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

1. The aim of the present study was to test the hypothesis that responses to BDF 9148, which prolongs the opening of sodium channels, are reduced in the spontaneously hypertensive rat (SHR) left ventricle in the presence of hypertrophy and failure. 2. We studied the effects of BDF 9148 on the action potentials and contractions of left ventricles from 5-week-old prehypertensive, 14-week-old hypertensive, 6- and 12-month-old hypertension-associated hypertrophy and 18-month-old hypertension-induced heart failure SHR and age-matched Wistar-Kyoto normotensive (WKY) rats. 3. Action potentials and left ventricular contractions did not alter in the early stages of hypertension (14-week-old SHR). The diastolic membrane potential did not change with hypertension-associated hypertrophy, but there was a reduction in amplitude and a prolongation of action potentials in the left ventricles of 6-18-month-old SHR. Cardiac stimulation responses and maximum contractions to 10(-6) mol/L isoprenaline were reduced at 6 months, whereas the maximum contractions to 10(-2) mol/L CaCl2 were only reduced in left ventricles of 18-month-old SHR. 4. At concentrations ranging from 10(-7) to 3 x 10(-6) mol/L, BDF 9148 increased the amplitude and prolonged the duration of action potentials and augmented the force in WKY rat left ventricles. The augmenting effects of BDF 9148 at 3 x 10(-6) mol/L were smaller than at 10(-6) mol/L, possibly because the high concentration of BDF 9148 was also blocking calcium channels. Similar effects were observed with BDF 9148 in the early stages of hypertension (14-week-old SHR). 5. In the presence of persistent hypertension-associated hypertrophy of the SHR left ventricle at > or = 6 months, the effects of BDF 9148 on action potentials and contractions were significantly reduced to a small extent. This impairment of the response to BDF 9148 may reflect the reduced contractility of the SHR left ventricle and/or it may indicate that the response to the opening of sodium channels is altered from 6 months of age. 6. In summary, most of the response of BDF 9148 is maintained in the presence of hypertrophy and failure. Thus, BDF 9148 may have some potential for the treatment of heart failure.
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PMID:Effects of BDF 9148 on the action potentials and contractions of left ventricles from normo- and hypertensive rats. 1008 16

Concern over dietary fat in processed meats led to the passage of the '40 per cent' rule in the United States. Substitution of NaCl, linked to hypertension, with divalent chloride salts such as MgCl2 and CaCl2 has shown limited success. Early studies showed that these divalent salts had a deleterious effect on the functional properties of meat when used at product levels that resulted in high aqueous phase ionic strengths (0.4-0.6). However, our research focus has been to determine the utility of low levels (0.05 per cent) of MgCl2, CaCl2 and ZnCl2 in improving the functional properties of processed meats. Effects of divalent salts have been evaluated in turkey breast and thigh minces, beef model systems, and frankfurter formulations containing heart muscle. To determine if time postmortem affects muscle's response to divalent cations, salts were added to broiler thigh muscle in the early postmortem period. The important findings were (1) MgCl2 increased myosin solubility, (2) CaCl2 enhanced gel forming ability in cooked batters, and (3) ZnCl2 dramatically decreased myosin solubility in the absence of food-grade phosphate (sodium tripolyphosphate).
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PMID:Improvement of muscle protein functionality in processed meats by magnesium and other divalent chloride salts. 1019 95

The influence and mechanisms of action of N-ethyl- and N-benzyl-1,2-diphenylethanolamines (compounds E and B, respectively) on the arterial blood pressure and the heart rate of the rat together with their effects on CaCl2-induced arrhythmias in the rat were investigated. Both E and B in doses of (1.5-12 micromol/kg IV) decreased the arterial blood pressure and the heart rate in a dose-dependent manner. Studies with various receptor blockers, enzyme inhibitors and CaCl2 revealed that E-induced cardiovascular depressant effects were mainly due to CaCl2 channel blocking action and activation of cyclic guanylyl cyclase or release of NO whereas the cardiovascular effects of B seemed to involve both blockade of Ca2+ channels and activation of parasympathetic ganglia. Both compounds (12-14.5 micromol/kg) completely protected the rat against CaCl2 (60 mg kg(-1))-induced tachyarrhythmias. The B compound seemed to be several times more potent than the E compound in its cardiovascular depressant actions. The results suggest the potential usefulness of both compounds in the treatment of hypertension and supraventricular arrhythmias.
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PMID:Studies on the cardiovascular depressant effects of N-ethyl- and N-benzyl-1,2-diphenylethanolamines in the rat: elucidation of the mechanisms of action. 1042 11

