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S Azar

Publications and source records attributed to S Azar.

At least 37 records · Page 2Linked to original sources
PubMed1983

Glomerular manifestations of diabetes in the BB rat.

Morphologic characteristics of the renal glomeruli and tubules of BB rats with spontaneous diabetes mellitus were studied at 30 weeks' duration of diabetes. Whereas the glomerular basement membrane (GBM) was significantly thickened, no changes in the diabetic glomeruli were seen in the peripheral capillary wall area and in the fractional volumes of the mesangial cells or of the mesangial matrix. Light microscopy of the diabetic kidneys were normal, and immunofluorescent examination of diabetic glomeruli showed no increased accumulation of albumin, C3, or IgG. Diabetic rats had increased renal blood flow and glomerular filtration rates. Diabetic rats at 7, 17, and 30 weeks excreted normal amounts of urinary albumin. Thus kidneys of the BB diabetic rat differ from other experimental models of diabetes in that GBM thickening occurs in the absence of mesangial changes and of increased albuminuria. These studies suggest that the mesangium may influence glomerular permeability in diabetes, while thickening of the GBM in diabetes does not necessarily coincide with increased urinary albumin excretion. Furthermore, these results are consonant with the hypothesis that genetic factors may influence the pathological expression of diabetic nephropathy in rats.

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PubMed1983

Open-field behavior in two models of genetic hypertension and the behavioral effects of salt excess.

In order to assess the relationship of behavior to blood pressure and salt intake, open-field behavior was studied in 123 rats of the spontaneously hypertensive (SHR), Wistar-Kyoto (WKY), Sprague-Dawley (SD), and Dahl resistant (DR) and sensitive (DS) strains. DS rats become hypertensive upon exposure to either high dietary salt or psychogenic stress, while DR rats remain normotensive. A circular photobeam open field was used under full room illumination. Three 5-min trials were given on consecutive days. Rats were tested with or without 5 days of an 8% NaCl diet. We found that DS rats were less active than DR rats, regardless of diet. In contrast, SHR rats were more active than WKY rats. However, DS and SHR rats were equally active. Thus, behavioral differences between these two models of hypertension are expressed by the normotensive control strains. The relative ranking of activity levels between strains was DR = SD greater than SHR = DS greater than WKY. High-salt-enhanced intertrial habituation, defined as the decrease in activity across trials (DS, 100%; SD, 82%; SHR, 90%; WKY, 1350%; but DR, -50%) as well as intratrial habituation, defined as the decrease from the first to the second half of the trial (14%, all subjects). Defecation was increased with high salt (DS, 975%; SD, 59%; SHR, 267%; WKY, 89%; but DR, 40%). These effects of high salt may reflect an increase in an emotionality factor. DR rats were largely resistant to the behavioral effects of salt. Total activity was positively correlated with blood pressure in hypertensive rats, r(42) = 0.33, p less than .01, but negatively correlated in normotensive rats, r(81) = -0.34, p less than .01. The proportion of total activity occurring in the first half of the trial for the initial test day was correlated with blood pressure in normotensive rats r(81) = 0.44, p less than .01. Dietary salt excess has behavioral as well as cardiovascular consequences.

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PubMed1981

Paraventricular--suprachiasmatic lesions prevent salt-induced hypertension in Dahl rats.

1. We studied the effects that lesions produced in the paraventricular and suprachiasmatic nuclei and intervening periventricular area had on 24 h mean circadian blood pressures in Dahl salt-sensitive and -resistant rats and their sham-operated controls. We measured blood pressures while the animals were on a low salt diet and after 1, 5 and 13 weeks of 8% NaCl diet. 2. Salt-sensitive rats with lesions had lower blood pressures than salt-sensitive sham-operated controls at all points of the study. In contrast, identical lesions in salt-resistant rats produced a transient pressor response to the diet. Twenty-four hour mean heart rate, determined after 13 weeks of 8% NaCl intake, was low only in salt-sensitive rats with lesions. Sodium intake and excretion per kg of body weight, as well as plasma sodium concentrations, were similar in all groups. 3. We conclude that the anteromedial hypothalamic area, which includes the paraventricular nucleus, the suprachiasmatic nucleus and the intervening periventricular area, participates in the development of Dahl hypertension. We suggest that a multifactorial mechanism is involved: (a) the facilitatory role of this region in ACTH release, (b) this region's participation in the baroreceptor reflex via vasopressinergic efferents to the nucleus of the tractus solitarius, and (c) the roles of the paraventricular and suprachiasmatic nuclei in the regulation of salt and water balance.

