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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We designed this study to establish the structural and functional characteristics of the hypertrophied left ventricle of middle-aged rats during mineralocorticoid-salt hypertension. Treatment was initiated at 12 months of age, and the rats were studied at either 13 or 15 months of age (after 1 or 3 months of treatment). All rats were unilaterally nephrectomized. One group received deoxycorticosterone acetate (DOCA) injections (30 mg/kg s.c.) biweekly and 1% NaCl drinking water (DOCA salt), and the other group was injected with the vehicle (sesame seed oil) and given tap water to drink (sham). During the first 4 weeks of DOCA-salt treatment, arterial pressure reached its peak and left ventricular enlargement was mainly due to increases of 47% in cardiocyte cross-sectional area in the middle layer of the left ventricular wall. The last 2 months were characterized by an accelerated endomyocardial growth. Because absolute left ventricular mass did not increase during the last 2 months of treatment, we conclude that cellular hypertrophy was accompanied by a focal loss of cardiocytes. Myocardial hydroxyproline concentration was initially elevated by 37% but normalized by the third month of treatment. Intracellularly, myofibril volume percent was not changed, but mitochondria volume percent declined (13% in the midmyocardium and 15% in the endomyocardium) and sarcoplasmic volume density increased by 25% and 39%, respectively, in these regions. Left ventricular hypertrophy was associated with enhanced peak cardiac and stroke indexes, measured during increased preload, after both 1 and 3 months of DOCA-salt treatment. Acceleration of flow, however, was depressed in the rats with left ventricular hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1990 Feb
PMID:Left ventricular structure and performance in middle-aged rats with deoxycorticosterone acetate-salt hypertension. 213 30

The effects of high salt intake (1.0% NaCl in the drinking water) on rats made hypertensive by 2-bromoethylamine hydrobromide (BEA) treatment (200 mg/kg, i.p.) were examined. BEA-induced medullary necrosis resulted in a mild hypertension (146 +/- 5 mm Hg) that was exacerbated by 4 weeks of high salt intake (163 +/- 6 mmHg). BEA-treated rats had significant salt-induced increases in urinary norepinephrine excretion and hypothalamic and brainstem norepinephrine content, that were not present in BEA-treated rats drinking tap water or control rats drinking saline. BEA treatment in combination with increased salt intake produced a decrease (p less than 0.05) in renal dopamine content and adrenal norepinephrine stores relative to BEA treatment alone. BEA treatment also significantly decreased renal norepinephrine stores and dopamine binding sites irrespective of salt intake. Renal alpha 2-adrenergic receptors and central nervous system stores of dopamine and serotonin were unaffected by BEA treatment. Renal function was well preserved as indicated by normal creatinine, glucose and protein excretion; however, significant (p less than 0.05) disruption of the urinary concentrating mechanism was present. These studies suggest that BEA-induced hypertension has a neural component that is exacerbated by high salt intake. The primary defect in BEA hypertension appears to be the lack of circulating antihypertensive lipids that attenuate the ability of salt loads to simulate sympathetic nervous system activity.
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PMID:Neural-renal interactions in the hypertension induced by papillary necrosis: role of dietary salt intake. 215 64

We examined the role of bradykinin in the onset and/or the maintenance of blood pressure and renal blood flow in deoxycorticosterone acetate (DOCA)-salt hypertensive rats by using a competitive antagonist of bradykinin [Arg-Pro-Hyp-Gly-Thi-Ser-Dphe-Thi-Arg; Hyp, L-4-hydroxyproline; Thi, beta-(2-theinyl-L-alanine)]. The intravenous injection of the bradykinin antagonist (25, 50 and 100 micrograms) produced an increase in mean arterial pressure in all rats treated with tap water, 1% NaCl and DOCA + 1% NaCl. However, the magnitude of the increase in mean arterial pressure was significantly lower in the DOCA-hypertensive rats than in the two groups of rats drinking tap water and 1% NaCl after 4 and 6 weeks, but there was no significant difference after 2 weeks. The bradykinin antagonist induced a decrease in renal blood flow in all rats. However, the extent of the fall in renal blood flow was reduced in the DOCA-hypertensive rats compared with the control rats drinking tap water. These results suggest that endogenous bradykinin is depressed in the established phase of hypertension in DOCA-hypertensive rats. It is also suggested that endogenous bradykinin may counteract the elevation of vascular resistance in the early stages of this model.
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PMID:Role of bradykinin in the regulation of blood pressure and renal blood flow in DOCA-salt hypertensive rats. 216 14

