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)

Endothelins are endothelial cell-derived peptides with potent vasoconstrictor properties. We investigated the actions of porcine/human endothelin-1 (ET-1) on the microvasculature of the guinea pig lung perfused at constant flow with Ringers-albumin. We measured the perfusion pressure, distribution of pulmonary vascular resistance (using the double occlusion method), lung weight change, and the pulmonary capillary filtration coefficient. At concentrations of greater than or equal to 10(-10) M, ET-1 produced dose-dependent increases in mean pulmonary artery pressure (EC50, approximately 10(-9.5) M), which were rapid in onset and biphasic (first phase peaking at 1-2 minutes; second phase peaking at 10-15 minutes) up to 60 minutes of the perfusion period. The vasoconstrictor response was sustained for the 60-minute perfusion period. The pulmonary vasoconstriction was inhibited by pretreatment with indomethacin (10(-5) M), the thromboxane A2 receptor antagonist SQ-29,548 (4 x 10(-6) M), or papaverine (10(-5) M). Nifedipine (10(-5) or 10(-7) M) had no effect on the first phase but prevented the second phase of the vasoconstriction. The vasoconstriction was primarily the result of a 10-fold increase in pulmonary venous resistance. Pulmonary edema developed after ET-1 challenge because of the venoconstriction and the resultant pulmonary capillary hypertension. However, the pulmonary capillary filtration coefficient was unchanged, indicating that pulmonary vascular permeability did not increase. ET-1 also had no effect on transendothelial 125I-albumin flux. The results indicate that ET-1 is a potent thromboxane-dependent venoconstrictor in the guinea pig lung.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of endothelin-1-induced pulmonary vasoconstriction. 205 31

Pulse wave velocity (PWV) is known to reflect the stiffness of the aorta, one of the major features of atherosclerosis. To clarify the severity and progression mechanism of atherosclerosis in hemodialysis patients and the preventive effect of nifedipine, PWV was annually measured for 2 years, and the change of PWV and contributory factors were analyzed. PWV in hemodialysis patients was faster than in age-matched normal controls. PWV was correlated with the duration of hemodialysis. delta PWV, which is obtained from the difference in PWV over 1 year, was positively correlated with age, high blood pressure, and serum cholesterol levels and was negatively correlated with HDL levels. The Ca x Pi value was also positively correlated with delta PWV. Nifedipine was administered to 47 patients for 2 years, and the change of PWV was compared with age-matched control hemodialysis patients. The PWV of the control group was gradually increased by 10%. The PWV of the group given nifedipine decreased by 2%. These results suggested that administration of nifedipine may prevent the progression of PWV in hemodialysis patients and may decrease the progression of atherosclerosis.
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PMID:Effect of nifedipine administration on pulse wave velocity (PWV) of chronic hemodialysis patients--2-year trial. 207 12

Nifedipine, in the gastrointestinal therapeutic system (GITS) formulation, a controlled-release formulation for once-a-day administration, was evaluated in the Modern Approach to the Treatment of Hypertension (MATH) trial. In this study conducted at 127 centers, 1155 patients with mild-to-moderate hypertension representative of the spectrum seen in practice were included in the analyses of effectiveness. After a 2 week placebo period, nifedipine GITS therapy was started at 30 mg/day and was titrated to a maximum dose of 180 mg/day over 6 weeks. Response criteria were a sitting diastolic blood pressure less than 90 mm Hg and a decrease of greater than or equal to 10 mm Hg. After titration, patients were observed for 12 weeks during treatment. At the final visit, nifedipine GITS significantly (P less than .0001) reduced sitting systolic blood pressure 17 +/- 14 mm Hg (mean +/- SD), and sitting diastolic blood pressure 14 +/- 8 mm Hg. Similar highly significant reductions in standing blood pressure were observed. For all subjects, 76% achieved goal blood pressure response during titration. More than 50% were controlled on doses of 30 to 60 mg/day. At the final visit blood pressure reductions in men and women were similar, except for a significantly greater decrease in sitting systolic pressure for women. A similar proportion of blacks responded compared with whites, and reductions in sitting systolic and diastolic blood pressure were also similar in the 2 groups. Nifedipine GITS had no effect on renal function, serum potassium, or total, HDL, or LDL cholesterol. Uric acid was reduced by 0.5 mg/dL (P less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nifedipine gastrointestinal therapeutic system in the treatment of hypertension. Results of a multicenter trial. The Modern Approach to the Treatment of Hypertension (MATH) Study Group. 207 18

