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At least 1,351 records · Page 75Linked to original sources
PubMed1986

Small kidney and hypertension: selection of patients for surgery.

We studied 37 patients with various degrees of hypertension and a small unilateral kidney. Renal vein renin studies were shown to be positive on 19 occasions and negative on 18. Of those positive, 10 had severe and 1 moderate hypertension. Surgery cured 63.3%. In 27% blood pressure improved and 1 patient failed to respond. Eight patients had mild hypertension with a positive renal vein renin ratio (RVRR), but on observation their home blood pressures were normal without medication and they were not considered for surgery. Eighteen patients with mild hypertension and negative RVRR were also not operated. We believe that RVRR is important for a surgical decision, but only in severe and moderate hypertensives. In mild hypertension, measurement of blood pressure at home is normal on most occasions. These are hyperreactive patients and should not have surgery, regardless of the results of their RVRRs.

Adolescent↗
PubMed1986

Serum beta-N-acetyl hexosaminidase levels in chronic renal failure.

Serum beta-N-acetyl hexosaminidase (beta-NAH) levels, the indirect indicators of hepatic endothelial and Kupffer cell function, were examined in 16 anuric chronic hemodialysis patients, and in 11 patients in different stages of chronic renal failure (serum creatinine 2-8.8 mg/dl). They were found to be lower than those of the healthy controls, contrary to expectation. It might be concluded that nonparenchymal liver cells are functioning well in chronic renal failure. However, the possibility that production of beta-NAH in these patients is abnormally reduced cannot be excluded.

Adult↗
PubMed1999

Vascular endothelin-1 gene expression and synthesis and effect on renal type I collagen synthesis and nephroangiosclerosis during nitric oxide synthase inhibition in rats.

BACKGROUND: The progression of hypertension during NO deficiency is associated with renal vascular fibrosis due to increased extracellular matrix (mainly collagen I) formation. The purpose of the present study was to investigate whether endothelin-1 (ET-1) is involved in this pathophysiological process. METHODS AND RESULTS: Treatment of rats for 4 weeks with the NO synthase inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME) 50 mg. kg-1. d-1 increased systolic blood pressure to 159+/-12 mm Hg. In animals treated with L-NAME, histological evaluation of renal sections revealed an increased formation of extracellular matrix (Masson's trichrome), and specifically of collagens (Sirius red). A part of this fibrosis was attributed to abnormal collagen I presence, because mRNA expression of the collagen I alpha1 chain (reverse transcription-polymerase chain reaction) and procollagen I formation (radioimmunoassay) were increased 3- and 2.5-fold, respectively, in the renal resistance vessels of hypertensive animals. In subsequent experiments, we examined whether ET-1 was involved in activation of collagen I formation. mRNA expression (RNase protection assay) of preproET-1 and ET-1 content (radioimmunoassay) were 10-fold and 3-fold increased, respectively, in renal microvessels of rats treated with L-NAME. Interestingly, in these vessels, ET-1 (immunostaining) was colocalized with sudanophilic lesions. Bosentan, an ET receptor antagonist (20 mg. kg-1. d-1), coadministered with L-NAME canceled the increased mRNA expression and synthesis of collagen I and attenuated the severity of renal vascular lesions without affecting L-NAME-induced high blood pressure. CONCLUSIONS: These data demonstrate that ET-1 synthesis is increased in renal microvessels when NO production is suppressed. In this model of hypertension, ET-1 is a major activator of collagen I formation in renal resistance vessels and participates in the development of renal fibrosis without affecting systolic blood pressure.

Animals↗
PubMed2004

Pathophysiology of hypertensive renal damage: implications for therapy.

Unlike the majority of patients with uncomplicated hypertension in whom minimal renal damage develops in the absence of severe blood pressure (BP) elevations, patients with diabetic and nondiabetic chronic kidney disease (CKD) exhibit an increased vulnerability to even moderate BP elevations. Investigations in experimental animal models have revealed that this enhanced susceptibility is a consequence of an impairment of the renal autoregulatory mechanisms that normally attenuate the transmission of elevated systemic pressures to the glomeruli in uncomplicated hypertension. The markedly lower BP threshold for renal damage and the steeper slope of relationship between BP and renal damage in such states necessitates that BP be lowered into the normotensive range to prevent progressive renal damage. When BP is accurately measured using radiotelemetry in animal models, the renal protection provided by renin-angiotensin system (RAS) blockade is proportional to the BP reduction with little evidence of BP-independent protection. A critical evaluation of the clinical data also suggests that the BP-independent renoprotection by RAS blockade has been overemphasized and that achieving lower BP targets is more important than the selection of antihypertensive regimens. However, achievement of such BP goals is difficult in CKD patients without aggressive diuresis, because of their proclivity for salt retention. The effectiveness of RAS blockers in lowering BP in patients who have been adequately treated with diuretics, along with their potassium-sparing and magnesium-sparing effects, provides a more compelling rationale for the use of RAS blockade in the treatment of CKD patients than any putative BP-independent renoprotective superiority.

