Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of vitamin E on platelet function and serum lipid peroxide levels were investigated in DOCA-salt hypertensive rats. In the hypertensive rats, ADP- and collagen-induced platelet aggregation in whole blood were markedly attenuated and accompanied by a reduction of serotonin content as compared with the normotensive controls. These facts indicated the appearance of exhausted platelets, which have already been activated in vivo, due to the hypertension. Platelet vitamin E levels were decreased by 50%, while serum lipid peroxide levels were increased 3.6-fold in the hypertensive rats. Vitamin E administration (10 times the dietary intake) during the experimental periods did not influence either the aggregability or the serotonin content of platelets from the hypertensive rats. However, vitamin E administration significantly prevented the elevation of serum lipid peroxides due to the hypertension. These results suggest that vitamin E administration has little effect on platelet activation in vivo due to DOCA-salt hypertension.
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PMID:Effects of vitamin E administration on platelet function and serum lipid peroxides in DOCA-salt hypertensive rats. 205 24

The hypotensive effects of N-[8-amino-1(S)-carboxyoctyl] -L-alanyl-L-proline (AB-47, CAS 120008-53-9) were examined in normotensive rats and various hypertensive rat models. The hemodynamic effect of AB-47 was also examined in anesthetized spontaneously hypertensive rats (SHR). In 2-kidney, 1-clip renal hypertensive rats (2K, 1C-RHR) and SHR, the single administration of AB-47 (10 mg/kg, p.o.) induced potent and long-lasting hypotensive effects. The repeated administration of AB-47 (1 to 10 mg/kg, p.o.) to SHR for 29 days produced a dose-dependently and sustained hypotensive effect of 20 to 70 mmHg. AB-47 (10 mg/kg, p.o.) had a weak hypotensive effect in DOCA-salt hypertensive rats but no effects in normotensive and 1-kidney, 1-clip renal hypertensive rats (1K, 1C-RHR). AB-47 (3 mg/kg, p.o.) reduced blood pressure in intact SHR but not in bilateral nephrectomized SHR. The single intravenous injection of AB-47 (10 to 100 micrograms/kg) dose-dependently lowered systemic blood pressure, left ventricular systolic pressure (LVSP) and dp/dtmax without affecting heart rate (HR) and these effects of AB-47 were more potent than those of captopril and enalaprilat. These results suggest that AB-47 is a potent and long-lasting hypotensive agent and may be useful for the therapy of both hypertension and congestive heart failure.
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PMID:Hypotensive and hemodynamic effects of the new non-sulfhydryl angiotensin converting enzyme inhibitor N-[8-amino-1(S)-carboxyoctyl]-L-alanyl-L-proline. 209 26

To validate a miniature swine model of sympathectomy, six swine that had chronic high blood pressures for unknown reasons and five DOCA hypertensive swine were treated with a single dose of the neurotoxin 6-hydroxydopamine (6-OHDA) (50 mg/kg i.v.). One week after 6-OHDA, conscious mean arterial pressure (MAP) had fallen by 47-49 mmHg and the pressor response to tyramine was attenuated in both groups. Norepinephrine content was significantly decreased in the kidneys (greater than 85%) and left ventricle (greater than 94%) in both 6-OHDA treated groups. These results indicate that 6-OHDA can be used to effectively sympathectomize adult swine. Chemical sympathectomy of swine with either unexplained high blood pressure or experimentally induced DOCA hypertension resulted in an equivalent fall in MAP in both of these populations. Further studies using 6-OHDA in miniature swine may help to elucidate the mechanisms involved in maintaining hypertension in this animal model.
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PMID:Effects of 6-hydroxydopamine in hypertensive adult miniature swine. 211 51

In various models of hypertension of genetic origin, a hypersensitivity of phospholipase C has been demonstrated to participate in the hyperreactivity of platelets toward a variety of vasoactive agents. Since this abnormality could not be observed in the absence of cell stimulation, it could not account for the increase in free Ca2+ which has been reported in resting platelets in primary hypertension. Likewise, in hypertensive subjects, platelets behave hyperactive when stimulated by ADP, although the stimulus has been demonstrated to be a poor activator of phospholipase C. In order to gain insight into the membrane alteration that could account for the cellular hyperactivity which characterizes hypertensive subjects, we investigated, in resting platelets, the kinetics of radioactive labeling of major membrane phospholipids. Isolated platelets were prepared from SHR (4w and 17w of age), SHR-SP, Dahl salt-resistant and salt-sensitive rats fed either a low or a high salt diet, DOCA-salt hypertensive rats and from the appropriate normotensive controls. Irrespective of the radioactive precursor used (32P-orthophosphate, 3H-glycerol, 3H-choline), the labeling of phosphatidylcholine (PC) was markedly (up to 20 fold) enhanced in SHR (whichever their age) and SHR-SP compared with WKY. This increase, specific of PC, could not be accounted for by differences either in the actual amount of PC or in the uptake of various labels, suggesting an increased PC turnover. Such an increase was also observed in platelets of Dahl hypertensive rats but not in those of DOCA-salt hypertensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Membrane abnormalities and cellular hyperreactivity in different models of hypertension]. 212 54

