately washed by gentle infusion of cold Krebs' bi carbonate solution through the renal artery until the solution coming out from the renal vein became colourless. After removal of the capsule, the kidney was cut longitudinally through the hilus, and cortex slices, 0.4 mm thick, were prepared with a razor blade under low temperature. Preparation of renin substrate Male mongrel dogs weighing 10 to 20 kg, were anesthetized with pentobarbital. Following heparinization (100 U/kg, i.v.) both kidneys were removed to reduce circu lating renin (4) and to increase renin substrate in plasma (5, 6). About 4 hours later the blood was slowly drawn from the carotid artery. The plasma was added by solid ammonium sulfate at a final concentration of 30% saturation and then pH was adjusted

Extracellular calcium exerts a dual effect on renin secretion from isolated mouse juxtaglomerular cells

“…This stimulatory effect resembles the classic effect of calcium in secretory cells in which elevations of calcium initiate, facilitate or maintain exocytotic processes [27]. In fact there are also a few reports on a stimulatory effect of calcium or calcium ionophores on renin secretion [13,17,24,26]. It could be speculated, in the light of our results, that in those instances the stimulatory effect of calcium may have overridden an inhibitory effect of calcium on renin secretion.…”

“…Unlike other enCorrespondence to: A. Kurtz docrine and exocrine cells, in which a rise of calcium initiates, facilitates, or maintains secretory activity [27], an increase in [Ca]~ is thought to inhibit secretion from JG cells, a phenomenon that is referred to as the "calcium paradox" [14]. This indirect evidence results from observations that renin secretion is (a) inhibited by calcium-mobilizing hormones [34,35], (b) inversely related to the extracellular calcium concentration [10,12,15,18,19,26], (c) inhibited by manoeuvres that are thought either to enhance calcium entry or to inhibit calcium extrusion [4-6, 9, 25, 28], and (d) enhanced by manoeuvres thought either to inhibit intracellular calcium release or calcium influx [i, 2,6]. It is an open question whether calcium has a unique directly inhibitory effect on exocytosis of secretory granules in JG cells or has, rather as it has in other secretory cells, a fusogenic effect that is overriden by a secondary calcium-dependent effect, which in turn acts inhibitorily in JG cells.…”

“…Another interpretation is based on the existence of calcium-activated chloride channels, which provide the basis for a powerful regulation of the JG cell volume [21], which in turn is known to influence renin secretion strongly [30]. That the inhibitory effect of calcium is not clear-cut is also suggested by a few studies reporting stimulation rather than inhibition of renin secretion by extracellular calcium or calcium ionophores [13,17,24,26].…”

Reversible hypertension caused by calcium overloading in a patient with postoperative hypoparathyroidism.

“…In the 7th hospital week, a calcium infusion test was performed in the morning after an overnight fast. Calcium was infused as calcium (Morimoto et al, 1970;Michelakis, 1971;Chen and Poisner, 1976). However, calcium infusion performed when the patient became normocalcemic, normoreninemic and normotensive did not increase PRA in spite of an increase in serum calcium.…”

Stimulation of renin release from dog renal cortical slices with L-isoproterenol and dibutyryl cyclic adenosine 3',5'-monophosphate.

“…Renin release studies using renal cortical slices have been reported in the rat, rabbit, dog, pig, and recently in the mouse of examine the direct stimuli on juxtaglomerullar cells not mediated by systemic effects. However, the evaluations of some of the essential characters of the experimental system, e.g., energy dependency (1, 2), Ca dependency (2-4), and oxygen demand (5,6) of renin secretion show discrepancies in some of the studies. Me thodological problems seems to be involved in some of the inconsistencies in the experi mental results.…”