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

The changes in the content of pyridine nucleotide coenzymes (NAD+ and NADH) in several models of experimentally induced hypertension, differing in mechanism (genetic spontaneous hypertension, renal one kidney Goldblatt hypertension, Adrenal-regeneration hypertension after INGLE-HIGGINS and Skelton, and NaC1 hypertension) were studied. An obvious difference between the changes in NAD+ and NADH in the various models of hypertension, was established: Thus in NaC1 hypertension a high level of the coenzymes in the kidneys and in the vessel wall was found, while the liver coenzyme content was in normal ranges. In ARH the coenzyme level was elevated not only in the kidneys and in the vessel wall, but in the liver as well. Treatment with hypotensive antilipolytic prostaglandin E1 decreased the coenzymes in ARH to normal values. Renal hypertension was characterized by a low content of oxidized NAD, an increased NADH, and a decreased NAD+/NADH ratio in the kidneys and the liver, while in the vessel wall the coenzyme level was moderately increased. The coenzyme changes in the kidneys of SHR were similar to those in renal hypertensive rats. However coenzyme level in the vessel wall of SHR was lower than in all the other forms of hypertension.
 ...
PMID:Coenzyme alterations in rats with experimental hypertension. 18 74

The prostaglandin synthetase inhibitor indomethacin was given orally or intravenously to pregnant ewes. This resulted in the fetal pulmonary to systemic arterial mean blood pressure difference across the ductus arteriosus rising significantly, presumably secondary to constriction of the ductus arteriosus. The pressure difference was due to pulmonary arterial hypertension, and not due to a fall in systemic arterial mean blood pressure. Fetal arterial blood gas tensions and pH values were normal throughout. In five experiments the pressure difference could be promptly but temporarily reversed by the administration of PGE1 into the fetal inferior vena cava. Indomethacin was present in fetal blood, and maternal plasma prostaglandin levels were suppressed. Indomethacin administration during pregnancy causes constriction of the fetal ductus arteriosus and fetal pulmonary arterial hypertension which, if severe, may cause rapid fetal death. It is possible that this mechanism may be one cause of persistent pulmonary hypertension or tricuspid insufficiency or both in the newborn infant.
 ...
PMID:Constriction of the fetal ductus arteriosus after administration of indomethacin to the pregnant ewe. 43 Mar 14

The prostaglandin synthetase inhibitor indomethacin was given orally or intravenously to pregnant ewes. This resulted in a significant rise in the fetal pulmonary-to-systemic arterial mean blood pressure difference across the ductus arteriosus, presumably secondary to constriction of the ductus arteriosus. In five experiments the pressure difference could be promptly but temporarily reversed by the administration of prostaglandin E1 (PGE1) into the fetal inferior vena cava. Fetal lungs from study and control animals were fixed by perfusion at measured pulmonary arterial mean blood pressure, and fifth-generation resistance vessels were studied. The medial width/external diameter ratio was significantly increased in the study vs the control lungs due to increased smooth muscle and decreased external diameter. In addition, study fetuses had acute degenerative myocardial changes in the tricuspid valve papillary muscles, the right ventricular free wall and the interventricular septum. Similar changes were not seen in control fetuses. Indomethacin administration during pregnancy causes constriction of the fetal ductus arteriosus, fetal pulmonary arterial hypertension, and right ventricular damage. If severe, this may cause rapid fetal death. If less severe, in the newborn infant, this mechanism may be one cause of persistent pulmonary hypertension due to vasoconstriction and increased pulmonary arterial smooth muscle and/or tricuspid insufficiency due to papillary muscle infarction.
 ...
PMID:Hemodynamic, pulmonary vascular, and myocardial abnormalities secondary to pharmacologic constriction of the fetal ductus arteriosus. A possible mechanism for persistent pulmonary hypertension and transient tricuspid insufficiency in the newborn infant. 44 54