Systemic and regional hemodynamics were studied in DOCA-treated Sabra hypertensive (SBH) and normotensive (SBN) rats. In SBH rats, mean arterial pressure (MAP) and total peripheral resistance index (TPRI) increased significantly. In SBN rats, MAP remained stable and TPRI decreased. Cardiac output and heart rate were unchanged. Opposed changes in TPRI were mediated mainly by changes in vascular resistance of the skin, skeletal muscles and splanchnic organs. Both strains developed significant biventricular hypertrophy. We conclude that SBH and SBN rats' susceptibility or resistance to DOCA-salt hypertension are associated with opposed changes in TPRI. The development of biventricular hypertrophy is apparently dissociated from systemic hemodynamic changes.
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PMID:Cardiac hypertrophy developing during DOCA-salt treatment is dissociated from systemic and regional hemodynamics. 213 2

The beneficial effect of angiotensin-converting enzyme (ACE) inhibitors on myocardial mass and contractility in hypertension and, possibly, congestive heart failure (CHF) may be related to their ability to induce a decreased afterload. This has been assessed in four experimental models--renovascular hypertension, DOCA-salt hypertension, spontaneously hypertensive rats (SHR) and myocardial infarction (MI)--and in normotensive mature rats. In renovascular hypertension, ACE inhibitors normalized blood pressure as well as left ventricular hypertrophy and hypocontractility. In the DOCA-salt model, blockade of the renin-angiotensin system by ACE inhibitors did not decrease blood pressure and therefore had no effect on cardiac mass and contractility. In the SHR model, the arterial smooth muscle cell is functionally and structurally abnormal; as a result, cardiac overload led, over time, to a terminal, decompensated phase of CHF. ACE inhibitors, by decreasing blood pressure, reversed cardiac hypertrophy, hyperfibrosis and atrial natriuretic factor (ANF) oversecretion and prevented overload and time-induced CHF. In the MI model, ACE inhibitors decreased blood pressure and thereby decreased overload and reversed cardiac hypertrophy, hypocontractility, hyperfibrosis and ANF oversecretion. In normal ageing, heart function and structure are modified over time. ACE inhibitors, by blocking a 'normal' signal upstream, allowed a 'normal' effector system to decrease blood pressure and prevented the development of age-dependent cardiac hypertrophy.
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PMID:Relationship between decrease in afterload and beneficial effects of ACE inhibitors in experimental cardiac hypertrophy and congestive heart failure. 214 18

The relation between blood pressure level and extracellular fluid volume and its distribution was studied in rats subjected to the following hypertensive stimuli--1K1C and 2K1C renal artery constriction, subtotal nephrectomy-salt and DOCA-salt. In all experimental groups the blood pressure increase was accompanied by increased extracellular fluid volume which was not always distributed proportionally between intravascular (PV) and interstitial (IFV) compartments. The blood pressure rise was further potentiated by plasma volume expansion so that the increased PV/IFV ratio was associated with a more pronounced hypertensive response (1K1C vs 2K1C, DOCA-salt vs subtotal nephrectomy-salt). However, adequate expansion of interstitial fluid is a necessary prerequisite for the hypertensive response. In DOCA-salt treated DI Brattleboro rats (lacking antidiuretic vasopressin action) plasma volume expansion per se was not accompanied by severe DOCA-salt hypertension. It is concluded that the expansion of both compartments of extracellular space, i.e. plasma volume and interstitial fluid volume, was necessary for a full development of severe hypertension. The expansion of only one of these compartments was accompanied by a mild blood pressure increase or blood pressure did not change significantly.
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PMID:Body fluids and their distribution in experimental hypertension. 214 92

