Identification of individual renocortical cells that secrete renin

Carey, Robert M.; Geary, K. M.; Hunt, M. K.; Ramos, Susan I.; Forbes, Michael S.; Inagami, Tadashi; Peach, Michael J.; Leong, Denis A.

doi:10.1152/ajprenal.1990.258.3.f649

Cited by 7 publications

(5 citation statements)

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“…b-Adrenergic receptors located in the juxtaglomerular apparatus of afferent arterioles (7,26) as well as NE receptors in the renal tubules that modulate sodium delivery to the macula densa (5) both control kidney renin secretion. Secretion of renin persists in the face of renal artery denervation, and the existence of a humeral factor secreted by an extrarenal site is postulated (3,4).…”

Section: Discussionmentioning

confidence: 99%

Blood pressure response to chronic episodic hypoxia: role of the sympathetic nervous system

Bao

Metreveli

et al. 1997

Journal of Applied Physiology

182

112

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Previous studies in several strains of rats have demonstrated that 35 consecutive days of recurrent episodic hypoxia (7 h/day) cause an 8- to 13-mmHg persistent increase in diurnal systemic blood pressure (BP). Carotid chemoreceptors and the sympathetic nervous system have been shown to be necessary for development of this BP increase. The present study was undertaken to further define the role of renal artery sympathetic nerves and the adrenal medulla in this BP increase. Male Sprague-Dawley rats had either adrenal medullectomy, bilateral renal artery denervation, or sham surgery. Rats from each of these groups were subjected to episodic hypoxia for 35 days. Control groups received either compressed air or were left unhandled. Adrenal demedullation or renal artery denervation eliminated the chronic diurnal mean BP response (measured intra-arterially) to episodic hypoxia, whereas sham-operated controls continued to showed persistent elevation of systemic BP. Plasma and renal tissue catecholamine levels at the end of the experiment confirmed successful adrenal demedullation or renal denervation in the respective animals. The chronic episodic hypoxia-mediated increase in diurnal BP requires both intact renal artery nerves as well as an intact adrenal medulla.

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Section: Discussionmentioning

confidence: 99%

Blood pressure response to chronic episodic hypoxia: role of the sympathetic nervous system

Bao

Metreveli

et al. 1997

Journal of Applied Physiology

182

112

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“…Male Sprague-Dawley rats (Hilltop Lab Animals, Inc., Scottdale, PA) weighing 100-120 g were used. Renal cortical cells were harvested using a modification of a method previously described by our laboratory (10). For each cell preparation, one rat was killed by decapitation, the abdominal or descending aorta was cannulated, and both kidneys were perfused with RPMI 1640 medium (GIBCO BRL, Gaithersburg, MD) containing 0.07% collagenase type A (Boehringer Mannheim Biochemicals, Indianapolis, IN), 0.12 mg/ml elastase (type III), 0.25 mg/ml soybean trypsin inhibitor, 0.16 mg/ml deoxyribonuclease I, and 0.3% crystallized BSA (all from Sigma Chemical Co., St. Louis, MO), and 100 g/ml penicillin and 100 g/ml streptomycin (Pen/Strep; GIBCO BRL) (enzyme solution).…”

Section: Methodsmentioning

confidence: 99%

“…Cells were cultured for 48 h on Permanox plastic-coated multi-well chamber slides (Nunc, Inc., Naperville, IL). Immunoperoxidase staining was performed using the avidin-biotin peroxidase complex (ABC) kit from Vector Laboratories, Inc. (Burlingame, CA), as described previously (10,11). Cells were fixed in methanol (4 Њ C) for 10 min, followed by a 10-s exposure to acetone (4 Њ C), and then air dried.…”

Section: Methodsmentioning

confidence: 99%

Biomechanical coupling in renin-releasing cells.

Carey¹,

McGrath²,

Pentz³

et al. 1997

J. Clin. Invest.

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The renin-angiotensin system is a major regulatory system controlling extracellular fluid volume and blood pressure. The rate-limiting enzyme in this hormonal cascade is renin, which is synthesized and secreted into the circulation by renal juxtaglomerular (JG) cells. The renal baroreceptor is a key physiologic regulator of renin secretion, whereby a change in renal perfusion pressure is sensed by these cells and results in a change in renin release. However, the mechanism, direct or indirect, underlying pressure transduction is unknown.We studied the direct application of mechanical stretch to rat JG cells and human renin-expressing (CaLu-6) cells on the release of renin. JG cells released a low level of baseline renin, comprising Ͻ 5% of their total renin content. By contrast, renin secretion from CaLu-6 cells comprised ‫ف‬ 30% of cellular stores, yet was also stimulated twofold by 10 M forskolin ( P Յ 0.001).In JG cells, mechanical stretch inhibited basal renin release by 42% ( P Ͻ 0.01) and forskolin-stimulated renin release by 25% ( P Ͻ 0.05). In CaLu-6 cells, stretch inhibited basal-and forskolin-stimulated renin release by 30 and 26%, respectively (both P Ͻ 0.01). Northern blot analysis demonstrated a stretch-induced reduction in baseline renin mRNA accumulation of 26% ( P Ͻ 0.05) in JG and 46% ( P Ͻ 0.05) in CaLu-6 cells.The data demonstrate that mechanical stretch in reninreleasing cells inhibits basal and stimulated renin release accompanied by a decrease in renin mRNA accumulation. Further studies will be necessary to characterize the intracellular events mediating biomechanical coupling in reninexpressing cells and the relationship of this signaling pathway to the in vivo baroreceptor control of renin secretion. ( J. Clin. Invest. 1997. 100:1566-1574.)

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“…Protein antigenicity may nevertheless be preserved by milder fixation, though at the cost of structural definition. Specific antibodies and the protein A-gold technique can then be used to detect renin and/or other proteins within granules (for details and illustrations see [10, 97, 98]).…”

Section: Techniques For Visualization Of Cellular Reninmentioning

confidence: 99%

“…The renin-antibody complex will then bind to protein A-conjugated sheep erythrocytes which will in turn be hemolyzed by complement attack. Renin secretion is visualized in a semiquantitative way as a circle of hemolyzed erythrocytes around individual renin-producing cells (complete technical description can be found in: [97, 101]).…”

Section: Visualization Of Single-arteriolar Single-cell or Singlmentioning

confidence: 99%

Methods for Imaging Renin-Synthesizing, -Storing, and -Secreting Cells

Casellas

2010

International Journal of Hypertension

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Renin-producing cells have been the object of intense research efforts for the past fifty years within the field of hypertension. Two decades ago, research focused on the concept and characterization of the intrarenal renin-angiotensin system. Early morphological studies led to the concept of the juxtaglomerular apparatus, a minute organ that links tubulovascular structures and function at the single nephron level. The kidney, thus, appears as a highly “topological organ” in which anatomy and function are intimately linked. This point is reflected by a concurrent and constant development of functional and structural approaches. After summarizing our current knowledge about renin cells and their distribution along the renal vascular tree, particularly along glomerular afferent arterioles, we reviewed a variety of imaging techniques that permit a fine characterization of renin synthesis, storage, and release at the single-arteriolar, -cell, or -granule level. Powerful tools such as multiphoton microscopy and transgenesis bear the promises of future developments of the field.

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Identification of individual renocortical cells that secrete renin

Cited by 7 publications

References 0 publications

Blood pressure response to chronic episodic hypoxia: role of the sympathetic nervous system

Blood pressure response to chronic episodic hypoxia: role of the sympathetic nervous system

Biomechanical coupling in renin-releasing cells.

Methods for Imaging Renin-Synthesizing, -Storing, and -Secreting Cells

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