Changes of hemodynamics and glomerular ultrafiltration in renal hypertension of rats

Schwietzer, G.; Gertz, K. H.

doi:10.1038/ki.1979.19

Cited by 74 publications

(30 citation statements)

References 38 publications

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“…It has been suggested that these increased pressures and flows may cause glomerular damage, eventuating in mesangial sclerosis and proteinuria. Micropuncture studies in hypertensive, salt-fed Holtzman rats (4) and 2-kidney, one clip Goldblatt hypertension (5) have demonstrated an augmented pattern of glomerular capillary perfusion similar to that observed after reduction in renal mass. Furthermore, in both salt-fed Holtzman rats (4) and 2-kidney, one clip Goldblatt hypertension (6), glomerular sclerosis eventually develops.…”

Section: Introductionmentioning

confidence: 73%

“…Finally, it has long been known that when hypertension is produced by constricting one renal artery in the rat, glomerular lesions are produced in the opposite kidney but not in the ipsilateral clipped kidney (6,29). Recent micropuncture studies (5) indicate that, in rats with this form of experimental hypertension, the unclipped kidney has augmented glomerular capillary pressures and flows and single nephron filtration rates, while, in contrast, these same parameters are reduced in the clipped "protected" kidney. Thus, the glomerular hemodynamic pattern observed in the unclipped kidneys of rats with 2-kidney Goldblatt hypertension closely resembles that observed in DOC-SALT hypertensive rats.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Hemodynamic basis for glomerular injury in rats with desoxycorticosterone-salt hypertension.

Dworkin¹,

Hostetter²,

Rennke³

et al. 1984

J. Clin. Invest.

256

102

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were not different than group 3 but significantly lower than group 4. QA and SNGFR were lower in group 5 (low protein) than in groups 3 and 4. Furthermore, proteinuria and glomerular structural lesions were abolished in group 5. Morphologic studies performed in groups 6 and 7 showed that early DOC-SALT lesions progress to focal glomerular sclerosis. These studies suggest that continued elevations in glomerular capillary flows and pressures predispose to glomerular injury in this model of systemic arterial hypertension.

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Section: Introductionmentioning

confidence: 73%

Section: Discussionmentioning

confidence: 99%

Hemodynamic basis for glomerular injury in rats with desoxycorticosterone-salt hypertension.

Dworkin¹,

Hostetter²,

Rennke³

et al. 1984

J. Clin. Invest.

256

102

View full text Add to dashboard Cite

show abstract

“…In rats with unilateral renal artery constriction, glomerular sclerotic lesions develop in the unclipped kidney but not in the clipped (nonhypertensive) kidney (37,38). Micropuncture studies have demonstrated that the unclipped kidney is exposed to augmented glomerular capillary pressure and flows, whereas these parameters are reduced in the clipped, "protected" kidney (39).…”

Section: Discussionmentioning

confidence: 99%

Control of glomerular hypertension limits glomerular injury in rats with reduced renal mass.

Anderson¹,

Meyer²,

Rennke³

et al. 1985

J. Clin. Invest.

857

382

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Micropuncture and morphologic studies were performed in four groups of male Munich-Wistar rats after removal of the right kidney and segmental infarction of two-thirds of the left kidney. Groups 1 and 3 received no specific therapy. Groups 2 and 4 were treated with the angiotensin I converting enzyme inhibitor, enalapril, 50 mg/liter of which was put in their drinking water. All rats were fed standard chow. Groups 1 and 2 underwent micropuncture study 4 wk after renal ablation. Untreated group 1 rats exhibited systemic hypertension and elevation of the single nephron glomerular filtration rate (SNGFR) due to high average values for the mean glomerular transcapillary hydraulic pressure difference and glomerular plasma flow rate. In group 2 rats, treatment with enalapril prevented systemic hypertension and maintained the mean glomerular transcapillary hydraulic pressure gradient at nearnormal levels without significantly compromising SNGFR and the glomerular capillary plasma flow rate, as compared with untreated group 1 rats. Groups 3 and 4 were studied 8 wk after renal ablation. Untreated group 3 rats demonstrated persistent systemic hypertension, progressive proteinuria, and glomerular structural lesions, including mesangial expansion and segmental sclerosis. In group 4 rats, treatment with enalapril maintained systemic blood pressure at normal levels over the 8-wk period and significantly limited the development of proteinuria and glomerular lesions. These studies suggest that control of glomerular hypertension effectively limits glomerular injury in rats with renal ablation, and further support the view that glomerular hemodynamic changes mediate progressive renal injury when nephron number is reduced.

