Renal Changes in Malignant Hypertension

Wilson, Campbell; Byrom, F.B.

doi:10.1016/s0140-6736(00)60143-5

Cited by 250 publications

(35 citation statements)

References 8 publications

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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: 88%

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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Section: -32mentioning

confidence: 88%

Renal morphological changes after sinoaortic denervation in dogs.

et al. 1993

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“…--This was done by the technique of Byrom and Wilson (9). This experiment was a repetition of one reported previously (3) and was done to make certain that no significant change in response had occurred in the R strain of rats in the intervening period.…”

Section: Methodsmentioning

confidence: 99%

Genetic Influence on the Development of Renal Hypertension in Parabiotic Rats

Iwai

Knudsen

Dahl

et al. 1969

The Journal of Experimental Medicine

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The relative roles of renal pressor and antihypertensive factors in the pathogenesis cf experimental renal hypertension remain a central, and disputed, issue.In our laboratory, we have evolved two strains of rats with opposite genetic predispositions to different forms of experimental hypertension including those produced by salt and unilateral renal artery constriction (1-4). But when a rat from each of the two strains was united in parabiosis, it was found that the reaction pattern to salt hypertension could be changed, i.e., the normally resistant animal not only developed significant hypertension but did so prior to its susceptible partner (5). This was interpreted to indicate that the genetic factors might act via a humoral agent, transmittable between rats from the two strains. The studies did not settle whether such factors were of a pressor or anti-pressor nature.In the current study, we have explored the effects of a variety of renal manipulations in single and parabiotic animals. Our results suggest that, although intact renal tissue has an antihypertensive action, the loss of this function is not alone sufficient to explain renal hypertension; a pressor agent must be involved. Since only animals from the sensitive strain were able to induce experimental hypertension in their intact parabiotic partners, we have speculated that, in animals from the sensitive strain there are two pressor principles: One agent is present in animals from this strain as well as in the one resistant to hypertension and is not transmitted through the parabiosis junction; a second agent is peculiar to the strain predisposed to hypertension and will traverse the junction. Material and MethodsThe rats belonged to two strains developed in this laboratory, called R and S because of their resistance or sensitivity, respectively, to experimental hypertension.

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“…At intervals of one week systolic blood pressures were measured in light ether anaesthesia by the plethysmographic method of Wilson & Byrom (1939). After stable blood pressure levels above 170 mm Hg were reached, the animals were divided into groups with mean blood pressure values of 178-209 mm Hg.…”

Section: Methodsmentioning

confidence: 99%