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

Imidazoline binding sites have been characterized in organs modulating blood pressure, such as brain and kidney with (3H)-p-aminoclonidine and (3H)-Idazoxan respectively. However, the pharmacological characteristics of the imidazoline-preferring binding sites differ considerably depending on the species investigated and the radioligand used. Little is known about the physiological relevance of the non-adrenergic (3H)-idazoxan binding sites. As some imidazolines and certain alpha-adrenoceptor agonists possess antihypertensive activity, an alteration of these binding sites should be considered as a possible causes in the development of hypertension. In the present study, we performed binding studies with the imidazoline ligand (3H)-idazoxan in renal cortex of hypertensive salt-sensitive (SBH) and normotensive salt-resistant (SBN) Sabra rats. (3H)-idazoxan binding capacities were higher in SBH than in SBN rats. Competition studies have shown for (3H)-idazoxan specific binding non-adrenergic characteristics exclusively. In these both substrains, (3H)-idazoxan binding exhibit pharmacological profile of imidazoline binding sites. However, theses sites have also high affinity for guanidino compounds and amiloride. Surprisingly, amiloride and some analogues were significantly more potent in SBN than in SBH rats. From this study, it is difficult to elucidate the physiological role of imidazoline binding sites in renal cortex. However, differences observed between SBN and SBH suggest that these sites may play a role in the development of hypertension in Sabra rats.
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PMID:[Binding sites of imidazolines. Study with (3H)-idazoxan in renal cortex of Sabra salt-sensitive (SBH) and salt-resistant (SBN) rats]. 197 30

Recent studies indicate that cardiac and renal hypertrophy develop during desoxycorticosterone acetate (DOCA)-salt (DOC) treatment in hypertension-prone (SBH) and -resistant (SBN) rats, irrespective of systemic hemodynamic changes. The effect of nitrendipine on the development of left and right ventricular hypertrophy (LVH and RVH, respectively) was evaluated in 16-week-old rats. Members of each strain were divided into six groups (n = 10): 1--control; 2--nitrendipine treated for 3 weeks; 3, 4, and 5--DOC for 10 days, 3 weeks, and 6 weeks, respectively; 6--DOC for 6 weeks and nitrendipine for the last 3 weeks. Cannulae were inserted into the left ventricle and abdominal aorta. The radioactive reference sample microsphere technique was used to measure cardiac index. Mean arterial pressure (MAP) and total peripheral resistance index (TPRI) were unchanged in all six groups of SBN rats, whereas MAP and TPRI increased progressively in the DOC-treated SBH groups. Concomitant administration of nitrendipine in Group 6 was associated with a reduction of MAP and TPRI to control levels. Cardiac index and heart rate did not change in any group. Despite the different hemodynamic changes, both SBH and SBN rats developed LVH and RVH. The concomitant administration of nitrendipine prevented the progression of LVH and allowed regression of RVH in both strains. It is concluded that nitrendipine can affect the pathogenesis of LVH through nonhemodynamic mechanisms.
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PMID:Nitrendipine prevents the development of cardiac hypertrophy in DOCA-salt-treated hypertension-prone (SBH) and -resistant (SBN) rats through nonhemodynamic mechanisms. 246 54

We report our experience in the management of children after orthotopic liver transplantation (OLT). From 03/84 to 04/87 50 patients (pts) were transplanted. Mean age was 4 3/12 years (8/12 to 13 2/12) and mean body weight 14.7 kg (5.8 to 40). Hospital mortality was 14%. Problems related to the surgery included: Abdominal complications: bleeding (8 pts), infection (18 pts), ascites and fistula (1 pt), need for secondary abdominal surgery (10 patients). Respiratory problems: lobar atelectasis (11 pts), right diaphragmatic paralysis (2 pts) and right pleural effusion (11 pts). Problems related to immunosuppression included: Bacterial infection (29 pts) fungal infection (5 pts), one patient died of disseminated cytomegalovirus infection. Side effect of cyclosporin A (CsA) were systemic blood hypertension (S.B.H.) (47 pts), sinusal bradycardia (37 pts), associated to SBH (24 pts), hypertensive encephalopathy (2 pts). Generalized seizures (2 pts in the absence of SBH). Renal side effects of CsA were hypercreatininemia, decreased sodium bicarbonate and hyperkaliemia. The nephrotoxicity of CsA was favoured by the use of other nephrotoxic drugs such as aminoglycosides, amphotericin B. Edematous pancreatitis was observed in 3 patients and related to the use of large doses of steroids. Problems related to the functioning of the graft included: Primary non-function of the graft (4 pts), hepatic artery thrombosis (8 pts) and severe acute rejection unresponsive to therapy (1 pt); these situations needed to be recognised early in order to organize a second OLT. Other causes of hepatic dysfunction were: portal vein thrombosis (1 pt), biliary tract obstruction (2 pts), angiocholitis (3 pts), right hepatic lobe necrosis (2 pts). Acute hepatic insufficiency in 7 children.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intensive care for children after orthotopic liver transplantation. 265 16

