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

Antihypertensive effects of chronic oral administration of adrenergic beta-blocking agents were assessed in SHR. Propranolol, pindolol, oxprenolol, atenolol and labetalol were used as beta-blockers and the effects of these compounds on the blood pressure and the heart rate were compared with those of hydralazine, a representative vasodilating antihypertensive agent. Propranolol, oxprenolol and atenolol produced a definite decrease in the heart rate; the development of hypertension was retarded. Pindolol produced antihypertensive effects only after a longer period of administration and such were associated with insignificant decrease in heart rate. With a shorter period of administration the drug produced only an insignificant fall of blood pressure with practically no change in the heart rate. With labetalol, a beta-blocker with alpha-blocking action, a fall of blood pressure appeared earlier and was of greater magnitude. Hydralazine produced a definite antihypertensive effect, which appeared immediately after administration and was associated with a tachycardia. In pithed rats, only pindolol produced a definite fall of blood pressure. On the basis of these findings, possible mechanisms of antihypertensive effects of beta-blockers were discussed.
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PMID:Effects of several beta-blocking agents on the development of hypertension in spontaneously hypertensive rats. 4 8

Spontaneously hypertensive rats (SHR) and two strains of normotensive rats were compared with respect to enzymatic activities and calcium accumulation of plasma membrane and endoplasmic reticulum enriched fractions from their mesenteric arteries. Increased specific activities of alkaline phosphatase, 5'-nucleotidase and Mg2+-ATPase, and increased ATP-dependent calcium accumulation were found in 5- to 6-month-old SHR as compared to both strains fo age-matched normotensive rats. Alkaline phosphatase was increased in 33-day-old "early hypertensive" and 3- to 4-month-old SHR, but 5'-nucleotidase, Mg2+-ATPase, and calcium accumulation were not. Hydralazine treatment of young SHR partially prevented the increase of both alkaline phosphatase activity and blood pressure that develops with age. The relationship between alkaline phosphatase activity and the alterations in vascular reactivity associated with hypertension remains to be determined.
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PMID:Relationship between blood pressure of spontaneously hypertensive rats and alterations in membrane properties of mesenteric arteries. 13 88

The effects of hydralazine (3 mg/kg) and the angiotensin I-converting enzyme (ACE) inhibitor captopril (SQ 14,225) (100 mg/kg) on mean arterial blood pressure, plasma renin activity, urinary volume and urinary Na+,K+, and aldosterone concentrations were examined in spontaneously hypertensive rats of the Okamoto and Aoki strain (SHR) after oral daily dosing for 2 weeks, 3 or 6 months. Captopril caused progressive cumulative reductions in blood pressure resulting in normalization of pressure after 6 months of dosing. Hydralazine also significantly reduced blood pressure but not to the level of normotensive rats of the Wistar-Kyoto strain (WKY). Reductions in heart size paralleled the changes in blood pressure, normalization of cardiac hypertrophy occurring after captopril but not hydralazine. Plasma renin activity increased approximately 2-3 fold after hydralazine and 15-fold after captopril. Neither hydralazine nor captopril had any consistent effects on 24-hr urine volume, urinary Na+,K+ or aldosterone excretion. These results indicate that chronic inhibition of ACE with captopril induces normalization of blood pressure in SHR, a normal-renin model of hypertension.
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PMID:Effects of chronic treatment with captopril (SQ 14,225), an orally active inhibitor of angiotensin I-converting enzyme, in spontaneously hypertensive rats. 23

