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Renal vascular effects of frusemide in the rat: influence of salt loading and the role of angiotensin II.
Exp Physiol. 2001 Sep; 86(5):611-6.EP

Abstract

We showed recently that post-frusemide (furosemide) natriuresis was associated with a major depression of medullary circulation. In the present study, prior to administration of frusemide the tubular transport of NaCl was modified by loading the animals with 5% saline to elucidate a possible interrelation between the tubular and vascular effects of the drug. Moreover, a possible involvement of the renin-angiotensin system was examined by pharmacological blockade using captopril, an inhibitor of angiotensin converting enzyme (1 mg x kg(-1), I.V.), or losartan, a selective inhibitor of angiotensin AT1 receptor (10 mg x kg(-1), I.V.). The effects of frusemide (0.25 mg x kg(-1) I.V., then the same dose given over 1 h) on renal medullary and cortical circulation (using laser-Doppler flowmetry) and renal excretion of sodium (U(Na)V), water and total solutes were measured in anaesthetised rats. With no pre-treatment, frusemide decreased the medullary flow (36.6 +/- 6.0%) significantly more than the cortical flow (10.1 +/- 1.0%; P < 0.001). The difference between the medulla and cortex was not significant in rats which showed high U(Na)V after hypertonic saline loading (2.0 +/- 0.4 vs. 0.4 +/- 0.1 micromol x min(-1) in non-loaded rats): 21.1 +/- 3.9% and 15.8 +/- 1.5%, respectively. At very high U(Na)V (9.5 +/- 1.1 micromol x min(-1)) the post-frusemide decrease in blood flow tended to be smaller in the medulla (7.6 +/- 7.7%) than in the cortex (16.2 +/- 2.6%). The fall in medullary blood flow was attenuated by pre-treatment with captopril (22.0 +/- 3.3%) and abolished by pre-treatment with losartan (2.8 +/- 11.8%). The decrease in cortical blood flow was not changed by hypertonic saline or angiotensin II blockers. The abolition of the post-frusemide depression of medullary blood flow by previous salt loading confirms the proposed link between tubular transport status and vasoconstriction. A similar modification of the response by blockade of the renin-angiotensin system suggests that the system is involved in the mechanism of medullary vasoconstriction.

Authors+Show Affiliations

Laboratory of Renal and Body Fluid Physiology, Medical Research Centre of the Polish Academy of Sciences, Pawiñskiego 5, 02-106 Warsaw, Poland. renal@cmdik.pan.plNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

11571489

Citation

Dobrowolski, L, et al. "Renal Vascular Effects of Frusemide in the Rat: Influence of Salt Loading and the Role of Angiotensin II." Experimental Physiology, vol. 86, no. 5, 2001, pp. 611-6.
Dobrowolski L, Badzyńska B, Grzelec-Mojzesowicz M, et al. Renal vascular effects of frusemide in the rat: influence of salt loading and the role of angiotensin II. Exp Physiol. 2001;86(5):611-6.
Dobrowolski, L., Badzyńska, B., Grzelec-Mojzesowicz, M., & Sadowski, J. (2001). Renal vascular effects of frusemide in the rat: influence of salt loading and the role of angiotensin II. Experimental Physiology, 86(5), 611-6.
Dobrowolski L, et al. Renal Vascular Effects of Frusemide in the Rat: Influence of Salt Loading and the Role of Angiotensin II. Exp Physiol. 2001;86(5):611-6. PubMed PMID: 11571489.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Renal vascular effects of frusemide in the rat: influence of salt loading and the role of angiotensin II. AU - Dobrowolski,L, AU - Badzyńska,B, AU - Grzelec-Mojzesowicz,M, AU - Sadowski,J, PY - 2001/9/26/pubmed PY - 2002/2/20/medline PY - 2001/9/26/entrez SP - 611 EP - 6 JF - Experimental physiology JO - Exp Physiol VL - 86 IS - 5 N2 - We showed recently that post-frusemide (furosemide) natriuresis was associated with a major depression of medullary circulation. In the present study, prior to administration of frusemide the tubular transport of NaCl was modified by loading the animals with 5% saline to elucidate a possible interrelation between the tubular and vascular effects of the drug. Moreover, a possible involvement of the renin-angiotensin system was examined by pharmacological blockade using captopril, an inhibitor of angiotensin converting enzyme (1 mg x kg(-1), I.V.), or losartan, a selective inhibitor of angiotensin AT1 receptor (10 mg x kg(-1), I.V.). The effects of frusemide (0.25 mg x kg(-1) I.V., then the same dose given over 1 h) on renal medullary and cortical circulation (using laser-Doppler flowmetry) and renal excretion of sodium (U(Na)V), water and total solutes were measured in anaesthetised rats. With no pre-treatment, frusemide decreased the medullary flow (36.6 +/- 6.0%) significantly more than the cortical flow (10.1 +/- 1.0%; P < 0.001). The difference between the medulla and cortex was not significant in rats which showed high U(Na)V after hypertonic saline loading (2.0 +/- 0.4 vs. 0.4 +/- 0.1 micromol x min(-1) in non-loaded rats): 21.1 +/- 3.9% and 15.8 +/- 1.5%, respectively. At very high U(Na)V (9.5 +/- 1.1 micromol x min(-1)) the post-frusemide decrease in blood flow tended to be smaller in the medulla (7.6 +/- 7.7%) than in the cortex (16.2 +/- 2.6%). The fall in medullary blood flow was attenuated by pre-treatment with captopril (22.0 +/- 3.3%) and abolished by pre-treatment with losartan (2.8 +/- 11.8%). The decrease in cortical blood flow was not changed by hypertonic saline or angiotensin II blockers. The abolition of the post-frusemide depression of medullary blood flow by previous salt loading confirms the proposed link between tubular transport status and vasoconstriction. A similar modification of the response by blockade of the renin-angiotensin system suggests that the system is involved in the mechanism of medullary vasoconstriction. SN - 0958-0670 UR - https://www.unboundmedicine.com/medline/citation/11571489/Renal_vascular_effects_of_frusemide_in_the_rat:_influence_of_salt_loading_and_the_role_of_angiotensin_II_ L2 - https://antibodies.cancer.gov/detail/CPTC-ATM-4 DB - PRIME DP - Unbound Medicine ER -