We studied the effect of nifedipine, a dihydropyridine calcium antagonist, on the hemodynamic changes induced by endothelin, in awake normotensive rats. Endothelin (0.07-1.40 nmol/kg, e.v.) caused an initial hypotensive effect, followed by long lasting hypertension. Renal blood flow was reduced immediately and still remained below basal levels, at 30 minutes after endothelin injection. Nifedipine (1 mg/kg, i.p.) significantly prevented the effect of endothelin on mean blood pressure and induced a right-ward shift in the dose response curve of renal hemodynamic changes induced by endothelin. We conclude that treatment with calcium antagonist could be very useful in all those conditions in which systemic and regional vasocostriction is provoked by endothelin.
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PMID:[Protective effect of a calcium antagonist against renal vasoconstriction induced by endothelin in the normotensive rat]. 208 61

Hypoxic pulmonary vasoconstriction is considered to be the primary cause of pulmonary hypertension and cor pulmonale in adult patients with cystic fibrosis (CF). The acute effect on pulmonary haemodynamics of a single sublingual dose of nifedipine 20 mg has been studied in 9 adult patients with CF. Nifedipine significantly attenuated the rise in mean pulmonary artery pressure and pulmonary vascular resistance induced by inhalation of a 13% oxygen gas mix. It also slightly reduced baseline pulmonary artery pressure and pulmonary vascular resistance and lowered pulmonary artery hypertension in the patients. Oxygen delivery was unchanged. Nifedipine is potentially useful for the treatment of hypoxic pulmonary hypertension in patients with CF.
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PMID:Acute effects on pulmonary haemodynamics of nifedipine in adult patients with cystic fibrosis. 209 44

Nifedipine is a new agent belonging to the calcium antagonist group of drugs, applied clinically to circulatory disorders, such as essential hypertension, renal hypertension and angina cordis and has been rapid in gaining popularity in Japan. On the other hand, as do all effective drugs, this drug has side effects, one of which is gingival hyperplasia. The clinical findings are extremely similar to the gingival hyperplasia induced by phenytoin used for the treatment of epilepsy. A 46-year-old man was referred to our hospital whose chief complaint was gingival swelling. He had been receiving nifedipine for his hypertension for about one year. He was diagnosed as having the side-effects of nifedipine due to being treated with 20 mg/day for a year. Nifedipine was discontinued and scaling and oral hygiene resulted in healing.
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PMID:[A case of gingival hyperplasia induced by nifedipine]. 213 36

The effect of long-term therapy of hypertension with antihypertensive drugs was investigated in 117 previously untreated patients (15 women, 102 men; mean age 46.4 +/- 9 years) with echocardiographically proven left-ventricular hypertrophy. 22 patients (group 1) received 100 mg/d Gallopamil, 25 (group 2) received 200 mg/d Metoprolol, 35 daily received both 50 mg Atenolol and 20 mg Nifedipine (group 3), 14 received daily 200 mg Acebutolol plus 20 mg Nifedipine (group 4), and 21 (group 5) 50 mg Atenolol plus 10 mg Enalapril daily. The treatment period lasted a mean of 38 (36.2-42.3) months. Left-ventricular muscle mass index (LVMI) as well as septal and posterior-wall thickness decreased significantly after 12.8 and 38.5 months (P less than 0.001). After a mean of 38.5 months LVMI had decreased by 36.7% in group 1, 35.1% in group 2, 42.3% in group 3, 45% in group 4 and 39.6% in group 5. LVMI was within normal range (less than or equal to 95 g/m2) in 81 of the 117 patients (69.2%) at the end of the treatment period. There was, however, no significant increase of the end-diastolic dimension of the left ventricle, but a significant increase of "fractional shortening" as a measure of myocardial contractility.
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PMID:[Regression of left ventricular hypertrophy in hypertensive patients under long-term therapy with antihypertensive agents]. 213 9