The Sabra hypertension resistant rats (SBN) have an outstanding ability to maintain normal blood pressure when exposed to procedures that ordinarily cause hypertension in normal rats. The following findings may be relevant to resistance to hypertension of these rats: 1) In SBN rats, cardiac norepinephrine content is not affected by DOCA-salt treatment. Since depletion of cardiac norepinephrine is an index of cardiac adrenergic nerve overactivity, the results suggest an attenuated cardiac sympathetic nerve activity in these rats. 2) In SBN rats, the sensitivity of the baroreflex control of the heart is markedly increased compared with other strains. Reduction of baro-receptor sensitivity by aortic-baroreceptor deafferentation renders them susceptible to DOCA-salt hypertension. The results suggest a strong relationship between baroreflex supersensitivity and resistance to hypertension in these rats. 3) The amount of alpha 2 adrenoreceptor densities in cerebral and renal cortical membranes of normal rats increased in vitro, in the presence of sodium and guanyl nucleotide (GTP). In SBN rats, the effect of sodium is markedly attenuated compared with SBH, while response to GTP is identical in the two strains. The demonstration of a similar pattern of response in the Dahl rats suggests that alpha 2 adrenoreceptor may be involved in the sensitivity or resistance to salt induced hypertension.
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PMID:[Hereditary resistance to salt-induced hypertension. What mechanisms?]. 283 85

Sodium ions and guanyl nucleotides play an important role in increasing alpha 2-adrenoceptor densities in cerebral and renal cortex of normotensive rats. The in vitro effect of Na+ and GTP was investigated on cerebral and renal alpha-adrenoceptors in hypertensive (SBH, salt-sensitive) and normotensive (SBN, salt-resistant) Sabra rats. In SBH and SBN rats, guanyl nucleotides increased cerebral and renal high-affinity alpha 2-adrenoceptor densities. Sodium ions, in contrast, markedly increased cerebral and renal high affinity alpha 2-adrenoceptor densities only in SBH rats. Under these conditions, alpha 1-adrenoceptor densities were unchanged. Thus, although Na+ and GTP both increase alpha 2-adrenoceptor densities, these agents appear to mediate their regulatory effects via different membrane components. Moreover, the absence of sodium regulation of alpha 2-adrenoceptors in SBN rats may be responsible for the resistance to salt-induced hypertension.
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PMID:Sabra rats as a model to differentiate between Na+ and GTP regulation of alpha 2-adrenoceptor densities. 299 Sep 68

Several studies have suggested a correlation between sodium accumulation and the development of hypertension. However, the mechanisms whereby sodium is able to increase blood pressure remain unclear. In the present study, alpha-adrenoceptors and noradrenaline contents have been studied in the cerebral cortex, hypothalamus and medulla oblongata in the Sabra rat strain in order to define their role in the resistance or sensitivity to sodium-induced hypertension. Alpha-Adrenoceptors were defined using the selective ligands 3H-prazosin and 3H-rauwolscine for alpha 1- and alpha 2-adrenoceptors, respectively. Under normal sodium diet, alpha 2-adrenoceptor density was higher in cerebral cortex and lower in hypothalamus and medulla oblongata of SBN (salt-resistant) compared to SBH (salt-sensitive) rats. Five weeks of high sodium intake induced a decrease in alpha 2-adrenoceptor density in cerebral cortex and an increase in hypothalamus only in SBN rats. These changes abolished the differences between SBH and SBN rats observed with a normal sodium diet. No changes in density and affinity of alpha 2-adrenoceptors were observed in medulla oblongata of SBN and SBH rats. Density and affinity of alpha 1-adrenoceptors were similar in SBN and SBH rats in all the tissues studied and they were unaffected by the high sodium diet. Noradrenaline contents in cerebral cortex, hypothalamus and medulla oblongata were also similar in the two rat substrains under normal sodium diet, but high sodium intake induced a decrease cerebrocortical noradrenaline content only in SBN rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in central alpha-adrenoceptors and noradrenaline content after high sodium intake in Sabra salt-sensitive and salt-resistant rats. 301 93

To determine whether the increased renal synthesis of thromboxane (Tx)A2 found in genetically hypertensive rats also occurred in rats with a sodium-dependent form of hypertension, the urinary excretion of 6-keto-prostaglandin F1 alpha (6KPGF1 alpha) and of TxB2 was measured by a sensitive and specific radioimmunoassay in hypertension-prone (SBH), -resistant (SBN) and unselected (SB) female rats of the Sabra strains. Rats of the three strains were studied before (9 weeks of age) and after five weeks of deoxycorticosterone (DOCA)-salt treatment. Before treatment, the urinary 6KPGF1 alpha did not differ among the three strains while a higher TxB2 excretion was seen in the SBN rats. After treatment, the urinary excretion of TxB2 increased significantly in SBH and SB but not in SBN rats, while the urinary 6KPGF1 alpha remained unchanged in SBH, increased moderately in SB and markedly in SBN controls. Consequently, DOCA-salt-induced changes in blood pressure and in urinary 6KPGF1 alpha observed in the three strains of rats were inversely related (r = -0.78; P less than 0.001). It is concluded that the high blood pressure developed after DOCA-salt treatment in SBH rats is more likely to depend upon a defect in the renal production of prostacyclin rather than upon an increased synthesis of thromboxane A2.
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PMID:Effects of DOCA-salt treatment on the urinary prostaglandins in Sabra rats. 339 82

