Biomedical subjects

J Bing

Publications and source records attributed to J Bing.

At least 37 records · Page 2Linked to original sources

PubMed1976

Vast and apparently paradoxical continuous rise in plasma renin after removal of gently manipulated submaxillary glands in nephrectomized mice.

Gentle manipulation of the submaxillary glands of previously nephrectomized mice results in a vast increase in plasma renin concentration. The concentration reaches 1 to 7 G.U. renin/ml, which is 1,000-fold higher than normal plasma concentrations. The rise is much less pronounced if the glands are removed after the manipulation, confirming the site of the release. However, an apparent paradox is seen: the renin concentration continues to rise even after removal of submaxillary glands as well as kidneys, indicating that a bound a form of renin is also released. The bound renin can be in the form of exocytosed granules or (and) in the form of "protein", the renin of which is activated with time. In spite of the very high renin concentrations the blood pressure is normal or only moderately increased. This disproportion between plasma renin and blood pressure can be caused by a simultaneous release of submaxillary kallikrein and renin, which have conteracting effects on the blood pressure.

Animals↗

PubMed1976

Participation of renal, but not of submaxillary renin in the homeostasis of the blood pressure after experimentally induced hypotension in mice.

While hypotension elicited a marked increase in plasma renin concentration in conscious normal mice, no increase was provoked in previously nephrectomized mice in spite of the high renin content of their submaxillary glands. The role of the increased release of renal renin for the homeostasis of the blood pressure was shown by the decrease in pressure which followed blockade of the renin system. Contrary to Saralasin which did not change the blood pressure in nephrectomized mice, injections of SQ 20.881 did in some mice result in a decrease in blood pressure, which was probably caused by its ability to inhibit bradykininases. Both Saralasin and SQ 20.881 elicited marked increases in plasma renin in normal, but not in nephrectomized mice, showing that, while renal renin release is controlled by the plasma angiotensin II concentration, this does not apply to submaxillary renin release.

Animals↗

PubMed1975

Time course of changes in plasma renin after blockade of the renin-system. Studies of conscious and anaesthetized, normal, adrenalectomized and spontaneously hypertensive rats.

Inhibition of the angiotensin I converting enzyme with SQ 20.881 results in a 2 to 35 fold increase in plasma renin concentration in normal rats and in spontaneously hypertensive rats. The effect is transient, lasting for 1 to 3 hours even in the presence of prolonged blockade. The relative increase is independent of the pretreatment plasma renin concentration. The blood pressure is unchanged in conscious rats in which the effect of SQ 20.881 on plasma renin is believed to be due to a blockade of the negative feedback of angiotensin II on renin release. In anaesthetized rats, SQ 20.88) has an additional hypotensive effect which augments the increase in plasma renin. Saralasin is without effect on blood pressure and plasma renin in conscious normal rats and in spontaneously hypertensive rats, while it causes a transient 3 to 27 fold increase in plasma renin concentration in anaesthetized rats. It is suggested that this increase is hardly due to an interception of the feedback, but to the concomitant fall in blood pressure, as a similar hypotension and increase in plasma renin is produced by dihydralazine. It is furthermore found that Saralasin blocks renin release induced by SQ 20.881. This demonstrates that Saralasin is bound to the receptors in the juxtaglomerular cells and has slight, agonistic properties there. Both in conscious rats and in anaesthetized adrenalectomized rats substituted with DOCA and salt, SQ 20.881 as well Saralasin causes transient increases in plasma renin concentration. If such rats are only substituted with salt and not with DOCA, the effects of both blockers are in the form of severe hypotension and a permanent elevation of plasma renin.

Adrenalectomy↗

PubMed1975

Different effects on renal and submaxillary renin release after blockade of the renin system in mice.

Ingibition of the angiotensin I converting enzyme with SQ 20,881 results in a rapid marked increase in plasma renin concentration in mice. The maximum effect is short-lasting, but the values are still elevated 2 hours after the injection, the time course being similar to that previously found in rats. The relative increase is the same in normal and sialo-adenectomized mice. The plasma renin concentration of nephrectomized mice with their submaxillary glands intact is, however, totally uninfluenced by injection of the blocker. This finding indicates that renin release from the submaxillary glands is not controlled by the plasma angiotensin II concentration as is that of the renin release from the kidneys.

Angiotensin II↗

PubMed1974