ETA receptor blockade attenuates the hypertension but not renal dysfunction in DOCA-salt rats.

@article{Allcock1998ETARB,
  title={ETA receptor blockade attenuates the hypertension but not renal dysfunction in DOCA-salt rats.},
  author={Graham H. Allcock and Richard C. Venema and David M. Pollock},
  journal={The American journal of physiology},
  year={1998},
  volume={275 1},
  pages={
          R245-52
        },
  url={https://api.semanticscholar.org/CorpusID:10877220}
}
ETA receptors appear to play a role in the maintenance and development of DOCA-salt hypertension but not in the accompanying reduction of renal function.
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Background Citations
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Methods Citations
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Results Citations
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ET(A) receptor blockade prevents renal dysfunction in salt-sensitive hypertension induced by sensory denervation.

The blockade of the ET(A) receptor ameliorates the impairment of renal excretory function and prevents the elevation in blood pressure in salt-sensitive hypertension induced by degeneration of sensory nerves, indicating that the activation of the E-A receptor impairs renal function and contributes to the development of a salt-induced increase in blood Pressure in this model.

Arterial Pressure Response to the Antioxidant Tempol and ETB Receptor Blockade in Rats on a High-Salt Diet

The data suggest that blood pressure lowering by tempol in rats on a high-salt diet may be unrelated to reductions in superoxide and that renal H2O2 may account for the limited ability of tempol to attenuate hypertension produced by ETB receptor blockade.

Different contributions of endothelin-A and endothelin-B receptors in the pathogenesis of deoxycorticosterone acetate-salt-induced hypertension in rats.

Results strongly support the view that ETA receptor-mediated action plays an important role in the pathogenesis of DOCA-salt-induced hypertension and seem likely that the ETB receptor- mediated action protects against vascular and renal injuries in this model of hypertension.

Endothelin A receptor blockade reduces diabetic renal injury via an anti-inflammatory mechanism.

Observations indicate that ETA receptor activation mediates renal inflammation and TGF-beta production in diabetes and are consistent with the postulate that Eta blockade slows progression of diabetic nephropathy via an anti-inflammatory mechanism.

Functional Role of ETB Receptors in the Renal Medulla

Results demonstrate that medullary vasodilation produced by Big ET‐1 is more prominent in rats on a high salt diet and are consistent with a contribution of ETB‐mediated events in the natriuretic response to high salt intake, which supports the hypothesis that endothelin plays an important role in regulating sodium excretion through activation of ETBs.

Role of ET-1 receptor binding and [Ca(2+)](i) in contraction of coronary arteries from DOCA-salt hypertensive rats.

The results suggest endothelin receptor uncoupling from signaling mechanisms and indicate that impaired [Ca(2+)](i) signaling contributes to the decrease in ET-1-induced contraction of coronary small arteries in DOCA-salt hypertensive rats.

Renal hemodynamics in renal artery stenosis and angiotensin II-dependent hypertension. Pathophysiological and diagnostic aspects.

The results suggest that selective ETA antagonists are more effective than combined ETA+B antagonists in this model and biomarkers of oxidative stress, and ET-1, in hypertensive patients with atherosclerotic RAS (ARAS) and the effect of renal angioplasty.

Assessment of the Effects of Race on Vascular Responses to ETA Receptor Blockade in Normal Subjects and in Hypertensive Patients

Hypertensive blacks have enhanced ETA-dependent vasoconstrictor tone, probably related to increased production of endothelin-1, given the negative vascular effects of ET-1.

Angiotensin II blockade prevents hyperglycemia-induced activation of JAK and STAT proteins in diabetic rat kidney glomeruli.

It is demonstrated that hyperglycemia induces activation of JAK2 and the STATs in vivo via an ANG II-dependent mechanism and that these proteins may be involved in the early kidney damage associated with diabetes.

Unique endothelin receptor binding in kidneys of ETB receptor deficient rats.

Rescued spotting-lethal rats that carry a naturally occurring deletion of the endothelin (ET) type B receptor gene resulting in a lack of functional renal ETB receptor expression have decreased renal cortical and outer medullary ETA receptor number.

47 References

ETA receptor-mediated role of endothelin in the kidney of DOCA-salt hypertensive rats.

ETA receptor blockade prevents hypertension associated with exogenous endothelin-1 but not renal mass reduction in the rat.

It is concluded that ETA receptor activation does not play a significant role in the functional derangements associated with renal mass reduction in the rat and can inhibit ETA-mediated hypertension, but has no effect on hypertension produced by a reduction in renal mass.

Endothelin antagonists in salt-dependent hypertension associated with renal insufficiency.

The results indicate that ET-A receptors play a role in glomerular function and confirm the importance of specific and nonspecific ET antagonists in decreasing blood pressure in models of salt-dependent hypertension.

Endothelin-A receptor antagonism attenuates the hypertension and renal injury in Dahl salt-sensitive rats.

Data indicate that endothelin-A receptor activation may play a role in the exacerbation of hypertension and development of renal injury in Dahl salt-sensitive (DS) rats.

Role of angiotensin II in cerebrovascular and renal damage in deoxycorticosterone acetate‐salt hypertensive rats

Although the hypertension in DOCA-salt hypertensive rats is independent of the renin-angiotensin system, the degree of cerebral and renal damage is associated with the activity of therenin-ANGiotens in system and has little relationship with the blood pressure level.

Effect of a nonselective endothelin antagonist on vascular remodeling in deoxycorticosterone acetate-salt hypertensive rats. Evidence for a role of endothelin in vascular hypertrophy.

It is concluded that a role for endothelin in the elevation of blood pressure and vascular hypertrophy and remodeling in DOCA-salt hypertensive rats may be suggested.

Effects of endothelin on blood pressure and renal hemodynamics in DOCA-salt hypertensive rats under conscious and unrestrained condition.

It is suggested that the marked increase in blood pressure and the altered renal hemodynamics induced by endothelin in DOCA-salt hypertensive rats are due in part to a decrease in endothelins clearance.

Ameliorating effect of an endothelin ETA receptor antagonist on renal function of DOCA-salt hypertensive rats.

Endothelin-1 expression in blood vessels of DOCA-salt hypertensive rats treated with the combined ETA/ETB endothelin receptor antagonist bosentan.

This study investigated the ir-ET-1 levels and the expression of the ET-1 gene in blood vessels of DOCA-salt hypertensive rats treated or not treated with bosentan, which respond to treatment with the combined ETA/ETB endothelin receptor antagonist bosenta with lowering of blood pressure.

Effects of endothelin on resistance arteries of DOCA-salt hypertensive rats.

Significant morphological and functional changes in small arteries of DOCA-salt hypertensive rats within 2 wk of developing hypertension and blunted reactivity to ET-1 are demonstrated.
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