Bertha Singer

Effect of renal nerve stimulation, renal blood flow and adrenergic blockade on plasma renin activity in the cat

1. The effect of electrical stimulation of the distal cut ends of the renal nerves of unilaterally nephrectomized, anaesthetized cats was studied. Using stimulation parameters of 15 pulses per second (pps), 15 V and 0·2 msec duration, there was an immediate sharp drop in renal blood flow, as determined by an electromagnetic flowmeter, which was maintained for about 2 min. Flow gradually returned to control values over approximately the next 10 min in spite of continued stimulation for up to 30 min.

Comparison of the effects of propranolol and ICI 66082 in blocking the renin releasing effect of renal nerve stimulation in the cat

The comparative effectiveness of propranolol and ICI 66082, in inhibiting the release of renin from the kidney resulting from renal nerve stimulation, has been studied in the cat. Over the dose range 0.17–0.68 × 10−5 mol/kg propranolol there was a dose‐response relationship with the increase of plasma renin activity (PRA) achieved after 10 min stimulation. Over the dose range 0.75–1.69 × 10−5 mol/kg ICI 66082 also inhibited the release of renin caused by nerve stimulation, but was about five times less effective than propranolol. It would appear from these data that the β‐adrenoceptors within the kidney mediating renin release are distinctly different from those of the heart.

Effect of propranolol and theophylline on renin release caused by furosemide in the cat.

Abstract Pretreatment with propranolol did not significantly modify the marked increase in plasma renin activity (PRA) produced by furosemide administration in anaesthetized, renally-denervated cats. Treatment with propranolol alone significantly lowered PRA. Theophylline, administered i.v. at the human therapeutic dose of 7 mg/kg, did not affect the level of PRA. When theophylline was superimposed on furosemide no potentiation of the effect on PRA was observed. Conversely, when furosemide was superimposed on theophylline the effect was similar to that produced by furosemide alone. These results indicate that, in contrast to neural stimulation, the release of renin in response to furosemide is not propranolol sensitive. Further, they suggest that the release of renin, in the renally-denervated cat, is not mediated through cyclic AMP, if the therapeutic level of theophylline effectively inhibits phosphodiesterase in the kidney.

The effect of angiotensin I converting enzyme inhibitor (SQ 20881) on the release of prostaglandins by rabbit kidney, in vivo.

1 Prostaglandin E‐ and F‐like material has been estimated in renal venous blood of the left kidney of anaesthetized rabbits following renal nerve section. Prostaglandins were estimated by bioassay following solvent extraction and column chromatography.

EFFECTS OF ADRENALINE, NORADRENALINE, ISOPRENALINE AND SALBUTAMOL ON THE PRODUCTION AND RELEASE OF RENIN BY ISOLATED RENAL CORTICAL CELLS OF THE CAT

1 Isolated renal cortical cells of the cat have been demonstrated to produce renin on incubation in vitro. After 2 h of incubation, without added agonist, the total amount of renin in the flask increased by a mean of 27.2%. The increase in renin content of the incubation flask was found to be present in the medium. 2 Noradrenaline (1.18 × 10−4 M) and adrenaline (1.09 ×; 10‐4 M) added to the incubation medium stimulated renin production by 45 and 34% respectively, compared with the incubated controls. Most of the increase in renin production was present in the incubation medium. 3 Isoprenaline did not stimulate renin production. However, when added to the incubation medium at a concentration of 0.72 × 10‐4 M there was a significant decrease in the cellular content and a significant increase in the medium content of renin. This increase was at least as great as that observed with adrenaline and noradrenaline. 4 Salbutamol had an effect similar to isoprenaline, i.e. it induced the release of renin into the medium without affecting production. In this respect it was about a third as potent as isoprenaline.