Factors influencing acute ischaemia-induced renal hypertension in rats

Giorgio Recordati, Federica Zorzoli, Olivia Pontara, Lucia Turolo, Alberto Zanchetti

Research output: Contribution to journalArticle

Abstract

Objective: To verify if the acute hypertension that occurs after reversal of complete renal ischaemia is related to the duration of ischaemia, is different in one-kidney (1K) and two-kidney (2K) rats, and is prevented by angiotensin receptor blockade. Methods: Four groups of Sprague-Dawley rats anaesthetized with pentobarbitone were studied before, during and after a reversible, complete renal ischaemia achieved by functional right nephrectomy. Results: In 1K rats (group 1, n = 21), reopening of right renal hilum after functional right nephrectomy of 180, 60 and 30 min was followed by peak increases in systolic blood pressure of 76.0 ± 10.1 mmHg, 36.5 ± 10.0 mmHg and 18.4 ± 4.4 mmHg, respectively (mean ± SEM). In 2K rats (group 2, n = 21), functional right nephrectomy of 180, 60 and 30 min was followed by smaller increases in blood pressure of 49.8 ± 7.6 mmHg, 5.9 ± 3.3 mmHg and 8.3 ± 2.1 mmHg, respectively. Plasma renin activity was directly related to the duration of functional right nephrectomy, and was greater in 1K rats. In group 3, irbesartan administered to 1K rats (n = 8) during functional right nephrectomy almost completely prevented the development of hypertension upon reopening. In group 4, labetalol injected intravenously in 1K rats (n = 3) did not prevent the blood pressure surge at reopening (49.2 ± 8.5 mmHg). Conclusions: An experimental acute renal hypertension may be elicited both in 1K and in 2K rats and for functional right nephrectomy of 30, 60 and 180 min duration. The increase in blood pressure is proportional to the duration of functional right nephrectomy and greater in 1K than in 2K rats. The experimental acute renal hypertension is due to acute release of renin and generation of endogenous angiotensin II, and is specifically prevented by the angiotensin II type 1 receptor blocker, irbesartan, but not by labetalol.

Original languageEnglish
Pages (from-to)2453-2463
Number of pages11
JournalJournal of Hypertension
Volume20
Issue number12
DOIs
Publication statusPublished - Dec 1 2002

Fingerprint

Renal Hypertension
Nephrectomy
Ischemia
irbesartan
Blood Pressure
Kidney
Labetalol
Renin
Hypertension
Angiotensin II Type 1 Receptor Blockers
Angiotensin Receptors
Pentobarbital
Angiotensin II
Sprague Dawley Rats

Keywords

  • Acute ischaemic renal failure
  • Experimental hypertension
  • Functional nephrectomy
  • Hypertensive crises
  • Nephrectomy
  • Post-transplantation hypertension
  • Renovascular hypertension

ASJC Scopus subject areas

  • Endocrinology
  • Internal Medicine

Cite this

Recordati, G., Zorzoli, F., Pontara, O., Turolo, L., & Zanchetti, A. (2002). Factors influencing acute ischaemia-induced renal hypertension in rats. Journal of Hypertension, 20(12), 2453-2463. https://doi.org/10.1097/00004872-200212000-00026

Factors influencing acute ischaemia-induced renal hypertension in rats. / Recordati, Giorgio; Zorzoli, Federica; Pontara, Olivia; Turolo, Lucia; Zanchetti, Alberto.

In: Journal of Hypertension, Vol. 20, No. 12, 01.12.2002, p. 2453-2463.

