Pathophysiology of renovascular hypertension.

Martinez-Maldonado, M.

doi:10.1161/01.hyp.17.5.707

Cited by 200 publications

(170 citation statements)

References 103 publications

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“…The RAS has a pivotal role in the development and maintenance of Goldblatt two-kidney one clip (G2K1C) hypertension: it increases plasmatic and tissue Ang II levels in both clipped and non-clipped kidneys [16]. In this model of hypertension, the non-clipped kidney is renin depleted but the intrarenal Ang II levels are not suppressed and Ang II concentrations in proximal tubular fluid remain high [20].…”

Section: Introductionmentioning

confidence: 99%

Angiotensinase activities in the kidney of renovascular hypertensive rats

et al. 2003

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In spite of the well-known contribution of angiotensin II (Ang II) in the pathogenesis of Goldblatt two-kidney one clip (G2K1C) hypertension, the importance of other Ang peptides, such as Ang III, Ang IV or Ang 2-10, is scarcely understood. The functional status of these peptides depends on the action of several aminopeptidases called angiotensinases. The metabolism of Ang III to Ang IV by aminopeptidase M (AlaAP) and of Ang I to Ang 2-10 by aspartyl aminopeptidase (AspAP) was evaluated in the renal cortex and medulla of normotensive (Sham-operated) and hypertensive (G2K1C) rats, treated or not with the AT 1 receptor antagonist valsartan. The results demonstrated a highly significant increase of membrane-bound (MEMB) AlaAP in the cortex of the non-ischemic kidney of G2K1C rats compared with the kidney of normal rats and with the clipped kidney of G2K1C rats. This suggests an increased formation of Ang IV in the non-clipped kidney of G2R1C rats. Valsartan reduced MEMB AlaAP and AspAP activities in the renal cortex of normotensive and in the clipped kidney of hypertensive rats. The reduced metabolism of Ang III may prolong its half-life in valsartan-treated animals. These results suggest a role for AlaAP in renovascular hypertension. In addition, the higher AspAP activity of the renal cortex compared to medulla reflects its relative functional difference between both locations.

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Section: Introductionmentioning

confidence: 99%

Angiotensinase activities in the kidney of renovascular hypertensive rats

et al. 2003

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“…tected because the elevated blood pressure and the progression of cardiac hypertrophy were mainly dependent on RAS activation in our experimental RHT model (18).…”

Section: Fig 8 Morphologic Changes Of Rat Coronary Vessels Sectionmentioning

confidence: 81%

Effects of Bradykinin on Cardiovascular Remodeling in Renovascular Hypertensive Rats

et al. 2004

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Angiotensin converting enzyme (ACE) inhibitors inhibit both the formation of angiotensin II and the catabolism of bradykinin (BK).sion of angiotensin I into angiotensin II (ATII). ACE inhibitors block not only ATII formation but also bradykinin (BK) degradation. Some pharmacological effects of ACE inhibitors are mediated by endogenous preservation of BK. BK is a potent vasodilator peptide, which possesses cardioprotective action via BK B2 receptor. The binding of BK to B2 receptor activates second messengers that induce a broad spectrum of biological effects, such as vasodilation, inflammation and cell proliferation (5, 6). In cardiovascular systems, BK mediates important effects, including increased vascular permeability, enhanced myocardial glucose uptake,

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“…The 2K1C hypertensive rat is a renovascular hypertensive model, which is characterized by elevated Ang II expression caused by ischemia in clipped kidney and shear stress in nonclipped kidney. The activity of RAS plays a key role in the development and maintenance of high BP through the production of Ang II [34,35] . Ang II has a high affinity for AT 1 receptors, which are responsible for Ang II-induced hypertension.…”

Section: Discussionmentioning

confidence: 99%

Effects of allisartan, a new AT1 receptor blocker, on blood pressure and end-organ damage in hypertensive animals

Yang

et al. 2009

Acta Pharmacol Sin

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Aim:To investigate the effects of allisartan, a new angiotensin II type 1 (AT 1 ) receptor antagonist, on blood pressure (BP) and end-organ damage (EOD) in hypertensive rats and dogs. Methods: First, a single dose of allisartan was given intragastrically to evaluate the BP reduction in spontaneously hypertensive rats (SHRs), two kidney-one clip (2K1C) renovascular hypertensive rats and dogs, and Beagle dogs with angiotensin II-induced hypertension. Second, allisartan was mixed in rat chow for long-term treatment. After 4 months of drug administration, rats were instrumented to determine BP and baroreflex sensitivity (BRS). Observation of morphologic changes was used to estimate EOD. Third, the acute toxicity of allisartan was compared with that of losartan in mice. Results: BP was significantly decreased after intragastric administration of allisartan in SHRs, 2K1C rats, 2K1C dogs and Beagle dogs with angiotensin II-induced hypertension. Compared with the control, SHRs that received long-term treatment with allisartan exhibited an improved BRS and organ protective effects. Mice who were administered allisartan experienced less acute toxicity than those treated with losartan. Conclusion: Allisartan is highly effective for BP reduction and organ protection with low toxicity.

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Pathophysiology of renovascular hypertension.

Cited by 200 publications

References 103 publications

Angiotensinase activities in the kidney of renovascular hypertensive rats

Angiotensinase activities in the kidney of renovascular hypertensive rats

Effects of Bradykinin on Cardiovascular Remodeling in Renovascular Hypertensive Rats

Effects of allisartan, a new AT1 receptor blocker, on blood pressure and end-organ damage in hypertensive animals

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