Animals↗
PubMed1995

Does keloid pathogenesis hold the key to understanding black/white differences in hypertension severity?

Repeated national surveys have shown that in the United States hypertension is more common and more severe in the black than in the white population. This discussion presents the hypothesis that the racial difference in hypertension severity is because of differences in growth factors (cytokines) affecting vascular smooth muscle cell growth. This hypothesis is derived from studies of keloids, which occur almost exclusively in blacks. Keloid fibroblasts in culture have growth characteristics that differ substantially from those of normal skin. Furthermore, there is evidence that peripheral blood mononuclear cells from patients with keloids produce different amounts of cytokines than do similar preparations from the blood of individuals without keloids. A growing body of evidence indicates that growth factors play a pivotal role in the pathogenesis of atherosclerosis, in experimental forms of hypertension, and in various renal diseases; it may be that they function in clinical hypertension as well.

Adolescent↗
PubMed1975

Effect of varying perfusion pressures on the output of sodium and renin and the vascular resistance in kidneys of rats with "post-salt" hypertension and Kyoto spontaneous hypertension.

Isolated kidneys from both "post-salt" normotensive and hypertensive rats were perfused with blood from donor rats at varying pressures. At 130 mm Hg inflow pressure 15 "post-salt normotensive" kidneys put out 0.75 muEq Na/min/g kidney while 14 "post-salt hypertensive" kidneys put out 0.28 mu-Eq Na/min/g (P less than 0.001), a 63% reduction. They also put out 55% less water (P less than 0.002). Thus, if "hypertensive" kidneys are perfused at normal pressures, they put out subnormal amounts of Na and H-2-O. Such Na and H-2-O retention maintains the hypertensive state. Normal Na output in these kidneys was only reached at hypertensive (160) inflow pressures. This shift in the "pressure natriuresis" curve explains in part how some "hypertensive" kidneys maintain hypertension. These "hypertensive" kidneys have grossly abnormal autoregulation curves, each increment of pressure actually producing progressively greater increments of blood flow. Isolated kidneys from Kyoto hypertensive and normotensive rats showed no difference in Na and H-2-O excretion at 130 mm Hg inflow pressure. Thus, a tendency to Na retention demonstrable in the isolated kidney is apparently not supporting Kyoto hypertension. Moreover, isolated kidneys form Kyoto hypertensive rats released significantly lower amounts of renin at all levels of inflow pressure, averaging a 70% lower rate than Kyoto normotensive kidneys (P less than 0.01). Hence, Kyoto hypertension is not supported by a supernormal renin release inherent in the kidney. One can speculate that Kyoto hypertensive rats normally have an elevated sympathetic tone which stimulates release of renin. The denervation which occurs in isolating kidneys might therefore produce a proportionally greater percentage loss of sympathetic influence in these kidneys, which could possibly account for some of their reduced renin release. These Kyoto hypertensive kidneys are apparently not "reset" to maintain hypertension with either Na or renin.

Animals↗
PubMed1970

On the influence of extracellular fluid volume expansion and of uremia on bicarbonate reabsorption in man.

The patterns of bicarbonate reabsorption during increasing plasma concentrations were studied in subjects with a range of glomerular filtration rates (GFR) from 170 to 2 ml/min. In a group of five subjects with GFR values above 30 ml/min, paired bicarbonate titration studies were performed first under conditions which minimized extracellular fluid (ECF) volume expansion, and second under conditions which were conducive to exaggerated expansion of ECF volume. In patients with GFR values below 30 ml/min, a single protocol was employed. Studies also were performed on two patients with far advanced renal disease who were nephrotic and exhibited a sodium-retaining state. When ECF volume expansion was minimized in the nonuremic subjects, values for bicarbonate reabsorption were well in excess of the usually accepted Tm level and over the range of plasma bicarbonate concentrations employed, no evidence of a Tm phenomenon was observed. A similar pattern emerged in the two nephrotic patients despite the presence of uremia. However, with both exaggerated expansion of ECF volume (GFR greater than 30) and in patients with advanced renal disease in the absence of exaggerated ECF volume expansion a tendency towards saturation kinetics for bicarbonate reabsorption was demonstrable. In comparing the minimized with the exaggerated expansion studies, evidence emerged for a decrease in both bicarbonate reabsorption per unit of GFR and the absolute rate of bicarbonate reabsorption. When ECF volume expansion was exaggerated in uremic patients after stable rates of bicarbonate reabsorption had been achieved, a decrease in reabsorption per unit of GFR and in absolute bicarbonate reabsorption occurred. The possible relationship of the factors controlling sodium excretion to the observed patterns of bicarbonate reabsorption is considered in the text.

Absorption↗