Renal morphological changes after sinoaortic denervation in dogs.

Abstract

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...

Renal Biopsy Findings in Presumed Hypertensive Nephrosclerosis

“…Focal segmental glomerular scar ring when associated with ischemic glomerular collapse is entirely consistent with the renal effects of benign essen tial hypertension. This is clearly demonstrated in the dog model of hypertension induced by sinoaortic denervation [13] , In contrast, it is difficult to attribute focal and seg mental glomerulosclerosis (FSGS) and hyalinosis to hy pertension when, as in our cases, enlarged glomeruli are present in the absence of ischemic collapse. The absence of collapse of the basement membrane suggests that the glomerular changes are not a consequence of benign essential hypertension, but are due to primary FSGS.…”

Myocardial hypertrophy, cardiac β‐adrenoceptors and adenylate cyclase activity during sinoaortic denervation in dogs

“…In fact, recent data have shown that this experimental model is associated with renal vascular and glomerular lesions (Orfila et al, 1990). Moreover, the early development of cardiac hypertrophy suggests that this phenomenon does not only depend on pressure overload.…”

Chronic absence of baroreceptor inputs prevents training‐induced cardiovascular adjustments in normotensive and spontaneously hypertensive rats

“…The present results show in addition that, besides blunting the sympathetic autonomic drive, SAD also blocked the beneficial training‐induced adjustments of skeletal muscle arterioles, an additional factor to cause a further pressure increase in trained SHR deprived of baroreceptor function. Knowing that target‐organ damage correlates to a greater degree with high pressure variability than with high pressure levels (Orfila et al 1993; Miao et al 2001; Tatasciore et al 2007), one may speculate that exercise training is a beneficial therapeutic tool even in the absence of baroreceptor reflex control of the circulation.…”

“…Knowing that target-organ damage correlates to a greater degree with high pressure variability than with high pressure levels (Orfila et al 1993;Miao et al 2001;Tatasciore et al 2007), one may speculate that exercise training is a beneficial therapeutic tool even in the absence of baroreceptor reflex control of the circulation.…”