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

Deoxycorticosterone acetate (DOCA)-salt hypertension was induced in Brown Norway (BN) kininogen-deficient rats (BN-Ka) and normal rats from the same strain (BN-Ki) after nephrectomy. Systolic blood pressure, which was determined by the tail-cuff method, of BN-Ki increased gradually during this treatment. In contrast, the blood pressure of mutant BN-Ka increased rapidly 2 weeks after the onset of the treatment. Urinary excretion of active kallikrein and prokallikrein increased at the same degree in rats of both strains during this treatment. Significant increase in urinary sodium excretion was observed with a tendency to increase in urine volume during the treatment in normal BN-Ki rats, whereas both parameters were essentially not increased in mutant BN-Ka rats, which could not generate urinary kinin. Aprotinin infusion by osmotic minipump to normal BN-Ki rats during the DOCA-salt treatment resulted in significant further increase in the systolic blood pressure.
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PMID:Essential role of kallikrein-kinin system in suppression of blood pressure rise during the developmental stage of hypertension induced by deoxycorticosterone acetate-salt in rats. 128 79

We investigated the chronic effect of bradykinin B2-receptor blockade on the antihypertensive actions of the angiotensin-converting enzyme (ACE) inhibitor ramipril in three different hypertensive rat models, the two-kidney/one-clip (2K1C) hypertensive Wistar rat, the kinin-deficient 2K1C hypertensive Brown Norway Katholieke (BN-K) rat, and the spontaneously hypertensive rat (SHR). Chronic blockade of bradykinin B2 receptors by subcutaneous infusion of the new bradykinin antagonist HOE 140 (500 micrograms/kg/day) attenuated the antihypertensive effect of ramipril only in 2K1C hypertensive Wistar rats, but not in 2K1C BN-K rats and SHR. Our data demonstrate for the first time that potentiation of endogenous kinins contributes to chronic antihypertensive actions of ACE inhibitors in experimental renal hypertension. Whether this holds also true for other forms of hypertension remains to be answered.
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PMID:Role of bradykinin in chronic antihypertensive actions of ramipril in different hypertension models. 128 37

The contribution of endogenous bradykinin to the chronic antihypertensive actions of the ACE-inhibitor, ramipril, was investigated in 2-kidney 1 clip (2K1C) hypertensive kinin-deficient Brown Norway Katholieke rats (BN-K) and 2K1C hypertensive Wistar rats (WI) as well as in spontaneously hypertensive rats (SHR). Treatment with ramipril plus the BK B2-receptor antagonist HOE 140 for 6 weeks significantly attenuated the antihypertensive effects of the ACE-inhibitor in 2K1C hypertensive WI rats, but not in 2K1C hypertensive BN-K rats and in SHR. Our data support the hypothesis that potentiation of endogenous kinins contributes to the chronic antihypertensive actions of ACE-inhibitors in experimental renal hypertension. Whether this holds also true for other forms of hypertension remains to be answered.
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PMID:Kinin contribution to chronic antihypertensive actions of ACE-inhibitors in hypertensive rats. 133 42

Previous studies from our laboratory have demonstrated that the intermediate phenotype of thermosensitivity is present in hypertensive mice and rats. Increased expression of hsp70 caused by increased transcription rate was demonstrated in vivo, in organs, and in cultured cells from spontaneously hypertensive rats and hypertensive mice. In this study, a polymorphism of this gene was revealed with BamHI enzyme by using a human hsp70 probe. A 4.4-kb fragment was visualized in normotensive rats (Brown-Norway BN.lx and Sprague-Dawley), and a 3.0-kb fragment was found in spontaneously hypertensive rats (SHR) of three different origins and in Wistar and Buffalo rats. Both fragments were present in the Wistar-Kyoto rat strain. The present study mapped the polymorphism of hsp70 into the RT1 complex in BN.1K and SHR.1N congenic strains. The hsp70 restriction fragment length polymorphism is associated with a blood pressure difference of 15 mm Hg in recombinant inbred strains. These results justify the search for a mechanism by which hsp70 could influence blood pressure.
Hypertension 1992 Jun
PMID:Restriction fragment length polymorphism of hsp70 gene, localized in the RT1 complex, is associated with hypertension in spontaneously hypertensive rats. 135 May 72

