Essential hypertension: a renal disease? A review and update of the evidence.

Luke, Robert G.

doi:10.1161/01.hyp.21.3.380

Cited by 62 publications

(24 citation statements)

References 84 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus in studies of normotensive relatives of patients with essential hypertension increased renal vasoconstriction in response to mental stress and postural changes has been shown. 23 Further, in spontaneously hypertensive rats, an experimental model of essential hypertension, chronic inhibition of nitric oxide synthesis, a renal vascular paracrine factor, resulted in a pathophysiological state indistinguishable from hypertensive nephrosclerosis. 24 Albumin excretion in hypertension is thought to be due to renovascular aberrations, as well as the loss of glomerular capillary permselectivity.…”

Section: Discussionmentioning

confidence: 99%

Microalbuminuria, renal function and waist:hip ratio in black hypertensive Jamaicans

et al. 1998

View full text Add to dashboard Cite

Objective: To investigate the relationship between blood pressure (BP), renal haemodynamics, anthropometric measures of obesity and urinary albumin excretion in hypertension and in a control group. Methods: Urinary albumin, BP and anthropometric measurements were carried out in patients attending the hypertension clinic of the University Hospital of the West Indies. A randomised stratified sample was then selected for renal haemodynamic assessment. A normoalbuminuric control group without hypertension or diabetes was also selected. Renal haemodynamics was assessed by measuring glomerular filtration rate using 51-chromium edetic acid (51Cr-EDTA) and renal blood flow using 125-iodohippurate (125-PAH). Results: Urinary albumin excretion was positively and significantly correlated with systolic pressure (␤ ‫؍‬ 0.011, P Ͻ 0.003, R ‫؍‬ 0.22), current body weight (␤ ‫؍‬ 0.014, P Ͻ 0.04, R ‫؍‬ 0.15) and the presence of diabetes (␤ ‫؍‬ 0.9, P Ͻ 0.001, R ‫؍‬ 0.3). In the sample selected for

show abstract

Section: Discussionmentioning

confidence: 99%

Microalbuminuria, renal function and waist:hip ratio in black hypertensive Jamaicans

et al. 1998

View full text Add to dashboard Cite

show abstract

“…Breathing with pure oxygen resulted in a significant increase of blood (EPO) was introduced in the treatment of anemia caused by renal failure, the most important side effect of the therapy was an increase of blood pressure or worsening of preexisting hypertension. 12 The proposed mechanisms of hypertension during EPO treatment were increased blood viscosity, loss of hypoxic vasodilation, and inappropriately reduced cardiac output after correction of anemia.…”

Section: Introductionmentioning

confidence: 99%

“…12 The proposed mechanisms of hypertension during EPO treatment were increased blood viscosity, loss of hypoxic vasodilation, and inappropriately reduced cardiac output after correction of anemia. 24 Furthermore, recent studies suggested that EPO could induce a direct or hormonally mediated vasopressor effect.…”

mentioning

confidence: 99%

Effect of isobaric hyperoxemia on erythropoietin secretion in hypertensive patients.

Kokot

Franek

et al. 1994

Hypertension

View full text Add to dashboard Cite

We assessed the influence of hyperoxemia on erythropoietin secretion in patients with various etiological forms of arterial hypertension (essential, n=15; renoparenchymal, n=16; renovascular, n=15) and in 15 healthy subjects. On the first day of the study, blood was withdrawn at 1-hour intervals for the estimation of erythropoietin during a total of 6 hours and at 2-hour intervals for the assessment of PO2. Three days later the same parameters were assessed again at identical time intervals, but the subjects were breathing pure oxygen during the first 2 hours. Breathing with pure oxygen resulted in a significant increase of blood (EPO) was introduced in the treatment of anemia caused by renal failure, the most important side effect of the therapy was an increase of blood pressure or worsening of preexisting hypertension. 12 The proposed mechanisms of hypertension during EPO treatment were increased blood viscosity, loss of hypoxic vasodilation, and inappropriately reduced cardiac output after correction of anemia.24 Furthermore, recent studies suggested that EPO could induce a direct or hormonally mediated vasopressor effect. 36The main stimulus for EPO secretion seems to be a decrease of oxygen supply to the renal tissue.7 As shown by Kurtz et al,7 EPO secretion is determined by the ratio of oxygen supply to oxygen demand in the kidney. The parameter that adequately reflects this ratio is Po 2 in small postcapillary peritubular veins. This local P02 is detected by a putative oxygen sensor regulating EPO secretion. -8 Limited information is currently available on the influence of hyperoxia on the regulation of EPO secretion.9 -" Changes in renal hemodynamics and tubular function are well described in hypertension. © 1994 American Heart Association, Inc.sive patients. In patients with essential hypertension, unlike in healthy subjects and patients with other etiological forms of arterial hypertension, only a very short-term suppression of erythropoietin levels was observed during hyperoxemia. No significant changes in blood pressure during breathing with pure oxygen were found in any of the studied groups. We conclude the following: (1) Isobaric hyperoxia exerts a significant suppressive effect on plasma erythropoietin levels both in patients with different etiological forms of arterial hypertension and in healthy subjects. (2) Patients with essential hypertension are characterized by a quantitatively different response of plasma erythropoietin to isobaric hyperoxia compared with healthy subjects and patients with renoparenchymal or renovascular hypertension. (3) Oxygen physically dissolved in blood plasma seems to be an important determinant of erythropoietin secretion independent of hemoglobin concentration and oxygen saturation. (Hypertension. 1994;24:486-490.) Key Words • erythropoietin • hypertension, essential • erythropoiesis • oxygen regulation of EPO production, both of these factors might influence EPO secretion. Limited available information on endogenous EPO in arterial hypertension did no...