There is experimental and epidemiologic evidence that some minerals and trace elements play a role in hypertension. We designed an experiment in which salt and water sources were manipulated to examine the possible impact of this relationship. A strain of rats (Dahl rats) known to become hypertensive with sodium chloride ingestion was used to study the effect of salt source and water source on the induction of hypertension. The group on tap water and table salt had blood pressures (184 mmHg +/- 19) significantly higher than every other group in the experiment. The experimental animals receiving tap water plus table salt had the highest blood pressure levels, although they consumed the lowest quantity of sodium. Analysis of the tap water samples showed "soft water" by analysis of calcium and magnesium concentration. This could adversely affect blood pressure. The relatively high magnesium concentration in sun evaporated sea salt may play a protective role in hypertension induction. The zinc and copper present in tap water may play an exacerbating role.
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PMID:Hypertension induction in Dahl rats. 228 Apr 29

Previous studies from our laboratories demonstrated that dietary NaCl supplementation in NaCl-sensitive spontaneously hypertensive rats elevates blood pressure, increases peripheral sympathetic nervous system activity, and depresses endogenous norepinephrine stores and turnover in the anterior hypothalamus. These findings suggest that reduced noradrenergic input to sympathoinhibitory neurons in anterior hypothalamus contributes to NaCl-sensitive hypertension in spontaneously hypertensive rats. The current study tested the hypothesis that dietary NaCl supplementation depresses endogenous norepinephrine stores and turnover in anterior hypothalamus of two other NaCl-sensitive models of hypertension, the Dahl salt-sensitive rat and the deoxycorticosterone acetate/NaCl hypertensive rat, thus increasing blood pressure by reducing noradrenergic input to the anterior hypothalamus. Dahl salt-sensitive rats were fed a high (8%) NaCl diet, and deoxycorticosterone acetate/NaCl rats rats drank 1% NaCl solution ad libitum for 2 or 4 weeks. Age-matched Dahl salt-sensitive rats fed a basal 1% NaCl diet and uninephrectomized Sprague-Dawley rats drinking tap water were controls. Regional brain catecholamines were determined by high-performance liquid chromatography with electrochemical detection. Norepinephrine turnover in hypothalamus (anterior, posterior, and ventral regions) and brain stem (pons and medulla) was assessed using the dopamine beta-hydroxylase inhibitor 1-cyclohexyl-2-mercapto-imidazole. High NaCl treatment caused significant elevations in blood pressure in Dahl salt-sensitive and deoxycorticosterone acetate/NaCl rats, but endogenous norepinephrine levels and turnover rates were not significantly different in anterior hypothalamus or any other brain region studied between the NaCl-supplemented and control groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1990 Jul
PMID:NaCl does not affect hypothalamic noradrenergic input in deoxycorticosterone acetate/NaCl and Dahl salt-sensitive rats. 236 46

Stroke-Prone spontaneously hypertensive rat strain (SHR-SP) always develops hypertensive retinopathy. The aim of the present work was to study the activity of a new antihypertensive drug, a synthetic furopyridine: cicletanine, in retinal hypertensive morphological lesions. The experiment was performed in 39 rats SHR-SP/A3N Iffa Credo, 11 weeks old, divided into 3 groups: group 1 was the control group, groups 2 and 3 were orally treated with cicletanine (respectively 100 and 150 mg/kg). All the rats had free access to tap water containing 1 p. 100 NaCl. During 6 weeks, blood pressure, body weight and survival were recorded, then all the rats were sacrificed. The eyes were removed, the posterior pole collected and fixed with Trump liquid for transmission election microscopy. In the SHR-SP control group, each layer showed neural body and/or process lesions: in the ganglion cell layer, some ganglion cells realized cytoid bodies corresponding to a lysed cell with nucleus degeneration, most of the axons were destroyed. In the inner and outer plexiform layers, most of the contacts between processes were lost because of fibrinous deposits. Numerous synapses were destroyed in the outer plexiform layer. These findings might explain the numerous dense bodies in the inner rod segment and the vesiculation of the rod outer segment. The capillaries showed markedly hypertensive lesions. Whereas, in both treated groups, rare and animal lesions were observed. The fact that these lesions were so few and so unimportant after 6 weeks of treatment, as well as for the photoreceptors which remained unimpaired, is closely related to cicletanine therapy, since it was so even though the treatment had been started with an already high blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Malignant hypertensive retinopathy in spontaneously hypertensive stroke-prone rats. Effect of treatment with cicletanine]. 251 Jun 62

1. The influence of deoxycorticosterone acetate (DOCA)-salt hypertension on brain atrial natriuretic factor (ANF) in rats was investigated to elucidate the role of central ANF in a renin-independent model of experimental hypertension. 2. Sprague-Dawley rats were subjected to uninephrectomy and given either tap water or saline [1% (w/v) NaCl] to drink plus weekly injections of either saline or DOCA (25 mg/kg, subcutaneously). After 32 days, the rats were decapitated and 18 different brain nuclei were removed by a micropunch technique. 3. The systolic blood pressure of the DOCA-salt rats was significantly higher than that of control rats [154 +/- 3 mmHg vs 104 +/- 2 mmHg (20.53 +/- 0.40 kPa vs 13.86 +/- 0.27 kPa), P less than 0.001]. 4. Plasma ANF levels were significantly (P less than 0.01) higher in DOCA-salt hypertensive rats compared with control rats. 5. In DOCA-salt hypertensive rats, the ANF content was increased in the organum vasculosum of the lamina terminalis (31.4 +/- 2.1 vs 22.1 +/- 2.5 pg/mg of protein, P less than 0.05), the subfornical organ (32.5 +/- 5.0 vs 24.2 +/- 2.4 pg/mg of protein, P less than 0.05), the medial amygdaloid nucleus (49.0 +/- 6.4 vs 34.0 +/- 2.0 pg/mg of protein, P less than 0.05) and the locus coeruleus (86.9 +/- 4.1 vs 64.4 +/- 4.2 pg/mg of protein, P less than 0.01) compared with control rats. The ANF content of 14 other brain areas investigated did not alter after treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic factor content of brain nuclei in deoxycorticosterone acetate-salt hypertension in the rat. 253 Oct 54

