The Production of Persistent Arterial Hypertension by Cellophane Perinephritis

Page, Irvine H.

doi:10.1001/jama.1939.02800480032008

Cited by 298 publications

(131 citation statements)

References 8 publications

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“…After the initial increase in GFR due to prostaglandinmediated vasodilation, there was a decrease in GFR due to a vasoconstriction phenomenon with an increase in intrarenal resistance resulting from a self-defence mechanism caused by vasoactive mediators, such as renin, angiotensin II and endothelins [22]. In the present study, the levels of renin, and more markedly aldosterone, increased after the ESWL session.…”

Section: Eswl Associated Injurysupporting

confidence: 50%

The protective role of coenzyme Q10 in renal injury associated with extracorporeal shockwave lithotripsy: a randomised, placebo‐controlled clinical trial

et al. 2014

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These results are protected by a patent at the Spanish Office of Patents and Trademarks (Reference: P201131992) Objective• To determine the efficacy of coenzyme Q10 (CoQ10) in preventing renal injury in patients with lithiasis undergoing extracorporeal shockwave lithotripsy (ESWL). Patients and Methods• Prospective, randomised, double-blind, placebo-controlled clinical trial of 100 patients with renal lithiasis who were treated with ESWL.• The patients were distributed randomly into two groups receiving either placebo or CoQ10 (200 mg/day), a powerful antioxidant with vasoactive properties, orally administered during the week before ESWL and for 1 week after.• Renal dysfunction markers, vasoactive hormones, oxidative stress, plasma levels of several interleukins and vascular resistance index (VRI) using Doppler ultrasound were evaluated the week before ESWL, 2 h before ESWL and at 2 h, 24 h and 7 days after ESWL. Results• There was a significant increase in glomerular filtration (P = 0.013), as well as a decrease in the albumin/creatinine ratio and the β2-microglobulin level (P = 0.02) after 1 week of treatment in the CoQ10 group. These changes were maintained at the follow-up after ESWL.• The administration of CoQ10 was associated with improvement in vasoactive hormone parameters, VRI and interleukin levels. These improvements were maintained until the end of the follow-up period.• However, the administration of CoQ10 was not associated with significant changes in the oxidative stress parameters. Conclusion• Our results indicate that CoQ10 administration improves renal function and vasoactive and inflammation parameter values, allowing for preconditioning before the tissue insult caused by ESWL.

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Section: Eswl Associated Injurysupporting

confidence: 50%

The protective role of coenzyme Q10 in renal injury associated with extracorporeal shockwave lithotripsy: a randomised, placebo‐controlled clinical trial

et al. 2014

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“…34 In our model, we did not observe a malignant phase with arteriolar fibrinoid degeneration and necrosis, which is observed in dogs with severe impairment of renal function and hypertension in Goldblatt's model. 35 These severe morphological changes were also described in dogs after unilateral renal artery constriction 36 and in wrapped kidney according to Page's model 37 in both rabbits and rats. 38 On the contrary, hypertension induced by injection of platelet aggregates 39 or Sephadex 40 was associated with microembolic renal lesions.…”

Section: -32mentioning

confidence: 89%

Renal morphological changes after sinoaortic denervation in dogs.

et al. 1993

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The present study investigates morphological renal lesions in sinoaortic-denervated dogs 1 (n=6) and 18 (n=5) months after sinoaortic denervation compared with sham-operated controls (n=8). After 1 month, a marked hyalinization and moderate thickening of the media of arterioles and small interlobular arteries were observed. These changes associated with edema and intimal thickening led to a narrowing of the lumen. In glomeruli, increase of mesangial matrix was focally present in all cases and associated with mesangial proliferation. In four of six cases, some glomeruli appeared retracted, with a large urinary space. A focal area of interstitial fibrosis occurred in just one case. After 18 months, similar but more pronounced vascular lesions were present, with marked hyperplasia of the media. Glomerular changes were characterized by mesangial lesions associated with focal glomerular sclerosis and thickening of Bowman's capsule. Tubulointerstitial lesions were more prominent in this group, with the presence of tubular epithelial changes and casts. Focal interstitial fibrosis, infiltrates, or both were demonstrated in all cases. These morphological lesions were associated with an increase in arterial blood pressure, proteinuria, and natriuresis and a decrease in urinary kallikrein. These results show that chronic sinoaortic denervation in dogs is associated with renal lesions similar to those observed in other well-established experimental and clinical hypertensive states. 1 By this surgical approach, hypertension has been induced in dog, 2 -3 rabbit, 4 and rat. 5 The mechanism of this experimental hypertension is still being discussed, and it may involve an increase in norepinephrine turnover and biosynthesis already reported in rabbits with neurogenic hypertension. 6 To our knowledge, renal modifications in this model of hypertension have received little attention. A recent report concerning urinary kallikrein excretion after chronic sinoaortic denervation in conscious dogs 7 has shown that urinary kallikrein excretion, which is of renal origin, is reduced after 32 weeks, thus suggesting renal dysfunction in this model of hypertension. With respect to the renal kallikrein-kinin system, a large number of reports 8 suggest a close relation between the decrease in renal kallikrein excretion and the development of hypertension. Although no causal relations have been clearly established between the decrease in urinary kallikrein excretion and the onset of hypertension, a decrease in urinary kallikrein excretion is a significant marker of established hypertension. Because the kidney is a key organ in the long-term control of blood pressure, ascertainment of renal damages could provide other evidence for the persistence of high blood pressure.An association between kidney disease and hypertension was reported by Bright 9 as early as 1836. More recently, the overriding dominance of the kidneys in long-term regulation of arterial pressure and in hypertension has been demonstrated by clinical and experimental studies. 10 I...