show abstract

“…2,4,10,11 Furthermore, many hypertensive patients have varying degrees of reduced renal function and compromised sodium excretion associated with excessive activation of the RAS. 12,13 …”

mentioning

confidence: 99%

Regulation of Intrarenal Angiotensin II in Hypertension

et al. 2002

View full text Add to dashboard Cite

Abstract-Intrarenal angiotensin II (Ang II) is regulated by several complex processes involving formation from both systemically delivered and intrarenally formed substrate, as well as receptor-mediated internalization. There is substantial compartmentalization of intrarenal Ang II, with levels in the renal interstitial fluid and in proximal tubule fluid being much greater than can be explained from the circulating levels. In Ang II-dependent hypertension, elevated intrarenal Ang II levels occur even when intrarenal renin expression and content are suppressed. Studies in Ang II-infused rats have demonstrated that augmentation of intrarenal Ang II is due, in part, to uptake of circulating Ang II via an Ang II type 1 (AT 1 ) receptor mechanism and also to sustained endogenous production of Ang II. Some of the internalized Ang II accumulates in the light and heavy endosomes and is therefore potentially available for intracellular actions. The enhanced intrarenal Ang II also exerts a positive feedback action to augment intrarenal levels of angiotensinogen (AGT) mRNA and protein, which contribute further to the increased intrarenal Ang II in hypertensive states. In addition, renal AT 1 receptor protein and mRNA levels are maintained, allowing increased Ang II levels to elicit progressive effects. The increased intrarenal Ang II activity and AGT production are associated with increased urinary AGT excretion rates. The urinary AGT excretion rates show a clear relationship to kidney Ang II content, suggesting that urinary AGT may serve as an index of Ang II-dependent hypertension. Collectively, the data support a powerful role for intrarenal Ang II in the pathogenesis of hypertension. Key Words: renin-angiotensin system Ⅲ angiotensinogen Ⅲ receptors, angiotensin Ⅲ hypertension, experimental I t is an honor and a privilege to be selected to present the Arthur C. Corcoran Memorial Lecture and I greatly appreciate this recognition that has been given to our research group. We all realize, however, that this year is very different for our country. The terrorist attacks have burned the date of September 11, 2001, indelibly in our minds. In the light of these tragic events, it has been difficult to move forward with the ordinary business of our lives. Compared with the sacrifices of the victims and their families, our activities have seemed irrelevant. Aside from moral and financial support, there is little that we personally can do. As scientists, however, we are comforted by the conviction that what we do collectively provides significant long-term benefits to the health and well-being of our citizens. Thus, going about our business and minimizing the disruptions is the most positive response that we can make. In doing so, however, we keep in mind that others less fortunate lost their lives or their loved ones while they were going about the ordinary business of their lives.As a renal physiologist, receiving this Corcoran Award is particularly meaningful because Dr. Corcoran performed so many interesting studies related to ...

show abstract

Essential hypertension: a renal disease? A review and update of the evidence.

Cited by 62 publications

References 84 publications

Microalbuminuria, renal function and waist:hip ratio in black hypertensive Jamaicans

Microalbuminuria, renal function and waist:hip ratio in black hypertensive Jamaicans

Effect of isobaric hyperoxemia on erythropoietin secretion in hypertensive patients.

Regulation of Intrarenal Angiotensin II in Hypertension

Contact Info

Product

Resources

About