Nitric oxide modulates the development and surgical reversal of renovascular hypertension in rats

Wann Chu Huang, Ren Yu Tsai, Te Chao Fang

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Objective. To evaluate the role of nitric oxide (NO) in the development and unclipping-induced reversal of blood pressure and bilateral renal function in two-kidney, one clip (2K1C) Goldblatt hypertensive rats. Methods. Goldblatt hypertensive rats were prepared by clipping the left renal artery 4 weeks before unclipping experiments. N(G)-nitro-L-arginine methyl ester (L-NAME) was administered after clipping and during unclipping to inhibit nitric oxide (NO) synthesis. Blood pressure and bilateral renal responses were measured. Results. Chronic L-NAME treatment accelerated and aggravated blood pressure elevations and increased plasma nitrite and nitrate levels in 2K1C rats. Surgical removal of the renal artery clip induced profound reductions in blood pressure in rats with and without L-NAME treatment. However, the magnitude of the unclipping-induced depressor response at the first postunclipping hour was significantly smaller in L-NAME-treated rats compared to those without L-NAME administration (15 ± 1 versus 22 ± 1%, P <0.05). Two hours after unclipping, blood pressure of both groups fell to a comparable, normal level. Acute intravenous infusion of L-NAME in established 2K1C hypertensive rats further increased blood pressure. Subsequent unclipping caused a depressor response similar to that observed in hypertensive rats treated chronically with L-NAME. Despite the marked decreases in blood pressure, unclipping induced striking increases in glomerular filtration rate (GFR), urine flow and sodium and potassium excretion rates in the ipsilateral kidney. However, the magnitudes of increases in GFR and the diuretic and natriuretic responses in rats without L-NAME treatment were significantly greater than in rats with L-NAME administration. In contrast, unclipping reduced these function indices in the contralateral kidney to a similar level in rats with and without L-NAME treatment. Conclusions. NO exerts vasodilator action and thereby lessens renal artery clipping-induced blood pressure elevation. Furthermore, unclipping-induced release of NO partially contributes to the early reduction in blood pressure and changes in bilateral renal function but does not directly mediate the normalization of blood pressure after unclipping in this hypertension model. (C) Lippincott Williams and Wilkins.

Original languageEnglish
Pages (from-to)601-613
Number of pages13
JournalJournal of Hypertension
Volume18
Issue number5
Publication statusPublished - 2000
Externally publishedYes

Fingerprint

Renovascular Hypertension
NG-Nitroarginine Methyl Ester
Nitric Oxide
Blood Pressure
Kidney
Renal Artery
Glomerular Filtration Rate
Surgical Instruments
Therapeutics
Nitrites
Vasodilator Agents
Diuretics
Intravenous Infusions
Nitrates
Potassium
Sodium
Urine

Keywords

  • Diuresis
  • Goldblatt hypertension
  • Natriuresis
  • Nitric oxide
  • Renal artery stenosis
  • Unclipping

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology

Cite this

Nitric oxide modulates the development and surgical reversal of renovascular hypertension in rats. / Huang, Wann Chu; Tsai, Ren Yu; Fang, Te Chao.

In: Journal of Hypertension, Vol. 18, No. 5, 2000, p. 601-613.

Research output: Contribution to journalArticle

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abstract = "Objective. To evaluate the role of nitric oxide (NO) in the development and unclipping-induced reversal of blood pressure and bilateral renal function in two-kidney, one clip (2K1C) Goldblatt hypertensive rats. Methods. Goldblatt hypertensive rats were prepared by clipping the left renal artery 4 weeks before unclipping experiments. N(G)-nitro-L-arginine methyl ester (L-NAME) was administered after clipping and during unclipping to inhibit nitric oxide (NO) synthesis. Blood pressure and bilateral renal responses were measured. Results. Chronic L-NAME treatment accelerated and aggravated blood pressure elevations and increased plasma nitrite and nitrate levels in 2K1C rats. Surgical removal of the renal artery clip induced profound reductions in blood pressure in rats with and without L-NAME treatment. However, the magnitude of the unclipping-induced depressor response at the first postunclipping hour was significantly smaller in L-NAME-treated rats compared to those without L-NAME administration (15 ± 1 versus 22 ± 1{\%}, P <0.05). Two hours after unclipping, blood pressure of both groups fell to a comparable, normal level. Acute intravenous infusion of L-NAME in established 2K1C hypertensive rats further increased blood pressure. Subsequent unclipping caused a depressor response similar to that observed in hypertensive rats treated chronically with L-NAME. Despite the marked decreases in blood pressure, unclipping induced striking increases in glomerular filtration rate (GFR), urine flow and sodium and potassium excretion rates in the ipsilateral kidney. However, the magnitudes of increases in GFR and the diuretic and natriuretic responses in rats without L-NAME treatment were significantly greater than in rats with L-NAME administration. In contrast, unclipping reduced these function indices in the contralateral kidney to a similar level in rats with and without L-NAME treatment. Conclusions. NO exerts vasodilator action and thereby lessens renal artery clipping-induced blood pressure elevation. Furthermore, unclipping-induced release of NO partially contributes to the early reduction in blood pressure and changes in bilateral renal function but does not directly mediate the normalization of blood pressure after unclipping in this hypertension model. (C) Lippincott Williams and Wilkins.",
keywords = "Diuresis, Goldblatt hypertension, Natriuresis, Nitric oxide, Renal artery stenosis, Unclipping",
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AU - Tsai, Ren Yu

