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

Injection of saralasin or converting-enzyme inhibitor produced a small variable reduction of blood-pressure in rats with two-kidney hypertension. Prolonged infusion of the inhibitors gradually reduced blood-pressure to normal. Control infusions of saralasin in normal animals and of dextrose in normal and hypertensive animals did not reduce blood-pressure. Plasma-renin concentration correlated significantly with the early but not with the later fall of blood-pressure. Plasma-concentrations of renin and angiotensin II were closely related except in rats receiving converting-enzyme inhibitor, when angiotensin II was relatively reduced. The gradual reduction of arterial pressure by saralasin was not associated with increased urinary sodium excretion.
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PMID:Correction of renal hypertension in the rat by prolonged infusion of angiotensin inhibitors. 7 29

Nitroglycerin is a vasodilating agent by virtue of its actions on vascular smooth muscle fibers. It may be administered intravenously (using either 5 p. cent dextrose, or propylene-glycol solvant), sublingually, orally or by topical administration. It is rapidly metabolized, principally by liver. Its is not toxic. The vasodilatation that is produced is both arterial and venous and is dose-related in dog (1 microgram to 100 micrograms/kg/min). However, resistance and tachphylaxis may occur. Its principal use is for angor treatment, but it has been used for the treatment of arteriopathy of the lower limbs, biliar hypertony and arterial hypertension. It has been recently administered for the treatment of acute phase of myocardial infarction and during pre, per- and post-operative periods in cardiac surgery, neurosurgery and hip surgery, as myocardial protector or anti-hypertensive agent or hypotensive agent. The absence of toxicity and the rapid reversibility of its cardio-vascular effects which are similar to the effects of sodium nitroprusside are important reasons for its use in anesthesia and cardiac intensive care.
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PMID:[Pharmacology of nitroglycerin (author's transl)]. 11 40

Abdominal aortic aneurysmectomy is being performed with progressively lower operative mortality and morbidity. Three hundred thirty seven patients have had elective aneurysm repair since 1954. Factors affecting mortality and morbidity in the last 108 cases are analyzed. Seventy-four per cent of patients had pre-existing disease, either cardiac, pulmonary, renal, cerebrovascular, diabetes mellitus, or hypertension. Six patients died following operation, a mortality rate of 5.5%. One died of pulmonary and 5 of cardiac causes. No patient died of renal failure or required dialysis. A signficant feature of management is the regimen of fluid therapy using dextrose in lactated Ringer's solution during and after operation to minimize hypotensive and renal complications. No patient developed a wound infection, graft infection, wound dehiscence, stroke, or intestinal ischemia. Serious postoperative complications were largely cardiac or pulmonary. Despite recent liberalization of indications for operation, comparative figures show continued reduction in operative mortality from 17% during 1954-1961, or 7.4% during 1962-1967, to 5.5% in the 1968-1974 era. This declining mortality is related to earlier diagnosis using non-invasive methods (sonogram), simplified operative techniques, improvement in fluid management, innovations in cardiopulmonary therapy, and recognition and proper handling of unusual manifestations of aortic aneurysms.
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PMID:Surgical management of abdominal aortic aneurysms: factors influencing mortality and morbidity--a 20-year experience. 12 60

1 Prolonged infusion (11 h) of both saralasin and angiotensin-converting enzyme inhibitor (SQ20881) gradually lowered BP in two-kidney hypertensive rats to levels similar to that in normotensive rats infused with dextrose. 2 Saralasin did not lower BP in DOCA-salt hypertensive rats. 3 These observations support the notion that in chronic renal hypertension, angiotensin II may maintain hypertension by a slowly developing action. 4 Plasma angiotensin II in rats infused with SQ20881 was suppressed relative to renin, but was not eliminated. 5 Chromatography of angiotensin II extracts from dogs infused with converting enzyme inhibitor (SQ14,225) showed that the very high levels of angiotensin I achieved after treatment with SQ14,225 can lead to falsely high estimated angiotensin II levels as a result of angiotensin I cross-reacting with the angiotensin II assay.
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PMID:Inhibitors of the renin-angiotensin system in experimental hypertension, with a note on the measurement of angiotensin I, II and III during infusion of converting-enzyme inhibitor. 22 15

