ATRIAL-NATRIURETIC-FACTOR AND ANGIOTENSIN-II STIMULATE NITRIC-OXIDE RELEASE FROM HUMAN PROXIMAL TUBULAR CELLS

J S MCLAY, P K CHATTERJEE, S K MISTRY, R P WEERAKODY, A G JARDINE, N G MCKAY, G M HAWKSWORTH

Research output: Contribution to journalArticle

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Abstract

1. It has been recently reported that angiotensin II can enhance atrial natriuretic factor-stimulated cyclic GMP release from brain capillary endothelial cells and stimulate directly the release of cyclic GMP by Neuro 2a cells. A possible mechanism mediating such cyclic GMP release could be via the production of nitric oxide and the resultant stimulation of soluble guanylate cyclase.

2. The ability of angiotensin II, atrial natriuretic factor and c((4-23)) atrial natriuretic factor to stimulate nitric oxide production was investigated in primary cultures of human proximal tubular cells.

3. Freshly prepared human proximal tubular cells were seeded onto 6-well plates and allowed to reach confluence, Cells were then incubated with incremental concentrations of either angiotensin II, atrial natriuretic factor or c((4-23)) atrial natriuretic factor alone for 1, 4, 12 or 24 h or in the presence of the nitric oxide synthase inhibitor N-G-monomethyl-L-arginine. Angiotensin II was also incubated with human proximal tubular cells in the presence of the AT(1) and AT(2) receptor antagonists DuP 753 and PD 123319.

4. Incubation of human proximal tubular cells with angiotensin II, atrial natriuretic factor or c((4-23)) atrial natriuretic factor produced a dose- and time-dependent increase in nitric oxide production, which was inhibited in the presence of N-G-monomethyl-L-arginine, A similar increase in nitric oxide production was observed after incubation with atrial natriuretic factor or c((4-23)) atrial natriuretic factor.

5. The angiotensin-induced increase in nitric oxide production was not inhibited in the presence of either the angiotensin AT(1) or AT(2) receptor antagonists DuP 753 or PD 123319.

6. This study demonstrates that primary cultures of human proximal tubular cells can be stimulated to produce nitric oxide by both atrial natriuretic factor and angiotensin II, Furthermore, the atrial natriuretic factor-induced response appears to be mediated via the atrial natriuretic factor-C receptor, while the angiotensin II-induced response appears to be mediated by a novel, as yet unidentified, angiotensin II receptor.

Original languageEnglish
Pages (from-to)527-531
Number of pages5
JournalClinical Science
Volume89
Issue number5
Publication statusPublished - Nov 1995

Keywords

  • ANGIOTENSIN II
  • ATRIAL NATRIURETIC FACTOR
  • ATRIAL NATRIURETIC FACTOR RECEPTOR
  • HUMAN PROXIMAL TUBULAR CELLS
  • NITRIC OXIDE
  • RECEPTOR SUBTYPES
  • RELAXING FACTOR
  • BRAIN
  • ACETYLCHOLINE
  • MECHANISMS
  • ACTIVATION
  • RELAXATION
  • PEPTIDES

Cite this

MCLAY, J. S., CHATTERJEE, P. K., MISTRY, S. K., WEERAKODY, R. P., JARDINE, A. G., MCKAY, N. G., & HAWKSWORTH, G. M. (1995). ATRIAL-NATRIURETIC-FACTOR AND ANGIOTENSIN-II STIMULATE NITRIC-OXIDE RELEASE FROM HUMAN PROXIMAL TUBULAR CELLS. Clinical Science, 89(5), 527-531.

ATRIAL-NATRIURETIC-FACTOR AND ANGIOTENSIN-II STIMULATE NITRIC-OXIDE RELEASE FROM HUMAN PROXIMAL TUBULAR CELLS. / MCLAY, J S ; CHATTERJEE, P K ; MISTRY, S K ; WEERAKODY, R P ; JARDINE, A G ; MCKAY, N G ; HAWKSWORTH, G M .

In: Clinical Science, Vol. 89, No. 5, 11.1995, p. 527-531.