Serial determinations of protein excretion rate and systolic blood pressure (SBP) were made in spontaneously hypertensive rats (SHR) uninephrectomized (UNX) at six weeks of age and given tap water (CON), or water with hydrochlorthiazide, hydralazine and reserpine (HHR), captopril (CAP) or enalapril (ENP). Compared to CON, significant hypertension was prevented, kidney weight was lower and there was less proteinuria in HHR, CAP and ENP rats followed for 30 weeks after UNX. Morphologic studies of these four groups revealed that antihypertensive therapy reduced the incidence of glomerular sclerosis in UNX SHR by 50%. Despite complete absence of systemic hypertension, there was striking medial thickening of lobular arteries and arterioles of rats given the angiotensin converting enzyme (ACE) inhibitor, captopril. These vascular abnormalities were present to a lesser degree in rats given ENP, but were entirely absent in untreated animals or in those ingesting the HHR combination. Micropuncture studies performed five weeks after UNX in four additional groups of CON, HHR, CAP and ENP rats revealed that glomerular capillary pressure was elevated in CON and reduced by all three drug regimens. These studies support the hypothesis that glomerular capillary hypertension and/or nephron hypertrophy predispose to glomerular injury in this model of hypertension and reduced renal mass. ACE inhibitors and HHR are equivalent in their ability to prevent glomerular hypertension and damage in these rats, but the former, and in particular captopril, produce abnormalities of cortical vessels via a mechanism not dependent on the presence of systemic hypertension.
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PMID:Renal vascular effects of antihypertensive therapy in uninephrectomized SHR. 254 Mar 76

1. Antihypertensive agents normalize blood pressure and restore depressed endothelium-dependent relaxations in experimental models of hypertension, but little is known regarding whether antihypertensive agents themselves can directly modulate responses to agonists of endothelium-dependent or independent relaxations, or contractions. 2. Normal rats were treated with either tap water, captopril, hydralazine or enalapril in their drinking water for 2 weeks, following which endothelium-dependent and endothelium-independent relaxations were tested with acetylcholine and sodium nitroprusside, respectively, in aortic rings suspended in organ chambers. 3. All antihypertensive agents caused slight but similar potentiation of sodium nitroprusside-induced relaxations. However, their effects on acetylcholine-induced relaxations were quite different: captopril had a marked potentiating effect, hydrazaline a slight potentiating effect, and enalapril had no significant effect on these relaxations. 4. The relaxations induced by acetylcholine and potentiated by captopril were not altered when indomethacin was included in the tissue bath. However, pyrogallol, an inhibitor of endothelium-derived relaxing factor (EDRF), markedly inhibited these relaxations suggesting that captopril's effect may involve EDRF. 5. SQ 14,534, a stereoisomer of captopril which is 100 fold less potent in inhibiting angiotensin converting enzyme, also significantly enhanced acetylcholine induced relaxations. Thus the effects of both captopril and SQ 14,534 upon EDRF appear independent of the effects of these compounds on the angiotensin converting enzyme. 6. We conclude that certain antihypertensive agents may modulate endothelium-dependent relaxations in response to agonists, and that these properties may be of therapeutic importance in cardiovascular diseases.
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PMID:Effects of antihypertensive agents on endothelium-dependent and endothelium-independent relaxations. 255 77

The effects of dietary K (food and tap water both containing 1% KCl) on blood pressure and renal prostaglandin-kallikrein-kinin system were investigated in Wistar rats made hypertensive by constriction of left renal artery. Dietary K attenuated the development of hypertension and increased urine volume accompanied by increased excretion of K, but by uninfluenced excretion of Na. Dietary K also increased the urinary excretion of kallikrein, PGE2 and aldosterone in Goldblatt hypertensive rats. There was no significant difference in the values of plasma Na between the two groups with and without dietary K. These results suggest that dietary K may attenuate the development of hypertension, increase urine volume via the mechanism of enhancing production of renal PGE2 and kallikrein in hypertensive rats.
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PMID:[Effects of dietary K on blood pressure, prostaglandin, and kallikrein in renovascular hypertensive rats]. 261 29


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