In order to determine the prevalence of arterial hypertension and clinical presentation of the hypertensive crisis, as well as the need and efficacy of treatment, 3626 patients who were seen at an Emergency care Unit during a period of 37 randomly chosen days in a total time period of three months, have been studied. Two hundred and fifty one patients presented arterial hypertension, defined as a systolic arterial pressure above 160 mmHg and/or diastolic above 95 mmHG, which represents 6,92% of medical emergencies and 1.79% of total emergencies. Only 104 patients (2.86%) seeked help for some pathology related to hypertension, of whom 49 (19.5% of hypertense patients) presented as a hypertensive emergency, being the acute lung edema and unstable angina the most frequently encountered emergencies. Nifedipine was the most frequently used drug in both groups and managed to control pressure levels in almost 90% of patients with a hypertensive emergency in a mean time of less than one hour.
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PMID:[Prevalence, forms of clinical presentation and treatment of arterial hypertension at an emergency unit]. 224 58

Treatment of hypertension may prevent many of the complications attributable to blood pressure elevation, particularly those that are "pressure-related," such as stroke. However, the atherosclerotic complications of hypertension, e.g., coronary artery disease manifested as coronary morbidity and mortality, have not been reduced significantly with antihypertensive therapy. This disappointing outcome may reflect the adverse metabolic effects of the traditional therapies, diuretics and beta blockers, and their lack of specific vasoprotective properties. Increasing attention is thus being paid to the newer antihypertensive agents, which typically have fewer adverse effects and perhaps more physiologic mechanisms of antihypertensive action. Since calcium plays a key role in the genesis of atherosclerosis, calcium antagonists may positively affect the course of vascular disease. Investigators have observed that calcium antagonists display clear antiatherosclerotic properties in experimental as well as clinical studies. In one recently published clinical study, coronary artery disease was shown to develop more slowly, with a slower progression of individual stenoses, higher regression rate and less frequent occurrence of new lesions in patients treated chronically with verapamil compared to those receiving conventional therapies. Other similar investigations are currently under way to evaluate the antiatherogenic properties of calcium antagonists, including the Frankfurt Isoptin Progression Study (FIPS), the Multicenter Isradipine Diuretic Atherosclerosis Study (MIDAS), the International Nifedipine Trial on Atherosclerosis Coronary Therapy (INTACT), and the large-scale Montreal Heart Institute Study. Results of these studies, which use precise end points such as myocardial infarction, cerebral infarction and peripheral vascular disease, may revolutionize the treatment of hypertension by identifying therapeutic approaches that control both the pressure-related and atherosclerotic complications of the disease.
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PMID:Anti-atherosclerotic and vasculoprotective actions of calcium antagonists. 225 66

The authors describe the case of a 57-year-old male patient with severe left ventricular dysfunction (ejection fraction of left ventricle--37%, left ventricular end diastolic pressure 32 mm Hg) as a result of an extensive anterior Q infarction of the heart muscle. The patient did not have signs of congestive heart failure. He was treated on account of angina pectoris on exertion, grade III according to NYHA, hypertension and diabetes. Nifedipine and diltiazem administration led to repeated attacks of cardiac asthma. Calcium channel blockers should be administered to patients with angina pectoris and severe left ventricular dysfunction only when nitrates alone do not eliminate ischaemia and pain. They should be administered carefully and with the knowledge that they may in rare instances cause clinical deterioration of left ventricular function.
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PMID:[Cardiac asthma after nifedipine and diltiazem]. 227 77


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