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At least 127 records · Page 7Linked to original sources
PubMed1978

[Oral contraceptives, hypertension and nephrosclerosis].

Oral contraceptives are of pathogenetic importance in hypertension of women aged 26 to 35 years. The hypertensive reaction occurs predominantly in those women who have hereditary predisposition to hypertension or diabetes mellitus, who suffer themselves from diabetes or who showed toxemia in previous pregnancies. Our findings are not in agreement with the suggestion that oral contraceptive hypertension in women is always reversible. Simultaneous administration of estrogen and progestogen accelerates Goldblatt-type hypertension in rats. Neither estrogen nor progestogen alone alters arterial blood pressure. In the hormonal combination the hypertensive effect of estrogen can be replaced by epsilon-aminocapronic acid. Estrogen is the only substance increasing plasma renin activity. There is no correlation between the increase of blood pressure and the plasma renin activity in the various groups of experimental animals receiving the different pharmacological substances. Estrogen and the synthetic progestogen cause sodium retention. Because of this, oral contraceptive hypertension may be supposed not to result from a stimulation of the renin-angiotensin-system. Oral contraceptive hypertension may result from a combination of endothelial lesions due to the estrogen's effect on blood coagulation leading to nephrosclerosis, and sodium retention produced predominantly by the synthetic progestogen.

Adult↗
PubMed1993

Hypertensive nephrosclerosis in the Dahl/Rapp rat. Initial sites of injury and effect of dietary L-arginine supplementation.

BACKGROUND: The Dahl/Rapp strains of salt-sensitive (SS/Jr) and salt-resistant (SR/Jr) rat were developed to examine pathogenetic mechanisms that produce hypertension in response to an increase in dietary salt. We have shown that providing SS/Jr rats with L-arginine, the metabolic precursor of nitric oxide, acutely prevented salt-sensitive hypertension, suggesting that SS/Jr rats developed hypertension because of inadequate nitric oxide production while on a high-salt diet. EXPERIMENTAL DESIGN: Male 23-day SS/Jr and SR/Jr rats were placed on chow that contained 8% sodium chloride. One group of SS/Jr rats also received L-arginine, 1.25 g/liter, in their drinking water. These three groups were examined at weekly intervals for 4 weeks. RESULTS: SS/Jr rats rapidly developed hypertension when placed on the high-salt chow. After 2 weeks on this diet, inulin clearance dramatically decreased, and albumin excretion rate increased. By the fourth week of study, SS/Jr rats on the high-salt diet had died or were dying. Coincident with the progressive decline in inulin clearance, renal morphologic analysis confirmed development of myointimal thickening, fibrinoid necrosis, and glomerulosclerosis. In contrast, over the 4 weeks of study, SS/Jr rats supplemented with oral L-arginine did not develop hypertension and any of the associated renal complications seen in age-matched SS/Jr rats on the high-salt diet. L-Arginine also corrected hypertension in SS/Jr rats exposed to the high-salt chow for 2 weeks before the inception of L-arginine. L-Arginine administration after 3 weeks on this chow, however, failed to reverse hypertension and the depressed inulin clearance and morphologic renal damage. CONCLUSIONS: Along with previous work (Chen PY, Sanders PW, J Clin Invest 88:1559-67), these studies were consistent with the hypothesis that hypertension and hypertensive nephrosclerosis developed in SS/Jr rats because, while on a high-salt diet, substrate (L-arginine) became a rate-limiting factor in the synthesis of nitric oxide.

Animals↗
PubMed1993

Nephrosclerosis in three cohorts of black and white men born 1925 to 1944, 1934 to 1953, and 1943 to 1962.

The prevailing levels of blood pressure among black and white men of ages 25 to 54 years were examined by two independent approaches in this study. Data on blood pressure obtained in national health surveys (National Health and Nutrition Examination Surveys, NHANES) do not show any appreciable upward or downward trend between 1960 and 1980 in men of these ages. The histologic examination of kidney samples obtained from coroner's autopsies offers an indirect way of estimating the levels of blood pressure that prevail in populations because of statistical relationships between nephrosclerosis and blood pressure. Samples of kidney tissues archived in New Orleans from 1968 to 1986 were evaluated by quantitative morphometry for the severity of the renovasculopathies that accompany high blood pressure. The outcome showed no significant secular trend among black and white men, confirming blood pressure survey findings that show no change in the hypertensive status of the population. The black-white difference in incipient signs of hypertension was seen to be well-established by ages 25 to 34 years in all cohorts of New Orleans subjects, as well as in the NHANES survey data. These result suggest that the adolescent and young adult ages are especially important in establishing the black-white difference in hypertension.

Adult↗
PubMed1997

Effects of the novel multiple-action agent carvedilol on severe nephrosclerosis in renal ablated rats.

