“No man's land” of the renal vasculature

Hollenberg, Norman K.; Epstein, Murray; Basch, Richard I.; Merrill, John P.

doi:10.1016/0002-9343(69)90199-5

Cited by 80 publications

(6 citation statements)

References 15 publications

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“…Justification for the latter is based on the fact that each individual angiographic film shows the stage of dispersal of contrast medium in the kidney at a particular instant in time, and therefore not only provides information regarding the structure of the renal arteries, cortex, medulla and veins, but also when films are examined as a sequential series provides a dynamic record of events which can be used to examine intrarenal blood flow. This approach is fully supported by the work of Hollenberg et al [7], Any abnormality in cither the arterial or nephrogram phase was confirmed by a second injection of contrast medium. …”

Section: Selective Serial Renal Angiographymentioning

confidence: 75%

Structural and Functional Changes in the Renal Circulation after Complicated Pregnancy

Burden¹,

Boyd²,

Aber³

1979

Nephron

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Angiographic and histological studies of the intrarenal circulation have been undertaken in 20 patients following complicated pregnancies: 12 patients had had hypertension of pregnancy (group 1); 7 acute renal failure due to either ante- or post-partum haemorrhage and 1 patient post-partum renal failure (group 2). 3 months after delivery all patients had angiographic evidence of structural and functional abnormalities involving intrarenal blood vessels and cortical blood flow. The severity of the structural changes was related to the degree of microangiopathic haemolytic anaemia noted in the acute obstetric complication but not to the height of the blood pressure at this stage. Histological abnormalities of the cortical blood vessels were minimal. At the time of the renal angiogram and biopsy, 3 of the 12 group 1 patients were hypertensive and 3 had impaired renal function, compared with 5 and 1, respectively, in the 8 group 2 patients. Although during the follow-up period (mean 5 years) no further deterioration in renal function in either group has been observed, hypertension developed in 50% of the group 1 patients compared with only 1 of the patients in group 2. The relationship between the late onset of hypertension and the intrarenal vascular and haemodynamic abnormalities is discussed.

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Section: Selective Serial Renal Angiographymentioning

confidence: 75%

Structural and Functional Changes in the Renal Circulation after Complicated Pregnancy

Burden¹,

Boyd²,

Aber³

1979

Nephron

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“…1). In addition, outer cortical perfusion improves somewhat with increasing pressure in the normal kidney (Robertson et al, 1972;Carrikre et al, 1966) but not in essential hypertension (Hollenberg et al, 1969a). Therefore, it seems unlikely that the changes in renal function in essential hypertension simply involve high pressure from extra-renal causes plus a normal renal response to the increased pressure.…”

Section: S Y N T H E S I Smentioning

confidence: 99%

“…Because of these results, changes in the fastest component of isotope washout are regarded as changes in outer cortical flow. Studies in essential hypertensives using these techniques show a marked decrease in the fastest component of isotope removal ; presumably therefore, the fraction of blood flow going to the outer renal cortex is reduced (Nomura et al, 1974;Hollenberg et al, 1969a;Hollenberg, et a[., 1969b;Ladefoged & Pedersen, 1969;Grunfeld, et al, 1972).…”

Section: Distribution Of Renal Blood $Owmentioning

confidence: 99%

The role of the kidney in essential hypertension

Guyton

et al. 1975

Clin Exp Pharma Physio

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1. Many forms of human and experimental hypertension begin with compromised renal function. Essential hypertension may be another such case. 2. The kidneys of subjects with essential hypertension excrete normal amounts of salt and water at higher-than-normal renal perfusing pressures. Other overt signs of renal dysfunction are few; renal disease is excluded by definition. However, renal blood flow and glomerular filtration rate are usually less than normal in essential hypertension. 3. Renal afferent resistance can be calculated from arterial pressure, renal blood flow, and an estimate of glomerular capillary pressure. These calculations indicate that afferent resistance is increased to two or more times normal in essential hypertension. 4. It is not clear whether afferent constriction causes hypertension or results from it. The ability of high pressure to produce vascular damage points to the latter. But, most essential hypertensives show low-to-normal plasma renin levels and a marked afferent dilation after saline loading. These observations do not suggest nephrosclerosis: they are consistent with a causal role for afferent constriction. 5. We can speculate that, in essential hypertension, there is a defect in one of the mechanisms that sets afferent resistance. Afferent constriction could result from extrinsic influences (neural or humoral) or something totally within the kidney, such as abnormal handling of information from the macula densa. 6. The effect of afferent constriction on salt-and-water excretion would theoretically be offset by elevated arterial pressure so that the actual salt-and-water excretion would be normal, but only so long as the arterial pressure remained elevated.

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“…The initial changes are functional and reversible, presumably mediated by neurohumoral mechanisms, including enhanced renal vascular response to circulating or endogenous norepinephrine and angiotensin II [23][24][25][26][27][28][29][30][31]. Subsequently, structural changes occur related to the severity of the hypertension and to the aging process [7,8,[12][13][14].Two vascular lesions are observed: hyperplastic elastic arteriosclerosis, most marked in the interlobular arteries, and hyaline arteriolosclerosis, primarily involving the afferent arterioles [15,16,[32][33][34][35]. Ultimately, as a result of reduced blood flow, the glomeruli undergo ischemic changes.…”

mentioning

confidence: 99%

“…Secondary tubular atrophy, thickening of tubular basement membranes, and interstitial fibrosis also occur [32][33][34][35]. Because the vascular lesions are usually distributed in a focal, irregular fashion throughout the renal cortex, the secondary ischemic changes assume a similar pattern of distribution [7,15,16,[32][33][34][35]. However, when the vascular lesions are severe and generalized, the entire kidney undergoes ischemic atrophy [15,16,[32][33][34][35].…”

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confidence: 99%

Acute and chronic effects of angiotensin converting enzyme inhibitors on the essential hypertensive kidney

Reams

Bauer

1990

Cardiovasc Drug Ther

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The natural course of essential hypertensive renal disease is characterized by a slowly progressive impairment of renal function. Initially, the changes are functional and reversible; however, structural changes gradually occur, leading to hypertensive nephrosclerosis. Similarities exist between the early functional hemodynamic changes observed in the essential hypertensive kidney and the physiologic renal effects of angiotensin II. To the degree that the initial functional changes are the result of excessive endogenous production of angiotensin II, interruption of the integrity of this humoral system could be expected to reverse the pathophysiologic sequence of events leading to hypertensive nephrosclerosis. This review focuses on the pathophysiology of the essential hypertensive kidney, the intrarenal effects of angiotensin II, and the acute and chronic effects of angiotensin converting enzyme (ACE) inhibition therapy on the essential hypertensive kidney. The data reviewed suggest that ACE inhibition therapy does reverse the initial functional hemodynamic changes observed in the essential hypertensive kidney and may protect the glomerulus from hemodynamically mediated injury.

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“No man's land” of the renal vasculature

Cited by 80 publications

References 15 publications

Structural and Functional Changes in the Renal Circulation after Complicated Pregnancy

Structural and Functional Changes in the Renal Circulation after Complicated Pregnancy

The role of the kidney in essential hypertension

Acute and chronic effects of angiotensin converting enzyme inhibitors on the essential hypertensive kidney

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