Propranolol administered subcutaneously in a dise of 30 mg/kg twice a day for 3 weeks did not significantly lower systolic tail blood pressure (STBP) in chronic two-kidney Goldblatt hypertension in rats. Plasma renin activity (PRA) measured at the end of the treatment was not significantly different in propranolol treated and dextrose treated rats, although there was marked bradycardia in propranolol treated rats. However, 3 out of 10 propranolol treated hypertensive rats had pressures in the normotensive range during the last week of therapy. PRA values in these three rats were significantly lower than those in dextrose treated hypertensive rats. STBP on day 20 showed a positive correlation with PRA in both propranolol (r = 0.90, p less than 0.01) and dextrose (r = 0.85, p less than 0.01) treated hypertensive rats. Hypertension was associated with an increase in heart weight, which was significantly blunted but not abolished by propranolol treatment. Thus, propranolol did not decrease blood pressure in most rats with chronic two-kidney Goldblatt hypertension; when it did lower blood pressure, its antihypertensive effect appeared related to its renin suppression effect. Furthermore, propranolol mitigated hypertension induced cardiac hypertrophy, independently of its antihypertensive effect.
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PMID:Effects of propranolol in chronic two-kidney Goldblatt hypertension in rats. 50 10

The hemodynamic effects of long term feeding of sympathomimetic amines (SPMA) to swine were studied. Three groups of female swine (N = 20 for each group) were fed either aminorex fumarate, d-amphetamine sulfate, or dextrose (control) for as long as 8 months in dosages up to 15 mg/kg/day. After 4 months of this feeding regiment, the weight gain of the pigs fed either aminorex or amphetamine was significantly less than the control animals. Hemodynamic measurements on awake swine indicated no elevation of pulmonary arterial blood pressure in the pigs fed SPMA. Measurement of systemic hemodynamics revealed that cardiac index was lower in the treated pigs than in control animals, but that heart rate and systemic arterial blood pressure were not altered by the drugs. In addition to baseline measurements of hemodynamic variables, the animals were exposed to acute hypoxia (12 percent O2 in N2) for 5 minutes. Although pulmonary arterial blood pressure increased similarly in the 3 groups of pigs, total pulmonary resistance increased to a greater extent in the pigs fed SPMA, indicating perhaps an enhancement of the hypoxic pulmonary pressor response after chronic ingestion of either amphetamine or aminorex. In a limited number of pigs, SPMA were fed for a period of 8 months, of which the last 3 months were during pregnancy. Hemodynamic measurements on sedated (metomidate, IV) swine revealed no difference in pulmonary arterial blood pressures between treated and control animals. We conclude that chronic ingestion of large doses of aminorex or amphetamine in swine does not lead to pulmonary arterial hypertension, but that slight reductions in cardiac output and subtle alterations in the pulmonary pressor response to acute hypoxia may occur.
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PMID:Hemodynamic effects of long term feeding of sympathomimetic amines to swine. 73 Nov 86

A large number of individuals currently diagnosed as having diabetes mellitus are asymptomatic. In order to provide rational therapy for this patient population, it is necessary to focus upon the differences between these patients and the classic prototypes with polyuria and weight loss, who require insulin for survival. Patients with asymptomatic diabetes do not need insulin for survival, and, by definition, they do not need it to alleviate symptoms. They tend to be middle-aged and overweight, but they can be young and thin. Their degree of hyperglycemia is moderate, often indistinguishable from that of normal individuals in their day-to-day existence. Indeed, they can often be differentiated from normal persons only on the basis of their blood glucose response to the stress of a large dextrose challenge; in this regard, the potential problem of over-diagnosing diabetes has been discussed. Since the major problem facing patients with asymptomatic diabetes is accelerated atherogenesis, the therapeutic approach must be based upon efforts to delay or prevent the onset of vascular disease. It has yet to be shown that any therapeutic intervention helps such patients, but an argument has been made in support of the following goals in subjects with asymptomatic diabetes whose fasting blood glucose level is less than 170 mg/100 ml: (1) stop smoking, (2) control hypertension, (3) attain ideal body weight, and (4) maintain blood triglyceride and cholesterol levels well within normal limits. Attempts to lower blood glucose with either insulin or oral agents do not seem indicated in the majority of patients within this defined diabetic population.
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PMID:Treatment of asymptomatic diabetes mellitus. 97 61