Red blood cell Na+ content as well as ouabain-resistant Na+ and Rb+ (K+) transport (susceptible or resistant to inhibition by loop diuretics) were determined in spontaneously hypertensive rats (SHR) and normotensive Brown Norway (BN) rats the erythrocytes of which were incubated in either saline or Mg(2+)-sucrose medium. Elevated ouabain-resistant Na+ net uptake contrasted with slightly decreased red blood cell Na+ content in SHR compared with BN rats. Acceleration of furosemide- and bumetanide-sensitive Na+ fluxes contributed to enhanced ouabain-resistant Na+ influx into SHR erythrocytes in saline medium, whereas higher furosemide- or bumetanide-resistant Na+ efflux caused greater ouabain-resistant Na+ efflux in Mg(2+)-sucrose medium. Furosemide- and bumetanide-resistant Rb+ leaks were augmented in SHR erythrocytes. The association of the disclosed ion transport alterations with blood pressure was examined in 20 recombinant inbred strains derived from F2 SHR x BN hybrids. Ouabain-resistant Na+ uptake as well as furosemide- and bumetanide-resistant Na+ inward leaks (but not red blood cell Na+ content or furosemide- and bumetanide-sensitive Na+ net uptake) cosegregated with systolic and pulse pressures but not diastolic pressure of the recombinant inbred strains. In contrast, neither ouabain-resistant Na+ efflux nor any component of ouabain-resistant Rb+ uptake correlated positively with blood pressure of the recombinant inbred strains. Increased ouabain-resistant Na+ influx was compensated for by accelerated ouabain-sensitive Na+ extrusion because red blood cell Na+ content was not elevated in the hypertensive strains. Thus, high cell Na+ turnover rates might be related to genetic hypertension if an altered Na+ inward leak would be less effectively compensated for in tissues involved in cardiovascular regulation.
Hypertension 1992 Oct
PMID:Association of red blood cell sodium leak with blood pressure in recombinant inbred strains. 139 93

In order to evaluate the quality of life (QOL) in hypertensive outpatients, we selected 78 patients with hypertension of various degrees of severity (WHO Classification I: 29 cases, II: 15, III: 34), 59 not ill healthy persons (N1) and 22 normotensive outpatients (N2) aged at 50 years and over, using the self-completed questionnaire (QUIK) which we developed. QUIK covers four domains including physical functioning (20 questions), emotional adjustment (10), interpersonal relationships (10) and attitudes toward life (10) totaling 50 questions. In this study the internal consistency of QUIK was alpha = 0.95 by the Kuder-Richardson formula 20 and it's repeatability was r = 0.89 by the Spearman-Brown formula. The QOL in hypertensive outpatients was definitely worse in terms of total score (N1 5.1 +/- 4.4 vs WHO II 9.3 +/- 7.2 and III 12.1 +/- 5.6, p < 0.05), for physical functioning (N1 2.5 +/- 2.1 vs WHO I 3.7 +/- 2.8, II 4.7 +/- 3.8, III 5.4 +/- 2.8 p < 0.05), for emotional adjustment (N1 1.2 +/- 1.4 vs WHO III 2.3 +/- 1.7, p < 0.01), for interpersonal relationships (N1 0.8 +/- 1.3 vs WHO III 1.6 +/- 1.5, p < 0.01) and for attitudes toward life (N1 0.7 +/- 1.2 vs WHO III 2.7 +/- 2.0 p < 0.01). The total QUIK score increased according to the severity of symptoms (WHO I 5.8 +/- 4.4, WHO II 9.3 +/- 7.2 and WHO III 12.1 +/- 5.6), respectively. The total score of WHO I was significantly lower compared with that of WHO III (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Quality of the life in hypertensive outpatients]. 146 Jul 79

Male F344BNF1 hybrid rats (F1 crosses between female Fischer 344 and male Brown Norway rats) aged 3 or 24 months were treated with vehicle (1 ml water/kg, IP) or fluoxetine (10 mg/kg, IP) once a day for 1 day or 27 consecutive days; body weights were recorded daily. Baroreceptor sensitivity was assessed in conscious unrestrained rats implanted with vascular catheters 24 hours after the single or 27th injection by measuring peak changes in mean arterial pressure (MAP) and heart rate (HR) elicited by graded doses of phenylephrine or nitroglycerin, IV. The results demonstrate that the effects of the serotonin uptake inhibitor fluoxetine, whether administered acutely or for 27 days, are similar in young and old rats: a relative decrease in body weight, a slight decrease in resting MAP without a change in HR, and no effect on baroreceptor sensitivity. In addition, this study in F344BNF1 hybrid rats supports previous reports in inbred rat strains by demonstrating that baroreceptor dysfunction, but not hypertension, is observed in old rats.
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PMID:Effects of the selective serotonin reuptake inhibitor fluoxetine on baroreceptor reflex sensitivity and body weight in young and old rats. 162 89

