Kinin influences on renal regional blood flow responses  to angiotensin-converting enzyme inhibition in dogs

Omoro, Sophia A.; Majid, Dewan S. A.; El‐Dahr, Samir S.; Navar, L. Gabriel

doi:10.1152/ajprenal.1999.276.2.f271

Cited by 27 publications

(37 citation statements)

References 19 publications

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“…Moreover, mainly due to the use of icatibant, a specific B 2 receptor antagonist, the contribution of kinins in the cardiovascular effects of ACE inhibitors has been documented experimentally, both on in vitro formation of endothelial nitric oxide and in vivo hypotensive and antihypertensive actions in animals (Linz et al 1995). Bradykinin also contributes to the renal vasodilator response to ACE inhibition (Fenoy et al 1991;Omoro et al 1999). Finally, in the isolated perfused rat kidney, we have reported that bradykinin is a potent renal vasodilator, the effects of which are potentiated by ACE inhibitors (Bagaté et al 1999a(Bagaté et al , 1999b.…”

Section: Discussionmentioning

confidence: 98%

Effects of icatibant on the ramipril-induced decrease in renal lithium clearance in the rat

Bagaté

Grima

Jong

et al. 2001

Naunyn-Schmiedeberg's Archives of Pharmacology

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The interaction between an inhibitor of angiotensin I converting enzyme (ramipril) and renal lithium handling was analysed in conscious, normotensive Wistar rats in the absence or the presence of a specific bradykinin B2 receptor antagonist, icatibant. The rats were treated for 5 days with ramipril (1 mg/kg/day p.o.) or its vehicle, alone or together with icatibant (0.1 mg/kg/day, s.c. infusion). Lithium chloride (8.3 mg/kg i.p.) was given as a single dose on day 5. Systolic blood pressure and heart rate were measured by tail plethysmography on day 3 (3, 9 and 15 h after ramipril administration) and renal function on day 4 (0-6 and 6-24 h urine sampling) and day 5 (0-6 h urine sampling). In another group of rats, 24 h sodium excretion was assessed during the first 4 days of ramipril treatment. Ramipril decreased renal lithium clearance (90+/-8 vs. 142+/-10 microl/min/100 g, P<0.001, n=24) and increased the fractional lithium reabsorption (74.3+/-1.9 vs. 66.7+/-1.7%, P<0.05) and plasma lithium concentration (0.108+/-0.006 vs. 0.085+/-0.004 mM, P<0.01). Alteration of renal lithium handling by ramipril was associated with a decrease in systolic blood pressure (-15% 3 h after ramipril administration) and sodium excretion (0-6 h after ramipril). The 24-h sodium excretion, however, tended to increase. Icatibant had no effect per se on renal function but attenuated the ramipril-induced decrease in renal lithium clearance (118+/-16 vs. 90+/-8 microl/min/100 g, n=12 and 24 respectively, P<0.05 one-tailed test) and systolic blood pressure. These results suggest that endogenous bradykinin contributes to the ramipril-associated alteration in renal lithium handling. Bradykinin B2 receptor-mediated vasodilation seems to be involved.

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Section: Discussionmentioning

confidence: 98%

Effects of icatibant on the ramipril-induced decrease in renal lithium clearance in the rat

Bagaté

Grima

Jong

et al. 2001

Naunyn-Schmiedeberg's Archives of Pharmacology

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“…In a sodium depleted organism plasma renin activity and plasma angiotensin II increases [17,18] and it may result vasoconstriction. However, cyclooxygenase expression [17,47] and kallikrein-kinin system activation [48,49] increases and these vasodilator agents may counterbalance the vasoconstriction produced by angiotensin II. As percent changes of blood flow and vascular resistance after NOS blockade does not differ significantly from those ones observed in normal rats we suppose that NO system has no role in adaptation of intrarenal blood flow in sodium restricted rats.…”

Section: Discussionmentioning

confidence: 99%

Intrarenal Distribution of Blood Flow in Sodium Depleted and Sodium Loaded Rats: Role of Nitric Oxide

Hably

Vág²,

Tost

et al. 2001

Kidney Blood Press Res

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The renal hemodynamic effects of nitric oxide synthase (NOS) inhibition and dietary salt were studied in rats. L-NAME (0.1 mg/ml in the drinking fluid, about 12 mg/kg/day) was given for 4 days to rats receiving low (sodium depletion, SD), normal (N) or high (sodium load, SL) NaCl diet. Intrarenal hemodynamics was studied in anaesthesia. NOS inhibition decreased renal blood flow and increased renal vascular resistance in each group. Cortical and outer medullary but not inner medullary blood flow increased in direct ratio to the sodium intake. NOS inhibition decreased the blood flow and increased the vascular resistance in all layers of the kidney in SD, N, and SL rats as well. In SD and N, but not in SL rats L-NAME induced vasoconstriction was higher in the outer (OM) and inner medulla (IM) than in the cortex (C) [SD: ΔCVR 43%, ΔOMVR 54%, ΔIMVR 84%; N: ΔCVR 54%, ΔOMVR 96%, ΔIMVR 106%; SL: ΔCVR 50%, ΔOMVR 64%, ΔIMVR 35%]; in normal rats blood flow shifts from the medulla toward the cortex. In conclusion, nitric oxide may have a role in the regulation of renal vascular tone not only in the case of regular sodium uptake but in the sodium depleted or loaded organism as well. However, nitric oxide has no role in the dietary salt evoked vascular adaptation in the kidney.

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“…In the kidney, kinins contribute to the renal vasodilatory actions of ACEIs, mainly in the medullary circulation [69][70][71][72][73].…”

Section: Angiotensin Converting Enzyme Inhibitorsmentioning

confidence: 99%

Intratubular Renin-Angiotensin System in Hypertension

Suzaki¹,

Prieto-Carrasquero²,

Kobori³

2006

CHYR

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It is well recognized that the renin-angiotensin system plays an important role in the regulation of arterial pressure and sodium homeostasis. Recent years, many studies have shown that local tissue angiotensin II levels are differentially regulated and cannot be explained on the basis of circulating concentrations. All of the components needed for angiotensin II generation are present within the various compartments in the kidney including the renal interstitium and the tubular network. The cascade of the renin-angiotensin system demonstrates three major possible sites for the pharmacological interruption of the renin-angiotensin system: the interaction of renin with its substrate, angiotensinogen, the angiotensin converting enzyme, and angiotensin II type 1 receptors. This brief article will focus on the role of the intratubular renin-angiotensin system in the pathophysiology of hypertension and the responses to the renin-angiotensin system blockade by renin inhibitors, angiotensin converting enzyme inhibitors and angiotensin II type 1 receptor blockers.

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Kinin influences on renal regional blood flow responses to angiotensin-converting enzyme inhibition in dogs

Cited by 27 publications

References 19 publications

Effects of icatibant on the ramipril-induced decrease in renal lithium clearance in the rat

Effects of icatibant on the ramipril-induced decrease in renal lithium clearance in the rat

Intrarenal Distribution of Blood Flow in Sodium Depleted and Sodium Loaded Rats: Role of Nitric Oxide

Intratubular Renin-Angiotensin System in Hypertension

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