Ultrastructure, renin status, contractile and electrophysiological properties of the afferent glomerular arteriole in the rat hydronephrotic kidney

Abstract

Histological, ultrastructural, immunohistochemical, intravital microscopic and electrophysiological techniques have been applied to study experimental hydronephrosis in rats in order to assess its value as a preparation for the investigation of renal microcirculation and of the electrophysiological properties of the renin-containing juxtaglomerular (JG) cells of the afferent glomerular arteriole. As hydronephrosis develops, the kidney parenchyma becomes progressively thinner owing to tubular atrophy. Twelve weeks after ureteral ligature, this process results in a transparent tissue sheet of about 150-200 microns in thickness. In this preparation, the renal arterial tree as well as the glomeruli can be easily visualized for intravital microscopic studies, e.g. the determination of kidney vessel diameters, or the identification of JG cells for penetration with an intracellular microelectrode. In contrast to the tubular atrophy, the vascular system is well preserved, and the JG cells and the sympathetic axon terminals are ultrastructurally intact. This is also true for the glomeruli, except for a certain confluence of the podocyte foot processes and a thickening of the basal laminae. Renin immunostaining and kidney renin content in the hydronephrotic organ correspond to those in control kidneys. In addition, there are no differences in the plasma renin levels of hydronephrotic and control rats. Intravital microscopic observations reveal that the renal vascular tree reacts in a typical, concentration dependent manner to the vasoconstrictor agent angiotensin II, mainly at the level of the resistance vessels. Electrophysiological recordings from juxtaglomerular granulated cells show a high membrane potential (-60 mV), and spontaneous depolarizing junction potentials, owing to random transmitter release from the nerve terminals. Angiotensin II, an inhibitor of renin release, depolarizes JG cells reversibly. Hence, we may infer that the hydronephrotic rat kidney is a suitable model for in vivo studies of the renal microcirculation as well as for in vitro investigations of the electrophysiological properties of the media cells of the afferent glomerular arteriole.

Differential effect of neuropeptide‐Y on membrane potential of cells in renal arterioles of the hydronephrotic mouse.

“…As described previously (Biihrle, Scholz, Nobiling & Taugner, 1986 c), in renincontaining (JG) cells as well as in VSMCs spontaneous depolarizing transients of small amplitude superimposed on the resting membrane potential were usually observed. These transients occurred in a random manner at frequencies between 30 and 200 min-', and their amplitudes ranged between 0-5 and 15 mV (noise level of the recording system with a typical 100 MQ electrode: 0-2-0-5 mV peak to peak).…”

The impaired renal vasodilator response attributed to endothelium-derived hyperpolarizing factor in streptozotocin - induced diabetic rats is restored by 5-methyltetrahydrofolate

“…About 8 to 10 weeks after the induction of hydronephrosis, the renal parenchyma becomes a thin translucent tissue sheet due to tubular atrophy. The microcirculation remains, however, intact [22,23] and is accessible for study by intravital microscopy. For the final experiments, the rats were anaesthetized with thiobutabarbital and cannulated as described above.…”

An Immunoelectron-Microscopical Observation of Mouse Juxtaglomerular Cells in the Case of Experimental Hydronrophrosis

“…The angiotensin series play several important roles in regulation of blood pressure and fluid volume in the body. In the control of renin release, four factors or receptor mechanisms have gener ally been recognized: (1) mechanical baroreceptors of afferent arterioles, (2) macula densa receptors providing feedback to JG cells, (3) renal sympathetic nerves and (4) several humoral factors including adrenaline, noradrena doles [9,10). More recently, the authors have investigated the mouse endocrine kidney using experimental obstruc tion of the ureter and demonstrated an elevation of renin activity in the ligated kidney 1 month after ligation [11].…”