Sixty-six patients with chronic hypertension were cared for during a total of 72 pregnancies. Patients were treated at home primarily by greater than or equal to 4 hours of bed rest daily in the left recumbent position. Only patients whose diastolic blood pressures remained greater than 110 mmHg were treated with hydralazine (Apresoline, Ciba). With this plan of treatment there were only 3 perinatal deaths for an uncorrected perinatal mortality of 4.1% (1.4% corrected). Twenty-nine percent of the patients had babies that were small for gestational age, 13.8% had positive oxytocin challenge tests, and 36.8% developed superimposed preeclampsia. When compared with the outcome of previous pregnancies, the program of bed rest lowered perinatal mortality from 16.8 to 8.8%. Thus, it is suggested that bed rest together with the avoidance of diuretics and the judicious use of hydralazine results in the most favorable fetal outcome.
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PMID:Evaluation of a program of bed rest in the treatment of chronic hypertension in pregnancy. 42 5

The electrophysiologic effects of hydralazine were evaluated in nine hypertensive patients with sinoatrial dysfunction. Intravenous hydralazine, 0.15 mg/kg, caused no significant reduction in arterial blood pressure. Yet this dose of hydralazine increased heart rate from 61.9 +/- 4.1 beats/min (mean +/- standard error of the mean) to 68.6 +/- 4.9 (P less than 0.001). Sinus nodal recovery time upon termination of atrial pacing shortened from 3,207 +/- 1,098 to 2,064 +/- 573 msec (P less than 0.05) and second escape cycles shortened as well (P less than 0.025). Acceleration of heart rate and abbreviation of recovery time did not closely correlate with change in blood pressure (r = 0.41 and 0.18, respectively). Junctional escape beats became more frequent and junctional escape time shortened from 2,525 +/- 692 to 1,705 +/- 382 msec (P less than 0.05). Sinoatrial conduction time tended to shorten, but a significant change was not observed. Atrial tachyarrhythmias did not occur and atrial refractoriness was unchanged. Thus, a minimal blood pressure response to hydralazine was associated with enhanced automaticity. Hydralazine merits clinical trial for treatment of sick sinus syndrome with concomitant hypertension.
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PMID:Electrophysiologic effects of hydralazine on sinoatrial function in patients with sick sinus node syndrome. 64 82

This study was undertaken to determine whether alterations in 45Ca kinetics, found previously in the aorta of spontaneously hypertensive rats (SHR), are the cause or the consequence of high blood pressure. SHR were treated for 3-6 weeks with hydralazine, propranolol or timolol before the uptake and efflux of 45Ca was measured in the aorta and compared with those in untreated animals. Hydralazine prevented the development of hypertension in the rats but did not alter the uptake or efflux of 45Ca. It is concluded that calcium handling in SHR is abnormal also in the absence of high arterial pressure.
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PMID:Effect of antihypertensives on calcium kinetics in the aorta of spontaneously hypertensive rats. 70 55

With improving standards of antenatal care, severe pre-eclampsia dn eclampsia are becoming less common and experience in the management of these conditions is lessening. Co-ordinated plans for the care of patients should be established by obstetricians and anaesthetists working as a team. A suitable regime for drug therapy in severe pre-eclampsia or eclampsia is the following: Initial management Diazepam 10 mg slowly i.v. Pethidine 100-150 mg i.m. or i.v. in incremental dosage, or extradural blocks, if analgesia is also required. Hydrallazine 20 mg i.v. initially, followed by 5 mg at intervals of 20 min until the diastolic pressure is less than 110 mm Hg. Then, preferably by syringe pump in a concentration of 2 mg/ml, at a rate of 2-20 mg/h. If vomiting occurs this can be controlled by administration of atropine. Subsequent management Sedation and anticonvulsant therapy. Continue diazepam and, in severe cases, institute chlormethiazole infusion. Continue analgesia with pethidine or extradural block. Control of hypertension by adjusting the dose of hydrallazine. If tachycardia exceeds 120 beat/min give propanolol 2-4 mg i.v. Plasma protein depletion with groww oedema is treated by administration of salt-free albumin or plasma protein fraction. Diuretic therapy is indicated if there is gross oedema or signs suggestive of acute renal failure. Oliguria associated with increased blood urea may be a result of renal failure or dehydration. The latter should be evident from the patient's condition and central venous pressure, but i.v. fluids and frusemide 20-40 mg can be used as a therapeutic test. Mannitol reduces cerebral oedema and may be given if diuresis has been first produced with frusemide. Potassium chloride is given if the plasma potassium decreases to less than 3 mmol/litre. Heparin therapy is considered if there is clinical evidence of disseminated intravascular coagulation.
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PMID:The management of severe pre-eclampsia and eclampsia. 83 44