The aim of this study was to determine whether parathyroidectomy (PTx) would modify hypertension secondary to adrenocorticotrophin (ACTH) administration. Male Sprague Dawley (SD) rats were randomly assigned to one of five groups; (i) sham (saline) treatment (NaCl 0.9% s/c 0.5 ml/kg/day), (ii) ACTH treatment (Synacthen Depot 0.5 mg/kg/day), (iii) saline/PTx/1% CaCl2 in water, (iv) ACTH/PTx/1% CaCl2 in water and (v) ACTH/1% CaCl2 in water. Tail cuff systolic blood pressure (SBP) and metabolic parameters were measured on alternate days for 4 control (C) and 11 treatment days (T0-T10). There was no change in SBP in the sham and saline/PTx/CaCl2 groups over T0-10. SBP increased in the ACTH treated groups. PTx did not modify ACTH-induced increases in SBP or metabolic effects. These results do not support a role for the parathyroids in the genesis of ACTH-induced hypertension in the rat.
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PMID:The role of the parathyroid glands in adrenocorticotrophin-induced hypertension in the rat. 1051 29

1. Hypertension leads to ventricular hypertrophy and, eventually, to heart failure. The present study has investigated the functional consequences of deoxycorticosterone acetate (DOCA)-salt hypertension in rats by defining the inotropic, chronotropic and vascular responses to noradrenaline (NA; beta1-adrenoceptor agonist), forskolin (adenylate cyclase activator) and theophylline (phosphodiesterase inhibitor). 2. Administration of DOCA (25 mg, s.c., every 4th day) and excess salt (1% NaCl in drinking water) to uninephrectomized rats increased left ventricular wet weight by 35 and 71% after 4 and 8 weeks, respectively. Addition of KCl (0.4%) or CaCl2 (1%) in the drinking water for 4 weeks attenuated blood pressure increases, but not ventricular weight increases (46 and 28%, respectively). 3. Positive inotropic responses in papillary muscles from uninephrectomized rats to NA (-log EC50 6.73+/-0.38; n = 7), forskolin (-log EC50 6.15+/-0.31; n = 7) and CaCl2 (-log EC50 2.40+/-0.02; n = 14) were unchanged in hypertrophied left ventricles of DOCA and DOCA-CaCl2 rats, although maximal responses to NA were decreased in DOCA-KCI rats (1.2+/-0.6 mN, n = 8; DOCA-salt 2.9+/-0.5 mN, n = 6); theophylline was less potent in DOCA-salt rats. Positive chronotropic responses to NA, forskolin and theophylline in right atria and negative inotropic responses to carbachol in papillary muscles were unchanged. 4. Maximal vasoconstrictor responses to NA in thoracic aortic rings were reduced in DOCA-KCI rats to 2.4+/-0.9 mN (n = 5), but were increased in DOCA-CaCl2 rats to 26.6+/-2.2 mN (n = 7; DOCA-salt 7.8+/-2.2 mN, n = 9). Vasorelaxant responses to forskolin and theophylline were unchanged. 5. These results show that cardiac responses are only minimally affected during the development of DOCA-salt hypertension-induced hypertrophy, despite the reported decreases in adenylate cyclase activity, in these rats. This is in contrast with the decreased responses reported in other rat models of cardiac hypertrophy and in the failing human heart. Thus, hypertrophy in hearts of DOCA-salt hypertensive rats does not produce similar changes to the failing human heart.
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PMID:Cardiac and vascular responses in deoxycorticosterone acetate-salt hypertensive rats. 1077 23