Research output: Contribution to journalArticle

MCLAY, JS, CHATTERJEE, PK, MISTRY, SK, WEERAKODY, RP, JARDINE, AG, MCKAY, NG & HAWKSWORTH, GM 1995, 'ATRIAL-NATRIURETIC-FACTOR AND ANGIOTENSIN-II STIMULATE NITRIC-OXIDE RELEASE FROM HUMAN PROXIMAL TUBULAR CELLS' Clinical Science, vol. 89, no. 5, pp. 527-531.
MCLAY JS, CHATTERJEE PK, MISTRY SK, WEERAKODY RP, JARDINE AG, MCKAY NG et al. ATRIAL-NATRIURETIC-FACTOR AND ANGIOTENSIN-II STIMULATE NITRIC-OXIDE RELEASE FROM HUMAN PROXIMAL TUBULAR CELLS. Clinical Science. 1995 Nov;89(5):527-531.
MCLAY, J S ; CHATTERJEE, P K ; MISTRY, S K ; WEERAKODY, R P ; JARDINE, A G ; MCKAY, N G ; HAWKSWORTH, G M . / ATRIAL-NATRIURETIC-FACTOR AND ANGIOTENSIN-II STIMULATE NITRIC-OXIDE RELEASE FROM HUMAN PROXIMAL TUBULAR CELLS. In: Clinical Science. 1995 ; Vol. 89, No. 5. pp. 527-531.
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abstract = "1. It has been recently reported that angiotensin II can enhance atrial natriuretic factor-stimulated cyclic GMP release from brain capillary endothelial cells and stimulate directly the release of cyclic GMP by Neuro 2a cells. A possible mechanism mediating such cyclic GMP release could be via the production of nitric oxide and the resultant stimulation of soluble guanylate cyclase.2. The ability of angiotensin II, atrial natriuretic factor and c((4-23)) atrial natriuretic factor to stimulate nitric oxide production was investigated in primary cultures of human proximal tubular cells.3. Freshly prepared human proximal tubular cells were seeded onto 6-well plates and allowed to reach confluence, Cells were then incubated with incremental concentrations of either angiotensin II, atrial natriuretic factor or c((4-23)) atrial natriuretic factor alone for 1, 4, 12 or 24 h or in the presence of the nitric oxide synthase inhibitor N-G-monomethyl-L-arginine. Angiotensin II was also incubated with human proximal tubular cells in the presence of the AT(1) and AT(2) receptor antagonists DuP 753 and PD 123319.4. Incubation of human proximal tubular cells with angiotensin II, atrial natriuretic factor or c((4-23)) atrial natriuretic factor produced a dose- and time-dependent increase in nitric oxide production, which was inhibited in the presence of N-G-monomethyl-L-arginine, A similar increase in nitric oxide production was observed after incubation with atrial natriuretic factor or c((4-23)) atrial natriuretic factor.5. The angiotensin-induced increase in nitric oxide production was not inhibited in the presence of either the angiotensin AT(1) or AT(2) receptor antagonists DuP 753 or PD 123319.6. This study demonstrates that primary cultures of human proximal tubular cells can be stimulated to produce nitric oxide by both atrial natriuretic factor and angiotensin II, Furthermore, the atrial natriuretic factor-induced response appears to be mediated via the atrial natriuretic factor-C receptor, while the angiotensin II-induced response appears to be mediated by a novel, as yet unidentified, angiotensin II receptor.",
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T1 - ATRIAL-NATRIURETIC-FACTOR AND ANGIOTENSIN-II STIMULATE NITRIC-OXIDE RELEASE FROM HUMAN PROXIMAL TUBULAR CELLS