Effect of tolmetin sodium on the pain-like responses caused by various nociceptive stimuli was examined in experimental animals. Tolmetin sodium showed a potent inhibitory activity on the acetic acid-induced writhing in mice and rats, and its potency, (ED50 = 23.4 and 3.01 mg/kg, p.o.) was about 2.4--10.3 times that of ibuprofen and aspirin. The hypertension induced by intraarterial injection of bradykinin toward the spleen of dogs was inhibited by tolmetin sodium (ED50 = 80 mg/kg, i.v.), but the hypertension by a simultaneous injection of bradykinin and PGE1 was not inhibited by tolmetin sodium and sulpyrine, though pentazocine inhibited both hypertensions. The pain-like response caused by pressing mechanically the inflamed paws or joints of rats induced by kaolin-carrageenin or adjuvant was inhibited by tolmetin sodium (30--100 or 20--40 mg/kg, p.o., respectively), and the potency was approximately equal that of ibuprofen and phenylbutazone. Tolmetin sodium produced a significant inhibition of the pain-like response induced by electrical stimulation of tooth pulp of dogs, but showed no effect when the methods of Haffner and D'Amour-Smith were applied to mice. Anti-writhing action of tolmetin sodium was not antagonized by naloxone. From these results, it was concluded that tolmetin sodium has a potent inhibitory activity on the pain-like responses induced by the chemical nociceptive stimuli and by the mechanical pressure stimulus of the inflamed tissue, especially on the writhing. The analgesic activity probably involves a peripheral mechanism.
 ...
PMID:[Analgesic activity of a non-steroidal anti-inflammatory agent, tolmetin sodium in experimental animals (author's transl)]. 53 31

The release of prostaglandin-like (PG-like) material by aorta strips of normotensive and hypertensive rats has been studied in vitro. When incubated in an oxygenated Krebs solution kept at 37 degrees C, aorta strips removed from 8- and 12-week-old spontaneously hypertensive (SH) rats generate 1.2-2.5 times more PG-like material than aorta strips from age-matched normotensive Wistar (NW) rats. The overproduction of PG-like material by aorta strips of SH rats did not precede the development of hypertension in SH rats. Aorta strips derived from renal and DOCA-salt hypertensive rats produced 1.5-3 times more PG-like material than aorta strips from NW rats. The production of PG-like material by aorta strips of renal and DOCA-salt hypertensive rats was largely reduced when hypertension was interrupted in these animals, thus suggesting that the alteration taking place in the arteries of hypertensive rats (namely increased production of PGs) during the development of hypertension was reversible. The production of PG-like material by aorta strips of hypertensive rats was inhibited by indomethacin. Analysis of the PG-like material by bioassays and thin-layer chromatography suggests the presence of PGE2 and PGE1. The possible involvement of these PGs in the pathogenesis of hypertension in rats is discussed.
 ...
PMID:The role of prostaglandins in hypertension. I. The release of prostaglandins by aorta strips of renal, DOCA-salt, and spontaneously hypertensive rats. 59 81

The purpose of the investigation was to study the alterations in the lipid and lipoprotein content in the blood serum, the liver and the aortic wall of rats with experimentally induced salt, renal (Goldblatt) and adrenal-regeneration hypertension. The experiments were carried out on 59 Wistar rats (25 normotensive controls). It was established that both the serum and the liver lipid patterns vary in the three experimental models of hypertension. Thus, while in salt-induced hypertension no hyperlipidaemia and hyperlipoproteinaemia were established, in renal hypertension the serum lipid and lipoprotein levels were significantly increased in comparison to the controls. The cholesterol content in the liver was increased in all the three models of hypertension. The remaining lipid fractions were within normal ranges or a little decreased in salt-induced hypertension, while in renal and adrenal-regeneration hypertension their quantity was significantly increased. A two weeks' treatment with hypotensive prostaglandin E1 diminished the lipid and lipoprotein contents in the liver of rats with adrenal-regeneration hypertension, only cholesterol remaining unaltered. The blood serum level of free fatty acids increased in all the three models of experimental hypertension, as did the cholesterol and beta-lipoprotein level in the aortic wall. The alterations in lipid and lipoprotein metabolism established in this study are regarded as specific for the hypertensive process itself, since no histological alterations characteristic of atherosclerosis were observed.
 ...
PMID:The action of arterial hypertension on lipid and lipoprotein metabolism. I. Salt, adrenal-regeneration and renal (Goldblatt) hypertension. 100 Sep 84