Antihypertensive drugs have differing effects on renal hemodynamics and morphology. We analyzed whether the use of a new beta adrenoceptor antagonist and vasodilator, carvedilol (CVD), slows the progression of nephrosclerosis and whether the renoprotective effect as well as reduction in cardiac hypertrophy is dependent on the degree of blood pressure reduction. Fifty-four adult male Sprague-Dawley rats were distributed among five groups: group I served as untreated controls with 5/6 nephrectomy (Nx); group II, sham (no renal ablation or drug treatment); group III, CVD 5 (5/6 Nx and treatment with oral CVD at 5 mg/kg/day); group IV, CVD 10 (5/6 Nx and treatment with oral CVD at 10 mg/kg/day); and group V, CVD 20 (5/6 Nx and treatment with oral CVD at 20 mg/kg/day). Tail-cuff blood pressure and 24-hr urine samples were obtained before and at 3, 5 and 11 weeks of treatment with CVD. At the end of the study period, blood was taken to measure serum creatinine, plasma renin activity and CVD levels, as well as the remnant kidney and heart for morphological studies. There was a significant reduction in 24-hr U(ProtV) in all the CVD-treated groups, and it was increasingly evident with the highest dose used. However, only rats receiving doses of 10 and 20 mg/kg/day of CVD exhibited significant decreases in blood pressure. Elevated serum creatinine levels seen in untreated controls were significantly decreased by CVD in treated rats (P < .01), indicating that glomerular filtration rate was improved by this drug. This was associated with a significant increase in U(NaV). Concomitant and significant (P < .01) decreases in plasma renin activity were observed in sham and CVD-treated rats. CVD-treated animals had considerably reduced renal damage (P < .01) and cardiac hypertrophy (P < .01) compared with untreated controls. These data indicate that CVD is effective in delaying progression of renal damage and provides beneficial effects in the remnant kidney and cardiac hypertrophy, even at nonhypotensive doses.

Adrenergic beta-Antagonists↗
PubMed1985

Effect of castration on the experimental renal hypertension of the rat. Blood pressure, nephrosclerosis, long-chain fatty acids, and N-acetylation of PAH in the kidney.

Rats were rendered hypertensive by clamping one renal artery. Both kidneys remained in situ ('two-kidney one-clip Goldblatt hypertension'). Half of the animals were simultaneously castrated. 18-24 weeks after the operation both castrated females and males had a lower level of hypertension than the uncastrated controls. The kidneys of castrates contained less connective tissue (measured as the content of hydroxyproline) and long-chain (C-18) fatty acids and had a higher specific activity of the enzyme N-acetylating p-aminohippurate (N-acetyltransferase) than those of uncastrated rats. Thus, castration seems to alleviate some renal effects of the Goldblatt hypertension. In all animals the clamped kidney contained more hydroxyproline and C-18 fatty acids and had a lower N-acetyltransferase activity than the contralateral untouched organ. These results are in accordance with the theory that renal fatty acid concentration interferes directly with the N-acetyltransferase activity of the kidney. The enhanced hydroxyproline content of the kidneys (nephrosclerosis) inhibits N-acetylation most probably indirectly by raising the tissue concentration of C-18 fatty acids.

Acetyltransferases↗
PubMed1996

Experimental studies on the role of intercellular adhesion molecule-1 and lymphocyte function-associated antigen-1 in hypertensive nephrosclerosis.

T helper cells and macrophages infiltrate into the renal cortical interstitium during the course of hypertensive nephrosclerosis. To investigate the mechanisms of mononuclear cell infiltration, we examined the expression of the intercellular adhesion molecule-1 (ICAM-1) and its counterpart lymphocyte function-associated antigen-1 (LFA-1) in the progression of hypertensive renal injury. We studied nonclipped kidneys of two-kidney, one clip renovascular hypertensive and sham-operated control rats immunohistochemically at 4, 7, 14, and 28 days after clipping (n = 5 per group and time point). Systolic pressure was significantly elevated by day 7 (154 +/- 4 versus 117 +/- 6 mm Hg in sham, P < .05). The development of hypertension resulted in a progressive increase of ICAM-1 expression in the perivascular and interstitial areas of the renal cortex and on proximal tubular brush borders. Only a few glomeruli showed augmented ICAM-1 staining. Increased ICAM-1 was associated with an accumulation of LFA-1-positive mononuclear cells in the perivascular region (day 14: 15 +/- 4 versus 2 +/- 0.2 cells/mm2 in sham, P < .005) and intertubular region (127 +/- 11 versus 32 +/- 3 cells per millimeter squared in sham, P < .005). The maximum was obtained at day 14 and remained elevated until day 28. In addition, the number of interstitial LFA-1-positive infiltrating cells was related to the degree of interstitial and tubular ICAM-1 expression and correlated with blood pressure (r = .75, P < .001, n = 18). Our data suggest that ICAM-1 is involved in the recruitment of macrophages/lymphocytes via specific interaction of ICAM-1 and LFA-1 in this model of hypertensive target-organ damage.

Animals↗