AU - MCLAY, J S

AU - CHATTERJEE, P K

AU - MISTRY, S K

AU - WEERAKODY, R P

AU - JARDINE, A G

AU - MCKAY, N G

AU - HAWKSWORTH, G M

PY - 1995/11

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N2 - 1. It has been recently reported that angiotensin II can enhance atrial natriuretic factor-stimulated cyclic GMP release from brain capillary endothelial cells and stimulate directly the release of cyclic GMP by Neuro 2a cells. A possible mechanism mediating such cyclic GMP release could be via the production of nitric oxide and the resultant stimulation of soluble guanylate cyclase.2. The ability of angiotensin II, atrial natriuretic factor and c((4-23)) atrial natriuretic factor to stimulate nitric oxide production was investigated in primary cultures of human proximal tubular cells.3. Freshly prepared human proximal tubular cells were seeded onto 6-well plates and allowed to reach confluence, Cells were then incubated with incremental concentrations of either angiotensin II, atrial natriuretic factor or c((4-23)) atrial natriuretic factor alone for 1, 4, 12 or 24 h or in the presence of the nitric oxide synthase inhibitor N-G-monomethyl-L-arginine. Angiotensin II was also incubated with human proximal tubular cells in the presence of the AT(1) and AT(2) receptor antagonists DuP 753 and PD 123319.4. Incubation of human proximal tubular cells with angiotensin II, atrial natriuretic factor or c((4-23)) atrial natriuretic factor produced a dose- and time-dependent increase in nitric oxide production, which was inhibited in the presence of N-G-monomethyl-L-arginine, A similar increase in nitric oxide production was observed after incubation with atrial natriuretic factor or c((4-23)) atrial natriuretic factor.5. The angiotensin-induced increase in nitric oxide production was not inhibited in the presence of either the angiotensin AT(1) or AT(2) receptor antagonists DuP 753 or PD 123319.6. This study demonstrates that primary cultures of human proximal tubular cells can be stimulated to produce nitric oxide by both atrial natriuretic factor and angiotensin II, Furthermore, the atrial natriuretic factor-induced response appears to be mediated via the atrial natriuretic factor-C receptor, while the angiotensin II-induced response appears to be mediated by a novel, as yet unidentified, angiotensin II receptor.

AB - 1. It has been recently reported that angiotensin II can enhance atrial natriuretic factor-stimulated cyclic GMP release from brain capillary endothelial cells and stimulate directly the release of cyclic GMP by Neuro 2a cells. A possible mechanism mediating such cyclic GMP release could be via the production of nitric oxide and the resultant stimulation of soluble guanylate cyclase.2. The ability of angiotensin II, atrial natriuretic factor and c((4-23)) atrial natriuretic factor to stimulate nitric oxide production was investigated in primary cultures of human proximal tubular cells.3. Freshly prepared human proximal tubular cells were seeded onto 6-well plates and allowed to reach confluence, Cells were then incubated with incremental concentrations of either angiotensin II, atrial natriuretic factor or c((4-23)) atrial natriuretic factor alone for 1, 4, 12 or 24 h or in the presence of the nitric oxide synthase inhibitor N-G-monomethyl-L-arginine. Angiotensin II was also incubated with human proximal tubular cells in the presence of the AT(1) and AT(2) receptor antagonists DuP 753 and PD 123319.4. Incubation of human proximal tubular cells with angiotensin II, atrial natriuretic factor or c((4-23)) atrial natriuretic factor produced a dose- and time-dependent increase in nitric oxide production, which was inhibited in the presence of N-G-monomethyl-L-arginine, A similar increase in nitric oxide production was observed after incubation with atrial natriuretic factor or c((4-23)) atrial natriuretic factor.5. The angiotensin-induced increase in nitric oxide production was not inhibited in the presence of either the angiotensin AT(1) or AT(2) receptor antagonists DuP 753 or PD 123319.6. This study demonstrates that primary cultures of human proximal tubular cells can be stimulated to produce nitric oxide by both atrial natriuretic factor and angiotensin II, Furthermore, the atrial natriuretic factor-induced response appears to be mediated via the atrial natriuretic factor-C receptor, while the angiotensin II-induced response appears to be mediated by a novel, as yet unidentified, angiotensin II receptor.

KW - ANGIOTENSIN II

KW - ATRIAL NATRIURETIC FACTOR

KW - ATRIAL NATRIURETIC FACTOR RECEPTOR

KW - HUMAN PROXIMAL TUBULAR CELLS

KW - NITRIC OXIDE

KW - RECEPTOR SUBTYPES

KW - RELAXING FACTOR

KW - BRAIN

KW - ACETYLCHOLINE

KW - MECHANISMS

KW - ACTIVATION

KW - RELAXATION

KW - PEPTIDES

M3 - Article

VL - 89

SP - 527

EP - 531

JO - Clinical Science

JF - Clinical Science

SN - 0143-5221

IS - 5

ER -