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

Hypertension in pregnancy has implications for both maternal and fetal welfare. Extrapolation from concepts of mechanisms operating in hypertension in general to pregnancy-related hypertension is not justified. In the latter, the major features are a hyper-adrenergic state, plasma volume reduction and an increased systemic resistance. A reduction in uteroplacental perfusion may result from or may activate the mechanisms that elevate blood pressure. Humoral factors (e.g. hormonal attenuation of vascular reactivity) and prostacyclin deficiency may be central to the disordered physiology. Treatment of hypertension in pregnancy should aim at avoiding the vascular damage due to blood pressure elevation but not cause a reduction in uteroplacental perfusion. Unlike earlier antihypertensive regimens using centrally acting sympatholytics, adrenergic neuron blockers or diuretics, regimens using beta-blockers or combinations of beta-blockers with alpha-blockers or vasodilating agents such as hydralazine permit effective blood pressure control, even in severe hypertension, and pregnancy can often proceed until term or until fetal maturity is secured. Adverse effects on the fetus (growth retardation, cardiorespiratory depression, hypoglycaemia, hyperbilirubinaemia) formerly attributed to beta-blockers are more likely related to poorly controlled hypertension. Specific benefits of maternal beta-adrenoceptor blockade are suggested by evidence for prevention of proteinuric deterioration and a decrease in the incidence and severity of respiratory distress in premature infants. Hypertension in pregnancy still presents a formidable therapeutic challenge and requires comprehensive management with close monitoring of fetal welfare. The presence or development of proteinuria in a hypertensive pregnant woman implies a major increase in risk to the fetus and warrants immediate admission to hospital for specialist management.
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PMID:Hypertension in pregnancy. Pathophysiology and management. 614 40

In theory, the pharmaceutical properties of beta-blockers would make their use in hypertension in pregnancy undesirable. Practically, however, these drugs are used more and more in pregnancy. This contradiction has been based on a whole number of clinical trials of which the results have been conflicting. This can be explained by the fact that many of these trials have not been carried out according to a scientific protocol for a trial of a drug. Only random studies are therefore analysed by this author. He concludes that beta-blockers can be used in pregnancy in some cases of hypertension.
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PMID:[Beta-blockers and arterial hypertension in pregnancy]. 615 59

Increased plasma levels of beta-thromboglobulin (beta TG) and fibrinopeptide A (FPA), markers of platelet release and thrombin generation respectively, were measured in normal women, women taking oral contraceptives, normal pregnancy and pregnant women with hypertension or pre-eclampsia. No significant increases in beta TG or FPA were found in women taking oral contraceptives. Significantly increased concentrations of beta TG, but not FPA, were found in normal pregnant women in the second and third trimester of pregnancy when compared with non-pregnant age-matched controls. In eleven women with pregnancy hypertension and thirteen women with pre-eclampsia significantly elevated levels of both beta TG and FPA were found when compared with age, parity and gestation-matched pregnant controls. Although the mean value for both beta TG and FPA in the group with pre-eclampsia was higher than the group with pregnancy hypertension, the difference was not statistically significant. These findings provide additional evidence that pre-eclampsia and pregnancy hypertension are associated with activation of the coagulation system and the platelet release reaction.
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PMID:Plasma fibrinopeptide A and beta-thromboglobulin in pre-eclampsia and pregnancy hypertension. 617 42

Labetalol is a combined alpha- and beta-adrenoceptor blocking agent for oral and intravenous use in the treatment of hypertension. It is a nonselective antagonist at beta-adrenoceptors and a competitive antagonist of postsynaptic alpha 1-adrenoceptors. Labetalol is more potent at beta that at alpha 1 adrenoceptors in man; the ratio of beta-alpha antagonism is 3:1 after oral and 6.9:1 after intravenous administration. Labetalol is readily absorbed in man after oral administration, but the drug, which is lipid soluble, undergoes considerable hepatic first-pass metabolism and has an absolute bioavailability of approximately 25%. There are no active metabolites, and the elimination half-life of the drug is approximately 6 hours. Unlike conventional beta-adrenoceptor blocking drugs without intrinsic sympathomimetic activity, labetalol, when given acutely, produces a decrease in peripheral vascular resistance and blood pressure with little alteration in heart rate or cardiac output. However, like conventional beta-blockers, labetalol may influence the renin-angiotensin-aldosterone system and respiratory function. Clinical studies have shown that the antihypertensive efficacy of labetalol is superior to placebo and to diuretic therapy and is at least comparable to that of conventional beta-blockers, methyldopa, clonidine and various adrenergic neuronal blockers. Labetalol administered alone or with a diuretic is often effective when other antihypertensive regimens have failed. Studies have shown that labetalol is effective in the treatment of essential hypertension, renal hypertension, pheochromocytoma, pregnancy hypertension and hypertensive emergencies. In addition, preliminary studies indicate that labetalol may be of value in the management of ischemic heart disease. The most troublesome side effect of labetalol therapy is posture-related dizziness. Other reported side effects of the drug include gastrointestinal disturbances, tiredness, headache, scalp tingling, skin rashes, urinary retention and impotence. Side effects related to the beta-adrenoceptor blocking effect of labetalol, including asthma, heart failure and Raynaud's phenomenon, have been reported in rare instances.
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PMID:Labetalol: a review of its pharmacology, pharmacokinetics, clinical uses and adverse effects. 631 May 29