STUDY OBJECTIVE - The aim was to examine the contractile state, the inotropic response to [Ca2+]e and the Ca2+ sensitivity of the contractile proteins in different models of hypertensive hypertrophy in an early stage of evolution (3-4 weeks). DESIGN - Renal hypertension was induced by placing a silver clip around the left renal artery. The contralateral kidney was either removed (1K-1C) or left untouched (2K-1C). Hypertension through sodium overload was produced by administration of deoxycorticosterone and 1% NaCl drinking water. (DOCA rats). Active and passive length-tension curves were performed to evaluate basal contractility at Lmax and passive stiffness of cardiac muscle. The inotropic responsiveness to [Ca2+]e and the Ca2+ sensitivity of the contractile proteins were also evaluated. EXPERIMENTAL MATERIAL - Papillary muscles and skinned trabeculae from the left ventricle of male Wistar hypertensive and age matched normotensive rats were used. MEASUREMENTS AND RESULTS - Cardiac hypertrophy was similar in all hypertensive groups. In 2K-1C and 1K-1C rats, basal contractility was not significantly different from controls. In DOCA rats, developed tension and time to peak tension (TTP) were significantly greater than controls. The inotropic response to [Ca2+]e was depressed in 2K-1C and increased in DOCA rats. In DOCA rats, increasing [Ca2+]e produced an increase in TTP greater than in controls. No differences were detected in muscle passive stiffness or in Ca2+ sensitivity of the contractility proteins among the different groups. CONCLUSIONS - In the earlier stages of hypertensive hypertrophy, differences in basal contractile state and/or inotropic responsiveness appear to be more related to the initiating cause of hypertensive hypertrophy than to the degree of hypertrophy itself. These differences cannot be attributed to changes in Ca2+ sensitivity of the contractile system.
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PMID:Calcium sensitivity of isometric tension in intact papillary muscles and chemically skinned trabeculae in different models of hypertensive hypertrophy. 214 71

Four experimental groups of rats treated with (1) DOCA-salt, (2) DOCA or (3) salt, and (4) controls were used to study the participation of brain natriuretic peptide (BNP) in the development of hypertension. Plasma and cardiac tissue concentrations of BNP as well as atrial natriuretic peptide (ANP) were measured in each group by using radioimmunoassays specific to rat BNP or ANP. Plasma BNP levels in DOCA-salt hypertensive group were higher than those in control (p less than 0.01), salt (p less than 0.01) and DOCA (p less than 0.01) groups. A positive correlation was observed between plasma BNP levels and blood pressure (r = 0.70, p less than 0.001) and between plasma ANP levels and blood pressure (r = 0.62, p less than 0.001). Plasma BNP/ANP ratio increased parallel with elevation of blood pressure. Plasma BNP levels correlated negatively with atrial BNP concentration (r = -0.33, p less than 0.05), but positively with ventricular BNP (r = 0.76, p less than 0.001). Compared with controls, tissue BNP-45/gamma-BNP ratio in the DOCA-salt rats was lower in atrium, but higher in ventricle. Thus, in DOCA-salt hypertension atrial BNP decreased with exhaustion of stored BNP-45, while ventricular BNP increased as BNP-45 accumulated. These results suggest that BNP is a novel cardiac hormone, synthesized, processed and secreted in response to changes in blood pressure. BNP may play different roles in controlling blood pressure than those assumed by ANP.
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PMID:Increased plasma brain natriuretic peptide levels in DOCA-salt hypertensive rats: relation to blood pressure and cardiac concentration. 214 83

This study was undertaken to verify the activity of plasma kininases in hypertension. Male Wistar rats (WIS) were used and three models of experimental hypertension were studied: spontaneously hypertensive rats (SHR), renal hypertensive rats, made according to the method of Goldblatt, DOCA-salt hypertensive rats. Normal Wistar rats, nephrectomized rats and sodium-loaded rats were used as control groups. Plasma from these animals was used to evaluate the kininase activities: kininase II activity (KII) was measured by the hydrolysis of hippuryl-L-histidyl-L-leucine (HHL); kininase I activity (KI) was measured by the hydrolysis of hippuryl-L-arginine (HLA) (CN1 activity) and of hippuryl-L-lysine (HLL) (CN2 activity). The three enzyme activities were characterized by their kinetic constants and the inhibitory pattern of various inhibitors. In normal WIS rats, hydrolysis of HHL proceeds with a Km of 2.55 +/- 0.22 mM and at a Vmax of 0.357 +/- 0.017 mumol/min/ml; the enzyme is inhibited by EDTA, 0-phenanthroline and captopril. HLA has a Km of 6.93 +/- 0.32 mM and a Vmax of 0.748 +/- 0.019 mumol/min/ml while the Km and Vmax values of HLL are 35.8 +/- 1.52 mM and 13.11 +/- 0.40 mumol/min/ml. The hydrolysis of both substrates is inhibited by EDTA, 0-phenanthroline and MERGETPA. KII activity is decreased in WKY and SHR rats (Vmax = 0.241 +/- 0.014 and 0.262 +/- 0.011 mumol/min/ml, respectively). In renal hypertensive rats and DOCA-salt hypertensive rats, the KII activity remained unchanged. CN1 activity was increased in 1K, 1C hypertensive animals (Vmax = 0.866 +/- 0.221 mumol/min/ml) and in DOCA-salt hypertensive rats (Vmax = 1.119 +/- 0.049 mumol/min/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Activity of plasma kininase I and kininase II in hypertensive rats]. 217 85


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