Research output: Contribution to journalArticle

Recordati, G, Zorzoli, F, Pontara, O, Turolo, L & Zanchetti, A 2002, 'Factors influencing acute ischaemia-induced renal hypertension in rats', Journal of Hypertension, vol. 20, no. 12, pp. 2453-2463. https://doi.org/10.1097/00004872-200212000-00026
Recordati, Giorgio ; Zorzoli, Federica ; Pontara, Olivia ; Turolo, Lucia ; Zanchetti, Alberto. / Factors influencing acute ischaemia-induced renal hypertension in rats. In: Journal of Hypertension. 2002 ; Vol. 20, No. 12. pp. 2453-2463.
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AU - Zorzoli, Federica

AU - Pontara, Olivia

AU - Turolo, Lucia

AU - Zanchetti, Alberto

PY - 2002/12/1

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N2 - Objective: To verify if the acute hypertension that occurs after reversal of complete renal ischaemia is related to the duration of ischaemia, is different in one-kidney (1K) and two-kidney (2K) rats, and is prevented by angiotensin receptor blockade. Methods: Four groups of Sprague-Dawley rats anaesthetized with pentobarbitone were studied before, during and after a reversible, complete renal ischaemia achieved by functional right nephrectomy. Results: In 1K rats (group 1, n = 21), reopening of right renal hilum after functional right nephrectomy of 180, 60 and 30 min was followed by peak increases in systolic blood pressure of 76.0 ± 10.1 mmHg, 36.5 ± 10.0 mmHg and 18.4 ± 4.4 mmHg, respectively (mean ± SEM). In 2K rats (group 2, n = 21), functional right nephrectomy of 180, 60 and 30 min was followed by smaller increases in blood pressure of 49.8 ± 7.6 mmHg, 5.9 ± 3.3 mmHg and 8.3 ± 2.1 mmHg, respectively. Plasma renin activity was directly related to the duration of functional right nephrectomy, and was greater in 1K rats. In group 3, irbesartan administered to 1K rats (n = 8) during functional right nephrectomy almost completely prevented the development of hypertension upon reopening. In group 4, labetalol injected intravenously in 1K rats (n = 3) did not prevent the blood pressure surge at reopening (49.2 ± 8.5 mmHg). Conclusions: An experimental acute renal hypertension may be elicited both in 1K and in 2K rats and for functional right nephrectomy of 30, 60 and 180 min duration. The increase in blood pressure is proportional to the duration of functional right nephrectomy and greater in 1K than in 2K rats. The experimental acute renal hypertension is due to acute release of renin and generation of endogenous angiotensin II, and is specifically prevented by the angiotensin II type 1 receptor blocker, irbesartan, but not by labetalol.

AB - Objective: To verify if the acute hypertension that occurs after reversal of complete renal ischaemia is related to the duration of ischaemia, is different in one-kidney (1K) and two-kidney (2K) rats, and is prevented by angiotensin receptor blockade. Methods: Four groups of Sprague-Dawley rats anaesthetized with pentobarbitone were studied before, during and after a reversible, complete renal ischaemia achieved by functional right nephrectomy. Results: In 1K rats (group 1, n = 21), reopening of right renal hilum after functional right nephrectomy of 180, 60 and 30 min was followed by peak increases in systolic blood pressure of 76.0 ± 10.1 mmHg, 36.5 ± 10.0 mmHg and 18.4 ± 4.4 mmHg, respectively (mean ± SEM). In 2K rats (group 2, n = 21), functional right nephrectomy of 180, 60 and 30 min was followed by smaller increases in blood pressure of 49.8 ± 7.6 mmHg, 5.9 ± 3.3 mmHg and 8.3 ± 2.1 mmHg, respectively. Plasma renin activity was directly related to the duration of functional right nephrectomy, and was greater in 1K rats. In group 3, irbesartan administered to 1K rats (n = 8) during functional right nephrectomy almost completely prevented the development of hypertension upon reopening. In group 4, labetalol injected intravenously in 1K rats (n = 3) did not prevent the blood pressure surge at reopening (49.2 ± 8.5 mmHg). Conclusions: An experimental acute renal hypertension may be elicited both in 1K and in 2K rats and for functional right nephrectomy of 30, 60 and 180 min duration. The increase in blood pressure is proportional to the duration of functional right nephrectomy and greater in 1K than in 2K rats. The experimental acute renal hypertension is due to acute release of renin and generation of endogenous angiotensin II, and is specifically prevented by the angiotensin II type 1 receptor blocker, irbesartan, but not by labetalol.

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KW - Post-transplantation hypertension

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