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“…Differential GFR renography documents decreased function of one kidney, presumably due to stenosis of the artery supplying that kidney. Captopril further decreases GFR in a stenosed kidney 35 ' 36 and increases function in the contralateral kidney, 37 which should accentuate the difference in GFR between the two kidneys. Our data confirm small reports that postcaptopril differential GFR renography detects renal artery stenosis with 92% sensitivity.…”

Section: Discussionmentioning

confidence: 99%

Prospective analysis of strategies for diagnosing renovascular hypertension.

et al. 1989

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Renovascular hypertension is a potentially curable form of high blood pressure. However, it is unclear how best to select patients who are likely to have renovascular hypertension, what diagnostic strategy to use in these selected patients, and how to predict the hemodynamic significance of a renal artery stenosis. We determined the prevalence of renovascular hypertension in adults who exhibited suggestive clinical features. In these clinically selected patients, we then determined the test characteristics of various diagnostic and potential screening tests. Renovascular hypertension was diagnosed if correction of renal artery stenosis resulted in decreased blood pressure. Of the 66 hypertensive adults evaluated, 11 (16.7%) had renovascular hypertension. Captopril-stimulated peripheral renln activity detected renovascular hypertension with 73% sensitivity, 72% specificity, 38% positive predictive value, and 92% negative predictive value. Less optimal combinations of sensitivity and specificity were found for differential glomerular filtration rate renography, differential effective renal plasma flow renography, and selective renal vein renin ratios, each performed after a single dose of captopril. Intravenous digital subtraction renal angktgraphy detected all patients with renovascular hypertension and was normal in 71% of patients with essential hypertension. To evaluate potential screening tests for renovascular hypertension, we calculated predictive values applied to a low prevalence population. If the observed sensitivities and specificities apply to a population with 5% prevalence of renovascular hypertension, captopril-stimulated peripheral renin would have a positive predictive value of 12% and a negative predictive value of 98%. In 16 patients with known renal artery stenosis, neither the captopril-stimulated renal vein renin ratio nor captopril-stimulated differential renography accurately predicted blood pressure response to correction of the stenosis. We conclude that clinical criteria can identify a subgroup with 16.7% prevalence of renovascular hypertension. In this high prevalence group, intravenous digital subtraction renal angiography will identify virtually all patients with renovascular hypertension, and a normal study will be sufficient to exclude renovascular hypertension. In unselected hypertensive patients, screening with captopril-stimulated peripheral renin activity may be the most useful and efficient procedure for identification of patients with renovascular hypertension. Functional tests do not accurately predict the hemodynamic significance of a renal artery stenosis. {Hypertension 1989;14:247-257) R enovascular hypertension (RVH) is a potentially curable form of high blood pressure. Its treatment, with angioplasty or surgery, provides the opportunity to prevent cardiovascular morbidity and mortality due to hypertension and to avoid the expense and potential morbidity of lifelong pharmacotherapy for hypertension. Therefore, this condition should be identified and treated whenever poss...

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Changes of hemodynamics and glomerular ultrafiltration in renal hypertension of rats

Cited by 74 publications

References 38 publications

Hemodynamic basis for glomerular injury in rats with desoxycorticosterone-salt hypertension.

Hemodynamic basis for glomerular injury in rats with desoxycorticosterone-salt hypertension.

Control of glomerular hypertension limits glomerular injury in rats with reduced renal mass.

Prospective analysis of strategies for diagnosing renovascular hypertension.

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