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“…The renal artery, vein, and ureter were ligated and cut on one side and the kidney removed; the contralateral kidney was wrapped with dialysis membrane as described previously. 12 The incision was closed in layers and the rabbits were allowed to recover. Eleven other rabbits had one kidney removed and the other kidney exposed but not wrapped and served as the shamoperated normotensive controls.…”

Section: Induction Of Hypertensionmentioning

confidence: 99%

Rapid baroreceptor resetting in chronic hypertension. Implications for normalization of arterial pressure.

et al. 1991

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The purpose of this study was to examine the ability of baroreceptors of renal hypertensive rabbits to reset rapidly during acute changes in arterial pressure. The carotid sinus (CS) was vascularly isolated and baroreceptor activity was recorded during slow ramp increases in CS pressure in hypertensive (one-kidney, one wrap; 127±3 mm Hg) and normotensive (one-kidney, no wrap; 85 ±3 mm Hg) rabbits anesthetized with chloralose. Control measurements were made after holding pressure for 10-15 minutes at the level of arterial pressure recorded before each experiment Baroreceptor threshold pressure (PtJ was higher in hypertensives (78 ±4 mm Hg) compared with normotensives (55 ±3 mm Hg, p<0.05), and nerve activity was less in hypertensives over a wide range of pressure. CS distensibility (sonomicrometers) was not significantly different in the two groups. After increasing holding pressure from control by 30 and 60 mm Hg for 10-15 minutes, the extent of baroreceptor resetting (A P^/A holding pressure x 100%) in normotensives was 39±6% and 33±2%, respectively, but only 14±5% and 9±3% in hypertensives (p<0.05). After decreasing holding pressure by 30 and 60 mm Hg, resetting was similar in normotensives (32±6% and 28±3%) and hypertensives (34±3% and 30±4%). In hypertensive rabbits, acute (10-15 minutes) exposure of baroreceptors to normotension (71 ± 4 mm Hg) decreased Pa, to 62 ±4 mm Hg and increased nerve activity to levels not significantly different from those of normotensive animals without altering CS distensibility. The results indicate that in chronic renal hypertension: 1) further upward resetting of baroreceptors during acute increases in pressure is suppressed; 2) in contrast, downward resetting during acute decreases in pressure is preserved; 3) baroreceptor activity is restored rapidly after brief exposure of the CS to normal pressure; and 4) changes in CS distensibility do not explain decreased baroreceptor activity in chronic hypertension nor restoration of activity after acute normalization of pressure. Impairment of acute upward resetting and preservation of downward resetting should be beneficial since they would oppose further increases in pressure and facilitate lowering of pressure. (Hypertension 1991;17:72-79) B aroreceptors buffer fluctuations in arterial pressure by causing reflexly mediated reciprocal changes in both heart rate and sympathetic nerve activity. 1 These changes keep the level of arterial pressure at a predetermined operating level or set point. When changes in pressure are sustained for several minutes, however, baroreceptors are reset rapidly and the baroreceptor pressure-activity curve shifts in the direction of pressure change to function at a new set point. 2 -5 This allows baroreceptors to buffer fluctuations of arterial pressure effectively because the new pressure set point remains on the steep portion of the reset pressure-activity curve. However, resetting provides positive feedback in the control of arterial pressure. During acute hypotension, baroreceptor activity increase...

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The Production of Persistent Arterial Hypertension by Cellophane Perinephritis

Cited by 298 publications

References 8 publications

The protective role of coenzyme Q10 in renal injury associated with extracorporeal shockwave lithotripsy: a randomised, placebo‐controlled clinical trial

The protective role of coenzyme Q10 in renal injury associated with extracorporeal shockwave lithotripsy: a randomised, placebo‐controlled clinical trial

Renal morphological changes after sinoaortic denervation in dogs.

Rapid baroreceptor resetting in chronic hypertension. Implications for normalization of arterial pressure.

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