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PubMed1978

The effects of Goldblatt hypertension on development of the glomerular lesions of diabetes mellitus in the rat.

Rats with classic Goldblatt (two-kidney) hypertension had diabetes induced by streptozotocin. After four months of diabetes, glomeruli of the unclipped kidney of hypertensive diabetic rats had markedly increased diabetic changes, including mesangial matrix thickening and mesangial immunoglobulin (IgG and IgM) and complement (C3) localization, when compared with glomeruli of the contralateral-clipped kidneys. Further, glomeruli of the unclipped kidneys of hypertensive diabetic animals had more mesangial thickening and IgG and IgM staining than glomeruli of normotensive diabetic rats. Although glomeruli of clipped kidneys in hypertensive diabetic rats had less mesangial thickening than glomeruli of normotensive diabetic rats, this did not reach statistical significance. However, these glomeruli did have significantly less IgG, IgM, and C3 staining compared with glomeruli of normotensive diabetic animals. Mesangial thickness in glomeruli of clipped and unclipped nondiabetic hypertensive rats did not differ from that in normal animals. However, there was less mesangial IgG staining in clipped than in unclipped kidneys of nondiabetic hypertensive rats or in kidneys of normal animals. We have interpreted these results to imply that alterations in nephron hemodynamics combine with the diabetic state to influence the rate of development of diabetic glomerulopathy in rats.

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PubMed1977

Evidence that prostaglandin synthesis inhibitors increase the concentration of sodium and chloride in rat renal medulla.

Thirty minutes after indomethacin (10 mg/kg, iv), a prostaglandin synthesis inhibitor, had been given to 10 rats, the Na concentration in renal papilla averaged 349 mEq/kg H2O, whereas it averaged only 181 in 14 "non-indomethacin" control rats (P less than 0.0001). Papillary plasma flow was closely similar in both groups. In a subsequent study, eight "indomethacin" rats had the same papillary flow as seven non-indomethacin rats but had a papillary Na concentration of 358 vs. 185 in the non-indomethacin controls (P less than 0.0001). In nine more rats, indomethacin increased Cl concentration in papillas by 66% (P less than 0.0001), while Na concentration increased 60% (P less than 0.0001). In eight other rats, micropuncture indicated that indomethacin does not greatly alter delivery of fluid out of late proximal tubule. Meclofenamate, another inhibitor, increased papillary Na just as much as indomethacin. Papillary urea is not changed with indomethacin. Thus, papillary Na concentration was almost twice as high in indomethacin rats, despite similar papillary plasma flow and late proximal flow. Apparently, inhibiting prostaglandin synthesis is associated with either a great increase in Na or Cl "pumping" or a great decrease in Na or Cl "leak" in either collecting duct or ascending limb, or in both. The collecting duct and papillary interstitial cells both synthesize prostaglandins, which seem to have a profound effect on medullary net Na transport.

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PubMedDate not supplied

The effects of normalization of dietary protein intake and carotid artery ligation on the renal autoregulatory abnormalities of streptozotocin diabetic rats.

We studied renal autoregulation in nondiabetic and streptozotocin diabetic Münich-Wistar rats 6 weeks after diabetes induction. We had previously shown that diabetic rats had greater preservation of renal blood flow (RBF) at reduced renal perfusion pressures (RPP) than control rats and speculated that this could be due to higher protein intake in the diabetic rats. Because of hyperphagia, the diabetic rats in the present study on a 24% protein diet (D-24) had 70% or greater increase in dietary protein intake compared to controls on the same diet (C-24). Diabetic rats on a 14% protein diet (D-14) had a dietary protein intake similar to C-24 and less than that of D-24 animals. Baseline glomerular filtration rate (GFR) and renal blood flow were lower and renal vascular resistance (RVR) was higher in the D-14 compared to the C-24 or D-24 rats. Nonetheless, at markedly reduced RPP both diabetic groups had better sustained RBFs and lower RVRs than the controls. Thus, increased dietary protein intake cannot explain the autoregulatory abnormalities in diabetes. Bilateral carotid artery ligation increased systemic blood pressure similarly in the C-24, D-24, and D-14 rats. All three groups responded with increased RVR to carotid artery ligation. Following carotid artery ligation, differences were no longer seen between diabetic and control rats for RBF at reduced RPPs. These studies indicate that diabetic rats are capable of generating increased RVR, ruling out impaired vascular constrictive capacity as an explanation of these hemodynamic abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS)

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