AU - Fang, Te Chao

PY - 2000

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N2 - Objective. To evaluate the role of nitric oxide (NO) in the development and unclipping-induced reversal of blood pressure and bilateral renal function in two-kidney, one clip (2K1C) Goldblatt hypertensive rats. Methods. Goldblatt hypertensive rats were prepared by clipping the left renal artery 4 weeks before unclipping experiments. N(G)-nitro-L-arginine methyl ester (L-NAME) was administered after clipping and during unclipping to inhibit nitric oxide (NO) synthesis. Blood pressure and bilateral renal responses were measured. Results. Chronic L-NAME treatment accelerated and aggravated blood pressure elevations and increased plasma nitrite and nitrate levels in 2K1C rats. Surgical removal of the renal artery clip induced profound reductions in blood pressure in rats with and without L-NAME treatment. However, the magnitude of the unclipping-induced depressor response at the first postunclipping hour was significantly smaller in L-NAME-treated rats compared to those without L-NAME administration (15 ± 1 versus 22 ± 1%, P <0.05). Two hours after unclipping, blood pressure of both groups fell to a comparable, normal level. Acute intravenous infusion of L-NAME in established 2K1C hypertensive rats further increased blood pressure. Subsequent unclipping caused a depressor response similar to that observed in hypertensive rats treated chronically with L-NAME. Despite the marked decreases in blood pressure, unclipping induced striking increases in glomerular filtration rate (GFR), urine flow and sodium and potassium excretion rates in the ipsilateral kidney. However, the magnitudes of increases in GFR and the diuretic and natriuretic responses in rats without L-NAME treatment were significantly greater than in rats with L-NAME administration. In contrast, unclipping reduced these function indices in the contralateral kidney to a similar level in rats with and without L-NAME treatment. Conclusions. NO exerts vasodilator action and thereby lessens renal artery clipping-induced blood pressure elevation. Furthermore, unclipping-induced release of NO partially contributes to the early reduction in blood pressure and changes in bilateral renal function but does not directly mediate the normalization of blood pressure after unclipping in this hypertension model. (C) Lippincott Williams and Wilkins.

AB - Objective. To evaluate the role of nitric oxide (NO) in the development and unclipping-induced reversal of blood pressure and bilateral renal function in two-kidney, one clip (2K1C) Goldblatt hypertensive rats. Methods. Goldblatt hypertensive rats were prepared by clipping the left renal artery 4 weeks before unclipping experiments. N(G)-nitro-L-arginine methyl ester (L-NAME) was administered after clipping and during unclipping to inhibit nitric oxide (NO) synthesis. Blood pressure and bilateral renal responses were measured. Results. Chronic L-NAME treatment accelerated and aggravated blood pressure elevations and increased plasma nitrite and nitrate levels in 2K1C rats. Surgical removal of the renal artery clip induced profound reductions in blood pressure in rats with and without L-NAME treatment. However, the magnitude of the unclipping-induced depressor response at the first postunclipping hour was significantly smaller in L-NAME-treated rats compared to those without L-NAME administration (15 ± 1 versus 22 ± 1%, P <0.05). Two hours after unclipping, blood pressure of both groups fell to a comparable, normal level. Acute intravenous infusion of L-NAME in established 2K1C hypertensive rats further increased blood pressure. Subsequent unclipping caused a depressor response similar to that observed in hypertensive rats treated chronically with L-NAME. Despite the marked decreases in blood pressure, unclipping induced striking increases in glomerular filtration rate (GFR), urine flow and sodium and potassium excretion rates in the ipsilateral kidney. However, the magnitudes of increases in GFR and the diuretic and natriuretic responses in rats without L-NAME treatment were significantly greater than in rats with L-NAME administration. In contrast, unclipping reduced these function indices in the contralateral kidney to a similar level in rats with and without L-NAME treatment. Conclusions. NO exerts vasodilator action and thereby lessens renal artery clipping-induced blood pressure elevation. Furthermore, unclipping-induced release of NO partially contributes to the early reduction in blood pressure and changes in bilateral renal function but does not directly mediate the normalization of blood pressure after unclipping in this hypertension model. (C) Lippincott Williams and Wilkins.

KW - Diuresis

KW - Goldblatt hypertension

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KW - Nitric oxide

KW - Renal artery stenosis

KW - Unclipping

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