Deoxycorticosterone pivalate (2.5 mg/kg) given intramuscularly on four occasions 10-15 days apart over a period of 45 days to unilaterally nephrectomized adult male mongrel dogs, receiving as drinking solution 0.9% NaCl in 5% dextrose, resulted in an average sustained rise in the mean arterial blood pressure of 30 mm Hg (1 mm Hg - 133 N/m2) in 60% of the animals. Hypertensive dogs had in their arterial tissues generally more sodium, potassium, magnesium, and calcium than the similarly treated but non-hypertensive dogs, but compared to the tissues of operated untreated or unoperated normotensive dogs, only sodium and calcium were significantly higher. The dogs who were similarly treated but did not develop hypertension had in their arterial tissues less sodium, potassium, and magnesium than operated untreated or unoperated normotensive dogs. Norepinephrine content in the branches of mesenteric arteries of all deoxycorticosterone- and NaCl-treated animals, irrespective of their blood pressure, was significantly lower, and in the myocardium significantly higher, than either the unoperated normotensive or operated but not further treated dogs. It is concluded, therefore, that in deoxycorticosterone + NaCl treatment the dogs which developed hypertension had more arterial sodium, potassium, magnesium, and calcium than those who were similarly treated but remained within the limits of normal blood pressure, and that there was no difference between hypertensive and non-hypertensive dogs in regard to their cardiovascular norepinephrine content.
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PMID:Water, cations, and norepinephrine content of cardiovascular tissues of unilaterally nephrectomized dogs treated with deoxycorticosterone and NaCl. 120 92

We assessed the vasodilator effect of endothelium-derived nitric oxide by inhibiting its formation with NG-monomethyl L-arginine (LNMMA) on systemic and regional hemodynamics in conscious, normotensive rats, using the radioactive microsphere technique. In rats injected with 10 mg/kg LNMMA (n = 8), mean blood pressure increased by 16.2 +/- 2.6 mm Hg, and heart rate decreased by 54.3 +/- 16.7 beats per minute. In comparison with rats injected with 5% dextrose (n = 14), cardiac index was lower by 35.6% (p less than 0.01), and total peripheral vascular resistance was higher by 51.6% (p less than 0.01); regional blood flows were lower and vascular resistance higher in most organs. Changes were significant in the heart, kidney, stomach, large intestine, skin, and adrenals (p less than 0.05). Preinjection of 100 mg/kg L-arginine prevented the pressor response but only partially attenuated the other hemodynamic effects of LNMMA. Combination of LNMMA with the bradykinin antagonist (D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Phe-Thi-Arg)trifluoroacetic acid (50 micrograms/min for 5 minutes) did not produce systemic or regional effects different from those obtained with LNMMA alone. Combination of LNMMA with indomethacin (10 mg/kg) resulted in additional changes in the cerebral circulation, blood flow decreasing by an additional 44.2% (p less than 0.01) and vascular resistance increasing by 75.3% (p less than 0.01) compared with changes produced by LNMMA alone.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Feb
PMID:Inhibition of nitric oxide, bradykinin, and prostaglandins in normal rats. 173 88

The current studies were designed to characterize calcium transport by intestinal brush border membrane in the spontaneously hypertensive rat (SHR) and normotensive control, the Wistar-Kyoto (WKY) rat. The biochemical and functional purity of the intestinal brush border membranes in SHR and WKY rats was validated by marker enzymes and the ability to transiently transport D-glucose in the presence of Na+ gradient. Calcium transport into duodenal and jejunal vesicles represented a minor binding component and transmembrane movement as evident by initial rate studies, A23187 studies, and lanthanum displacement experiments. Initial rate and time course of calcium uptake was lower in SHR compared with WKY rats. Kinetic analysis of calcium uptake by the jejunum (total uptake minus binding component) showed a Vmax of 6.98 +/- 0.2 and 1.8 +/- 0.2 nmol/mg protein/7 sec in WKY rats and SHR, respectively (P less than 0.001), whereas Km values were 0.76 +/- 0.04 and 0.87 +/- 0.1 mM for WKY rats and SHR, respectively. Similar kinetic analysis of calcium uptake by the duodenal segments showed a Vmax of 10.3 +/- 0.8 and 2.8 +/- 0.2 nmol/mg protein/7 sec in WKY rats and SHR, respectively (P less than 0.01). Km values were 0.7 +/- 0.2 and 0.3 +/- 0.06 mM (P greater than 0.05). Vmax of calcium uptake in the 2-week-old rats (prehypertensive period) was 6.0 +/- 0.3 and 3.53 +/- 0.3 nmol/mg protein/7 sec in WKY rats and SHR, respectively (P less than 0.001), whereas Km values were 0.60 +/- 0.07 and 0.5 +/- 0.01 mM, respectively. These results suggest that calcium binding and uptake by duodenal and jejunal intestinal brush border membranes of SHR is significantly decreased compared with WKY rats. The decrease in transmembrane calcium uptake is secondary to decrease in Vmax and is present before the appearance of hypertension, implying a genetically determined defect in calcium uptake in intestinal brush border membranes of the SHR.
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PMID:Intestinal brush border calcium uptake in spontaneously hypertensive rats and their genetically matched WKY rats. 198 42


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