The cardiotonic and antidysrhythmic effects of four triterpenoid derivatives, namely oleanolic acid (OA), ursolic acid (UA), and uvaol (UV), isolated from the leaves of African wild olive (Olea europaea, subsp. africana) as well as methyl maslinate (MM) isolated from the leaves of Olea europaea (Cape cultivar) were examined. The derivatives showed low toxicity on brine shrimp test. They displayed significant, dose-response vasodepressor effect and sinus bradicardia, most prominent for OA and MM. The derivatives acted as beta-adrenergic antagonists, blocking the effect of adrenaline and isoprenaline. The established positive inotropic and dromotropic effects were most distinctive for OA and MM. The antidysrhythmic effects were evaluated on CaCl2- and adrenaline-induced chemical arrhythmias, and on ischemia-reperfusion arrhythmia. OA and UA displayed antidysrhythmic effects on both types of chemical arrhythmia; OA and UV in dose 40 mg/kg conferred significant antidysrhythmic activity on ischemia and reperfusion arrhythmias. The effect was comparable to that of propranolol and suggestive of beta-adrenergic antagonistic activity. On the basis of the vasodepressor, cardiotonic and antidysrhythmic effects of these compounds, it was concluded that OA and UV isolated from wild African olive leaves, or crude extract containing all components, can provide a cheap and accessible source of additive to conventional treatment of hypertension, complicated by stenocardia and cardiac failure.
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PMID:Cardiotonic and antidysrhythmic effects of oleanolic and ursolic acids, methyl maslinate and uvaol. 1507 Jan 61

Postmenopausal estrogen deficiency increases the incidence of cerebrovascular disease. However, hormone replacement therapy is associated with an increased cardiovascular risk. Tamoxifen is a selective estrogen receptor modulator with estrogenic effects on cardiovascular risk factors, but its long-term impacts on cerebral vasculature are unknown. We hypothesized that chronic 17beta-estradiol or tamoxifen treatment exerted similar effects in reducing cerebrovascular tension in ovariectomized rats. We therefore determine whether (1) chronic 17beta-estradiol treatment could influence vasomotor activities, (2) chronic tamoxifen therapy could exert an estrogen-like or estrogen-antagonistic effect, and (3) acute exposure to estrogen could mimic the effect of 17beta-estradiol. Isometric tension was measured in cerebral arteries from female rat groups: control, ovariectomy, ovariectomy plus 17beta-estradiol treatment, ovariectomy plus tamoxifen treatment, and ovariectomized rats treated with tamoxifen and 17beta-estradiol. Ovariectomy enhanced cerebrovascular contractions to endothelin-1 or CaCl2, but not to U46619 or phenylephrine. 17beta-Estradiol therapy reversed these effects. Chronic tamoxifen treatment exerted estrogen-like actions by reversing ovariectomy-induced enhancement of vessel tone without antagonizing the effect of chronic 17beta-estradiol treatment. Ovariectomy enhanced the relaxing potency of nicardipine, and 17beta-estradiol treatment prevented this effect. Acute exposure to 10(-9) mol/L 17beta-estradiol or 10(-8) mol/L tamoxifen did not modulate contractions in rings from nonoperated female rats. In conclusion, ovariectomy differentially enhances agonist-induced cerebrovascular tone, an effect that was reversed by estrogen therapy. Tamoxifen does not act as an estrogen antagonist; instead, it functions as an estrogen agonist during estrogen deficiency. Thus, tamoxifen may confer beneficial effects similar to estrogen in cerebrovascular vessels.
Hypertension 2004 Jul
PMID:Estrogen and tamoxifen modulate cerebrovascular tone in ovariectomized female rats. 1515 80