A study was made of the possible mechanisms underlying bupicomide- and hydralazine-induced increase of plasma renin activity. Six patients with mild to moderate hypertension were treated with both bupicomide and hydralazine on separate occasions in random order. Bupicomide lowered mean arterial pressure from 124.2 +/- 3.7 mm Hg (mean +/- SE) to 107.2 +/- 3.9 mm Hg (P less than 0.001). The associated increase in plasma renin activity was 1.27 ng/ml per hour and the increase in heart rate was 16.5 beats/min. Hydralazine reduced mean arterial pressure from 124.2 +/- 3.7 mm Hg to 107.0 +/- 2.0 mm Hg (P less than 0.01). The associated increase in plasma renin activity was 2.20 ng/ml per hour and the increase in heart rate was 22.4 beats/min. Plasma renin activity during bupicomide and hydralazine administration correlated positively with control plasma renin activity (r = 0.98, P less than 0.001). The log of plasma renin activity correlated positively with heart rate (r = 0.51, P less than 0.02) and negatively with mean arterial pressure (r = -0.62, P less than 0.005). We conclude that control plasma renin activity is a major determinant of change in plasma renin activity during administration of bupicomide or hydralazine. Both an increase in sympathetic activity and a decrease in perfusion pressure may contribute to the bupicomide- and hydralazine-induced increase in plasma renin activity, possibly by a baroreceptor-mediated increase in adrenergic tone.
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PMID:Physiologic mechanisms of bupicomide- and hydralazine-induced increase in plasma renin activity in hypertensive patients. 87 65

During phenylephrine-induced hypertension in 6 near-term pregnant ewes, nitroprusside rapidly lowered the blood pressure to control values with no accompanying change in uterine blood flow. Hydralazine slowly lowered the blood pressure to control values. This change was accompanied by a statistically significant (15%) increase in uterine blood flow. Hydralazine also had a more pronounced effect than nitroprusside on cardiac output, heart rate, and total peripheral resistance. There were no significant acid-base changes in mother or fetus throughout the study.
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PMID:Comparison of nitroprusside and hydralazine in hypertensive pregnant ewes. 90 67

This study was designed to investigate the effects of antihypertensive drugs on vascular hypertrophy and vascular angiotensin II in vivo in spontaneously hypertensive rats (SHR). Hydralazine (10 mg/kg/day), delapril (angiotensin converting enzyme inhibitor; 20 mg/kg/day), manidipine (calcium channel blocker; 10 mg/kg/day), and vehicle were given by gavage to four groups of SHR between 4 and 5 months of age. The aortic angiotensin II level was measured by highly sensitive radioimmunoassay coupled with high pressure liquid chromatography; aortic morphologic studies were performed. Each drug treatment effectively lowered blood pressure to the same level. However, the aortic wall thickness, medial-intimal areas, and wall to lumen ratio of abdominal aorta decreased significantly (p < 0.05, p < 0.01, p < 0.01, respectively) with delapril and manidipine but not hydralazine. Delapril significantly decreased aortic angiotensin II levels (p < 0.05), whereas manidipine treatment significantly increased them (p < 0.05). The aortic angiotensin II level was not changed by hydralazine. These results show that delapril and manidipine caused regression of hypertension-induced vascular hypertrophy in SHR. The probable mechanism of regression of aortic hypertrophy by delapril was inhibition of vascular angiotensin II formation, but the mechanism for manidipine was unclear.
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PMID:Regression of hypertension-induced vascular hypertrophy by an ACE inhibitor and calcium antagonist in the spontaneously hypertensive rat. 134 88


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