An increasing amount of anatomical, physiological, and pharmacological evidence suggest that pain inhibitory circuitry is linked with cardiovascular regulatory systems in man and laboratory animals. Induction of hypertension in rats by different methods (mineralocorticoid treatment, stenosis of renal artery, or social deprivation) is associated with reduced responsiveness to noxious thermal stimuli (hot-plate) or to noxious mechanical stimuli (paw pressure). Genetically hypertension-prone rats derived from the SABRA strain and spontaneously hypertensive rats derived from Wistar/Kyoto strain also display a similar hypoalgesia. Acute increases in blood pressure are associated with reduced sensitivity to painful stimuli. Additionally, the interaction between blood pressure and pain perception has also been supported by the demonstration that various experimental interventions that diminish the magnitude of hypertension also attenuate the hypoalgesia. Recent clinical findings are also in agreement with the laboratory animal findings since sensory and pain thresholds have been shown to be significantly higher in unmedicated essential hypertensive subjects compared to normotensive controls. Thus, the human data corroborate animal data and suggest that a relation between blood pressure and pain sensitivity is likely to be a general phenomenon. It is unlikely that damage to peripheral pain fibers caused by a change in blood pressure contributes to the observed hypoalgesia. Naloxone, which has no effect on blood pressure, returns the pain sensitivity to normal levels. Behavioral tests (open field and motor activity cage) of normotensive and of renal and genetically (SBH and SHR) hypertensive rats exclude the possibility of a general motor deficit in hypertensive rats. Endogenous opioid peptides in central and peripheral nervous systems as well as in endocrine organs are implicated, although non-opioid mechanisms are also evident. Activation of baroreceptor afferents by acute or chronic increases in arterial or venous blood pressure may play an important role in the somatosensory responses associated with the increase in blood pressure. Coordinated cardiovascular-pain regulatory responses may be part of an adaptive mechanism that helps the body to face stressful events.
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PMID:The relationship between cardiovascular and pain regulatory systems. 352 85

The effects of chronic dietary salt-loading and nifedipine therapy on hypertension-prone (SBH), -resistant (SBN) and parental (SB) Sabra rats were investigated. Salt diet for 12 weeks resulted in a sustained hypertension and heart hypertrophy only in SBH. Nifedipine therapy (300 p.p.m. = 300 mg/kg of food) introduced after week 7 on a salt diet, achieved small changes in salt-loaded SBN and SB rats, but resulted in a marked decrease in blood pressure in SBH rats within 1 week and in a regression of cardiac hypertrophy. Plasma renin activity rose slightly in nifedipine treated SB and SBN rats, but decreased significantly in treated SBH rats. Histopathological investigations revealed hypertensive vasculopathy in three out of nine untreated SBH rats, whereas there were no morphological changes in the treated rats.
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PMID:Salt-induced hypertension in the 'Sabra' rat strain: influence of nifedipine treatment. 388 35

The effect of desoxycorticosterone (DOC)-NaCl treatment upon sympathetic neuronal uptake of norepinephrine (uptake1) was evaluated in strains of hypertension-resistant (SBN) and -prone (SBH) rats. Uninephrectomized animals were given either a placebo pellet sc and tapwater (untreated) or a 25-mg DOC pellet and 1% NaCl. Four weeks later, tail systolic pressure was significantly higher in DOC-NaCl SBH, 183 +/- 3 mm Hg, than SBN, 141 +/- 2 (P less than 0.01). [3H]Norepinephrine (NE) uptake was determined in heart slices of all four groups by incubation in Krebs buffer at 37 degrees C for 20 min at several concentrations. Preliminary studies confirmed that this is a measure of uptake1. Heart slices of DOC-NaCl-treated SBN and SBH rats had significantly reduced NE uptake at concentrations of 10-80 nM (P less than 0.01); there was no significant difference between SBN and SBH in this regard. Untreated SBH rats have been shown to have a defect in baroreflex regulation when normotensive. The results raise the possibility that the greater increase in arterial pressure caused by DOC-NaCl in SBH compared to SBN may be related to both the inborn difference in reflex function and an acquired reduction in inactivation of norepinephrine by sympathetic neuronal uptake.
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PMID:Reduced sympathetic neuronal uptake (uptake1) in a genetic model of desoxycorticosterone-NaCl hypertension. 396 82


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