Coexistence of Hyperplasia of Renomedullary Interstitial Cells and Juxtaglomerular Cells after Acute Occlusion of Renal Artery

Hypertension in rats produced by constriction of one renal artery was associated with degranulation of juxtaglomerular cells in the contralateral, undamped, kidney. These findings are consistent with those of other investigators. Furthermore, the degree of granulation (JGI) in the unclamped kidney was inversely correlated with the level of blood pressure (r = –0.7). Degranulation of JG cells also occurred in rats made hypertensive by application of a "figure-of-eight" ligature to one kidney and removal of the other one, except when the interference in blood supply was so severe that scarring resulted. In these damaged areas, granules persisted or increased in number even though they were decreased in adjacent relatively normal areas. Occlusion of one ureter in rats produced severe hydronephrosis in the homolateral kidney and an elevation in blood pressure. Juxtaglomerular cell granules persisted in the hydronephrotic kidney but were decreased in the contralateral one. This finding confirmed the results of the above experiments. Unilateral nephrectomy in comparable rats had no effect on the degree of granulation of JG cells in the remaining kidney or on the level of blood pressure under the conditions of these experiments. The possibility that degranulation of JG cells in the contralateral kidney in the rats described above was due to compensatory hypertrophy was thereby excluded. An elevation in blood pressure was therefore implicated as an important factor in causing degranulation of juxtaglomerular cells.

Download Full-text

Recovery of renal function after delayed revascularisation of acute occlusion of the renal artery

BMJ ◽

10.1136/bmj.296.6636.1591 ◽

1988 ◽

Vol 296 (6636) ◽

pp. 1591-1592 ◽

Cited By ~ 5

Author(s):

B Williams ◽

J Feehally ◽

A R Attard ◽

P R F Bell

Keyword(s):

Renal Function ◽

Renal Artery ◽

Acute Occlusion

Download Full-text

Evidence for an intrarenal beta receptor in control of renin release

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1976.230.2.410 ◽

1976 ◽

Vol 230 (2) ◽

pp. 410-418 ◽

Cited By ~ 43

Author(s):

JA Johnson ◽

JO Davis ◽

RW Gotshall ◽

TE Lohmeier ◽

JL Davis ◽

...

Keyword(s):

Blood Flow ◽

Arterial Pressure ◽

Renal Artery ◽

Adrenergic Receptors ◽

Adrenergic Receptor ◽

Renin Secretion ◽

Renin Release ◽

Juxtaglomerular Cells ◽

Alpha Adrenergic Receptors ◽

K Concentration

Infusion of isoproterenol intravenously in normal dogs at rates of 0.10 or 0.018 mug/min per kg body wt increased renin secretion; at the lower infusion rate arterial pressure (AP) and renal blood flow (RBF) were unchanged. Isoproterenol was also infused into the renal artery in normal dogs at 0.10 mug/min per kg; renin secretion increased in association with an increase in RBF but AP was unchanged. Plasma K concentration was consistently decreased in all three of the above experiments and because hypokalemia is known to increase renin release isoproterenol was not infused intrarenally at the lower rate; the decrease in plasma K level precluded relating the entire response in renin release to isoproterenol. Intrarenal infusion of propranolol at 0.05 mg/kg per h in Na-depleted dogs decreased renin secretion whereas intravenous infusion at the same dose failed to alter renin release. Intrarenal infusion of propranolol at this rate in Na-depleted dogs with a denervated, nonfiltering kidney also decreased renin release. In contrast, intrarenal infusion of phentolamine or phenoxybenzamine in normal dogs failed to alter renin secretion in doses that blocked alpha-adrenergic receptors. These experiments provide strong evidence for an intrarenal beta-adrenergic receptor that mediates renin release, and it seems likely from the experiment in the denervated, nonfiltering kidney that the receptor is located in the juxtaglomerular cells.

Download Full-text