We conducted a prospective and serial study of blood pressure (BP) and of the changes in the renin-angiotension-aldosterone system (RAAS) and of one factor in the kallikrein-kinin system during normal pregnancy and in patients with pre-existing or developing hypertension in pregnancy. Strict diagnostic criteria were used to define pre-eclampsia (PE), essential hypertensives (EH) and other hypertension (OH) in pregnancy. In normotensive pregnant women (n = 26) there was a rise in all components of the RAAS measured: plasma renin activity (PRA), plasma aldosterone concentration (PAC) and urinary aldosterone excretion (tU-Aldo), from week 12 to week 20 of pregnancy, compared with non-pregnant control subjects (n = 24) of similar age. Peak values were observed at week 30, whereafter fairly constant levels were maintained. Plasma and urinary aldosterone levels were increased 6-10 fold. Urinary kallikrein excretion (tU- Kall ) was increased at weeks 12-20, but at weeks 30-36 roughly the same mean values were observed as for non-pregnant control subjects. On the other hand, different results were obtained in the hypertensive patients, especially those with PE (n = 18). PRA was depressed in the PE group to values about those observed in non-pregnant control subjects. PRA was also significantly lower in the PE group than in EH (n = 8) or OH (n = 16) groups. PAC and tU-Aldo were also much lower in PE patients than in normal pregnant women at comparable gestational ages, but not significantly different from EH patients, whereas those with OH had both PAC and tU-Aldo values comparable to normal pregnant women.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in the renin-angiotensin-aldosterone and kallikrein-kinin systems during normal and hypertensive pregnancy. 637 41

We studied retrospectively the case records of 442 women who were followed because of hypertension during a pregnancy. Pregnancy hypertension was more frequent in white european than in black or arabic women. It occurred more frequently in women with an important professional activity than it did in housewives. 58% of patients had a familial history of high blood pressure, 35% were obese, 12% had glucose intolerance and 18% had hypercholesterolemia. Those frequencies were out of proportion with those in the control population. Finally, 32% of patients remained hypertensive after pregnancy. It is concluded that pregnancy hypertension occurs mainly in women whose genetic and metabolic background is that of essential hypertension.
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PMID:[Epidemiologic aspects of hypertension in pregnancy. Study of 442 cases]. 644 39

This study evaluates the perinatal outcome of infants born to ninety-five mothers with hypertension in pregnancy whose blood pressure was treated in a double blind trial comparing clonidine hydrochloride (C) and alpha-methyldopa (A). There were no fetal deaths and two neonatal deaths, giving a perinatal mortality of 2%. There was no significant difference between Groups C and A with regard to the gestation or weight at birth, incidence of intrauterine growth retardation, or condition at birth as judged by Apgar scores and acid-base status. No infant in either group developed significant hypotension or rebound hypertension. The blood pressure was not significantly different between Groups C and A, and controls. In each of these three groups there was a similar significant rise in systolic blood pressure with age.
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PMID:Effect of antihypertensive drugs on neonatal blood pressure. 651 65

Cardiovascular adaptations to the circulatory and volume changes of pregnancy have been studied in late normal and hypertensive pregnancy and postpartum. There has been evidence of a marked plasma volume expansion in normal pregnancy, blunted in preeclampsia; an increased capillary permeability during normal pregnancy; augmented left ventricular mass, which is increased in mild preeclampsia; and similar increases in peripheral venous distensibility during normal and preeclamptic pregnancy. In mild preeclampsia the enlarged ventricle has been shown to be capable of maintaining a normal cardiac output despite elevated afterload. The forearm vascular bed appears to play little part in these adjustments, because forearm venous distensibility has been shown to be higher during normal pregnancy than during postpartum; in hypertensive individuals there was no difference during pregnancy and postpartum. It is evident from this brief review that it is too early to draw clear-cut conclusions regarding the vascular, volume, and cardiac response to normal and hypertensive pregnancy. Research in this field, including two-dimensional echocardiography and plethysmography in larger homogeneous groups, will probably lead to a better understanding of the pathophysiological mechanism of pregnancy hypertension.
Hypertension
PMID:Vascular, volume, and cardiac response to normal and hypertensive pregnancy. 651 52

40 Gravidae with hypertension were treated with clonidine . Placental blood flow measurements were performed to study the effect of clonidine on uteroplacental blood flow. The results show a significant decrease of the gestosis-index and a significant improvement of placental perfusion type during medication. Therefore, clonidine is suitable for treatment of hypertension in pregnancy and has no negative effect on uteroplacental blood flow.
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PMID:[Measurement of uteroplacental circulation in antihypertensive therapy with clonidine]. 653 28

Blood pressure; extracellular fluid volume; renal plasma flow; glomerular filtration rate; plasma concentrations of renin, angiotensin, aldosterone, desoxycorticosterone, and prostaglandins; responses to infused angiotensin; and many other factors are altered during normal and hypertensive gestation. The diagnosis of the exact disease process responsible for hypertension in pregnancy in an individual patient is extremely difficult if based solely on clinical criteria. The American College of Obstetricians and Gynecologists has suggested the following clinical classifications: (1) preeclampsia-eclampsia, (2) chronic hypertension of whatever cause, (3) chronic hypertension with superimposed preeclampsia, and (4) late or transient hypertension. The three broad categories of renal disease responsible for these clinical syndromes are: (1) preeclampsia-eclampsia, (2) hypertensive changes, and (3) various primary renal diseases. Controversy abounds regarding the aggressiveness of therapy in this syndrome. We prefer a middle-of-the-road approach, bringing blood pressure down to the range of 95 to 100 mm Hg. Hydralazine and Aldomet are the usual drugs of choice. Any intervening nervous system hyperexcitability suggests impending eclampsia and should be immediately treated with magnesium sulfate. The long-term prognosis for the mother with pure preeclampsia appears to be excellent. Most infants born of hypertensive gestations are small for date, with a prognosis that is also affected by the underlying disease of the mother.
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PMID:Hypertension in pregnancy. 655 34


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