The effects of prostaglandin E1 on fluid and sodium excretion, creatinine clearance and renin release were examined in 26 hypertensive patients including 9 cases of essential hypertension, 10 of renovascular hypertension and 7 of primary aldosteronism. When prostaglandin was infused intravenously in a total dose of 120 mug in 60 min, urine volume was increased in 70% of cases, and sodium excretion in 61%, but little changes were observed in creatinine clearance. The most prominent diuresis and natriuresis were obtained in primary aldosteronism (mean increase was 319% in urinary volume, and 222% in sodium output). The average increases in urinary volume were 61% in patients with essential hypertension and 97% in renovascular hypertension. And urinary output of sodium was increased by 63% in the former and 56% in the latter. The remarkable renal effects of prostaglandin E1 in primary aldosteronism were completely abolished after the administration of spironolactone. Significant elevation of plasma renin activity resulted from prostaglandin E1 infusion in essential hypertension, while no constant effect was obtained in renovascular hypertension and primary aldosteronism. The present experiments indicate that prostaglandin E1 has different effects on the kidney according to the types of hypertension and the effects correlate closely with patient's status of extracellular fluid volume or sodium balance.
 ...
PMID:Renal effects of prostaglandin E1 in hypertensive patients. 118 18

The effects of prostaglandin E1 on renal function were studied in surgical patients under general anesthesia. The patients were over 20 years old, and had ischemic heart disease, hypertension and/or liver dysfunction. In 67 patients (PGE1 group), prostaglandin E1 (PGE1) was in fused at a rate of 0.02 mcg.kg-1.min-1. In 55 patients (control group), only lactated Ringer solution was infused at a rate of 10 ml.kg-1.h-1. Urine output and fractional sodium excretion in PGE1 group were significantly higher than those in control group. There were no significant differences in creatinine clearance and free water clearance between the two groups. The increase in urine output in PGE1 group could be attributed to the decrease in the water reabsorption in the proximal renal tubule.
 ...
PMID:[The effects of prostaglandin E1 on renal function]. 143 69

The effect of oral prostaglandin E1 (limaprost) on erectile function was studied in a double-blind placebo controlled trial. Fifty one patients who agreed to participate were examined for their subjective symptoms and nocturnal erection was recorded using an erectometer at the beginning of the study, after an initial 6 week period, and again after a second 6 week period. Patients were randomly assigned to a group which received placebo followed by limaprost or to a group which received limaprost followed by placebo. Ten cases dropped out. In the remaining forty one patients, NPT during the limaprost phase was significantly different from that during the placebo phase. Patients with the history of diabetes mellitus, hypertension, or pelvic surgery showed relatively poor responses to oral prostaglandin E1. Oral prostaglandin E1 achieved 42.9% effectiveness in the psychogenic impotence, and this effectiveness is significantly higher than that of placebo. Oral prostaglandin E1 was suggested as an additional or alternative therapy in the management of psychogenic impotence. Psychogenic impotent who didn't respond to sex therapy and patients with slight organic causes would seem to benefit from oral prostaglandin treatment.
 ...
PMID:[Double-blind trial of oral prostaglandin E1 on impotence]. 143 68

The case history of a woman, who at the age of 25 years on the birth of her second child was found to be diabetic, is reported. Over the subsequent 30 years the patient had been treated with insulin, the dose administered being monitored at regular intervals. At the age of 52 years, the patient was diagnosed as suffering from hypertension and diabetic nephropathy of the nephrotic type. The patient's condition gradually deteriorated and at 55 years of age 40 micrograms/day prostaglandin E1 was given intravenously for 84 days. Treatment resulted in a decline in urinary protein without a reduction in creatinine clearance. Renograms confirmed an improvement in the vascular and secretory phases of both kidneys.
 ...
PMID:Does a dose of 40 micrograms/day prostaglandin E1 reduce creatinine clearance in a patient with diabetic nephropathy of the nephrotic type? 152 75


1 2 3 4 5 6 7 8 9 Next >>