It has recently been proposed that sequence variation in the gene coding for tissue kallikrein might be involved in the pathogenesis of hypertension. However, molecular evidence of an association between a sequence alteration in the kallikrein gene family and the transmission of increased blood pressure has never been reported. In 32 recombinant inbred (RI) strains derived from the spontaneously hypertensive rat (SHR) and the normotensive Brown Norway rat (BN), we investigated whether a restriction fragment length polymorphism (RFLP) marking the kallikrein gene family cosegregated with blood pressure. In the RI strains that inherited the kallikrein RFLP from the SHR progenitor strain, the median systolic, diastolic, and mean arterial pressures were significantly greater than in the RI strains that inherited the kallikrein RFLP from the BN progenitor strain. These findings suggest that in the rat, sequence variation in the kallikrein gene family, or in closely linked genes, may have the capacity to affect blood pressure.
Hypertension 1991 Feb
PMID:Cosegregation of blood pressure with a kallikrein gene family polymorphism. 167 81

It has recently been suggested that in the rat, sequence variation in the renin gene or closely linked genes may have the capacity to affect blood pressure and contribute to the pathogenesis of hypertension. To map the chromosomal location of the rat renin gene and to investigate its relationship to the inheritance of increased blood pressure, we studied a panel of rat x mouse somatic cell hybrids and a large set of recombinant inbred (RI) strains derived from spontaneously hypertensive rats (SHR) and normotensive Brown-Norway (BN) rats. We have found that in the rat, the renin gene is located on chromosome 13 and that it belongs to a conserved synteny group located on chromosome 1 in man and mouse. We have also found the median blood pressure of the RI strains that inherited the renin allele of the SHR to be greater than that of the RI strains that inherited the renin allele of the normotensive BN rat. These findings, together with the results of previous studies, suggest that in the rat, sequence variation in the renin gene, or in genes linked to the renin locus on chromosome 13, may have the capacity to affect blood pressure.
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PMID:The rat renin gene: assignment to chromosome 13 and linkage to the regulation of blood pressure. 167 97

Brown Norway kininogen-deficient rats had very low levels of plasma kininogens and lower levels of plasma prekallikrein, compared with those of normal rats of the same strain. Systolic blood pressure, determined by the tail-cuff method, of 5-week-old kininogen-deficient rats (106 +/- 0.4 mm Hg, n = 7) and the rate of systolic blood pressure increase with age were not different from those in normal rats. Weekly injections of deoxycorticosterone acetate (5 mg/kg s.c.) with 1% sodium chloride solution in drinking water after uninephrectomy at 7 weeks of age caused a gradual increase in the blood pressure of normal rats, reaching a plateau at 18 weeks of age, whereas that of deficient rats rose rapidly to 158 +/- 6 mm Hg 2 weeks after the start of treatment and continued to increase slightly, becoming significantly higher than normal rats at 8, 9, 10, 11, and 12 weeks of age (p less than 0.05 or 0.01). The levels of urinary prokallikrein and active kallikrein were slightly higher in deficient rats before deoxycorticosterone acetate-salt treatment but were not significantly increased after this treatment, whereas these levels in normal rats were increased 3.6- and 4.7-fold by this treatment. Urinary free kinin, collected from the ureter in untreated deficient rats, was below the detection limit. The plasma level of low molecular weight kininogen, the substrate of glandular kallikrein, was decreased in normal rats during the treatment. Continuous subcutaneous injection of aprotinin by an osmotic pump to normal rats induced significant increase in blood pressure. These results indicate that glandular kallikrein may play a suppressive role in deoxycorticosterone acetate-salt hypertension.
Hypertension 1991 Jun
PMID:Suppression of rat deoxycorticosterone-salt hypertension by kallikrein-kinin system. 171 Jun 5


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