Intravenous diltiazem can be used to treat myocardial ischemia, hypertension, and supraventricular dysrhythmias, but significant adverse effects including atrioventricular block and hypotension have been reported. At the present time, there is controversy as to which drug is most effective in reversing these sequelae. This study was designed to assess the effectiveness of calcium chloride v epinephrine in reversing these side effects. The hemodynamic and electrophysiologic effects of diltiazem infusion were investigated in eight dogs anesthetized with fentanyl and nitrous oxide/oxygen. This study confirmed that diltiazem infusions in high concentrations produced predominantly atrioventricular conduction depression followed by profound hypotension. Epinephrine infusion proved to be most effective in attenuating and eliminating each of these deleterious side effects. In contrast, calcium chloride did not significantly increase heart rate or blood pressure or reverse atrioventricular block. In two instances calcium chloride produced further depression of atrioventricular conduction, leading to severe bradycardia and sinus arrest. Although calcium chloride increased left ventricular contractile force (LV dP/ dt) and cardiac index (CI), mean arterial pressure was not affected and SVR was further decreased. This study indicates that calcium chloride should not be given to reverse the side effects of diltiazem in the presence of atrioventricular conduction block or profound hypotension. Calcium chloride is indicated only when isolated myocardial depression is present and after the calcium channels have been reopened by epinephrine.
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PMID:Reversal of the adverse cardiovascular effects of intravenous diltiazem in anesthetized dogs. 1717 30

Hypertension is a common cardiovascular disease and can induce many complications, such as stroke and coronary heart disease. The purpose of the present study was to investigate the effect of ischemia/hypoxia on mesenteric artery vasomotor function in spontaneously hypertensive rats (SHR). Rat mesenteric arterial rings were cultured in modified ischemia-mimetic solution in a hypoxia incubator for a certain time period. Isometric tension changes of isolated mesenteric arterial rings were recorded continuously by a myograph system. The results obtained were as follows: In SHR group, the maximum contractions to KCl and phenylephrine (PE) were increased, and the maximum relaxation to acetylcholine (ACh) was decreased, compared to those in Wistar-Kyoto (WKY) rats group. Compared with SHR group and WKY with acute ischemia/hypoxia (WKY+H) group, SHR with acute ischemia/hypoxia (SHR+H) increased the maximum contractions induced by KCl and PE and inhibited the maximum relaxations by ACh. In SHR+H and SHR groups, the vasodilation induced by ACh was unaffected by N(G)-nitro-L-arginine methylester (L-NAME), whereas in WKY group, the relaxation to ACh was attenuated by L-NAME. CaCl2-induced contraction in depolarized rings in SHR+H group significantly shifted to the left compared with SHR group. In Ca(2+)-free K-H solution, the maximum contractions induced by PE and caffeine were increased in SHR+H group compared to those in WKY+H group; the PE- and caffeine-induced contractions were also enhanced in SHR group versus WKY group; the maximum contraction induced by PE was significantly increased in SHR+H group versus SHR group. These findings suggest that acute ischemia/hypoxia aggravates mesenteric artery dysfunction in SHR. The mechanism may be related to the decreased NO generation and increased sarcoplasmic reticulum Ca(2+) release.
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PMID:[Effect of ischemia/hypoxia on mesenteric vasomotor function in spontaneously hypertensive rats and its possible mechanism]. 2219 49

The research of biological activity of peptide geroprotector Slavinorm on the basis of calf aorta extract was conducted in experimental models of hypertension and chloride-calcium arrhythmia. The research results showed that in experimental model of arrhythmia in rats induced by pituitrin administration, intraventricular and intramuscular introduction of Slavinorm in therapeutical dose had caused to leveling of hypertension symptoms. That was expressed in normalization of blood pressure characteristics, body weight, heart and kidney weight. In the experimental model of chloride-calcium arrhythmia in rats inrtaventricular and intramuscular introduction of Slavinorm showed the ability to predict the arrhythmia development caused by the Calcium Chloride administration. The research results testify to availability of the medication research in the capacity of the medication for treatment of age related pathology conditioned by vessels impaired function.
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PMID:[The natural peptide geroprotector antiarhythmic action]. 2313 May 33


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