The role of calcium channel blockers in the treatment of women with preeclampsia

1996 ◽  
Vol 8 (1) ◽  
pp. 19-27 ◽  
Author(s):  
R Lewis ◽  
M Belfort ◽  
B Sibai
Keyword(s):  
Smooth Muscle ◽  
Gestational Hypertension ◽  
Fetal Distress ◽  
The United States ◽  
Chronic Hypertension ◽  
Channel Blockers ◽  
Appropriate Therapy ◽  
Mild Preeclampsia ◽  
Smooth Muscle Relaxant

Preeclampsia was originally known as a process whereby an unknown “toxin” was responsible for a variety of responses. While this toxin has yet to be determined, many theories have prevailed as to the appropriate therapy for this condition.Recently, antihypertensive therapy has become increasingly regarded as an important component of the medical management of women with preeclampsia. Initially, the ideal therapy for peripartum acute hypertensive emergencies was felt to be a smooth muscle relaxant and the most commonly prescribed agent was hydralazine. This drug was felt to be beneficial because of its action on vascular smooth muscle, decreasing vasospasm. Outside of the United States diazoxide was also used for this purpose, although this drug has been replaced because of the high incidence of fetal distress. Another agent that was frequently used was α-methyldopa which was initially considered to be the treatment of choice in the treatment of patieats with moderate and severe preeclampsia. Recently, α-methyldopa has been reserved for the outpatient management of gestational hypertension, especially in women with mild preeclampsia or chronic hypertension.

Role of extracellular calcium and calmodulin in prolactin secretion induced by hyposmolarity, thyrotropin-releasing hormone, and high K+ in GH4C1 cells

1990 ◽  
Vol 123 (2) ◽  
pp. 218-224 ◽  
Author(s):  
Xiangbing Wang ◽  
Noriyuki Sato ◽  
Monte A. Greer ◽  
Susan E. Greer ◽  
Staci McAdams
Keyword(s):  
Smooth Muscle ◽  
Muscle Relaxant ◽  
Prolactin Secretion ◽  
Thyrotropin Releasing Hormone ◽  
Dependent Manner ◽  
Cell Toxicity ◽  
High K ◽  
Dose Dependent ◽  
Smooth Muscle Relaxant

Abstract. The mechanism by which 30% medium hyposmolarity induces PRL secretion by GH4C1 cells was compared with that induced by 100 nmol/l TRH or 30 mmol/l K+. Removing medium Ca2+, blocking Ca2+ channels with 50 μmol/l verapamil, or inhibiting calmodulin activation with 20 μmol/l trifluoperazine, 10 μmol/l chlorpromazine or 10 μmol/l pimozide almost completely blocked hyposmolarity-induced secretion. The smooth muscle relaxant, W-7, which is believed relatively specific in inhibiting the Ca2+-calmodulin interaction, depressed hyposmolarity-induced PRL secretion in a dose-dependent manner (r = −0.991, p<0.01 ). The above drugs also blocked or decreased high K+-induced secretion, but had much less effect on TRH-induced secretion. Secretion induced by TRH, hyposmolarity, or high K+ was optimal at pH 7.3-7.65 and was significantly depressed at pH 6.0 or 8.0, indicating that release of hormone induced by all 3 stimuli is due to an active cell process requiring a physiologic extracellular pH and is not produced by nonspecific cell toxicity. The data suggest hyposmolarity and high K+ may share some similarities in their mechanism of stimulating secretion, which is different from that of TRH.

Interactions between nitroglycerin and endothelium in vascular smooth muscle relaxation

1991 ◽  
Vol 260 (3) ◽  
pp. H698-H701 ◽  
Author(s):  
J. L. Dinerman ◽  
D. L. Lawson ◽  
J. L. Mehta
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Muscle Relaxation ◽  
Smooth Muscle Relaxation ◽  
No Production ◽  
Cyclic Monophosphate ◽  
The Mean ◽  
Smooth Muscle Relaxant ◽  
Vascular Smooth Muscle Relaxation

To evaluate the role of endothelium in nitroglycerin (NTG)-mediated vascular relaxation, epinephrine-contracted rat thoracic aortic segments with and without intact endothelium were exposed to NTG (10(-10) to 10(-5) M). Aortic segments with intact (endo+, n = 15) and denuded endothelium (endo-, n = 9) exhibited typical NTG-induced relaxation. However, the mean effective concentration of NTG was lower for endo- than for endo+ segments (P less than 0.001). To determine if this phenomenon related to nitric oxide (NO) generation by endothelium, six endo+ segments were treated with NG-monomethyl-L-arginine (L-NMMA), an inhibitor of NO production. These endo+ segments exhibited greater (P less than 0.001) relaxation in response to NTG than the untreated endo+ segments. Oxyhemoglobin, an inhibitor of guanylate cyclase activation, greatly diminished NTG-mediated relaxation of all aortic segments. To determine if the enhanced NTG-mediated relaxation of endo- segments was unique to the guanosine 3',5'-cyclic monophosphate-dependent vasodilator NTG, other endo+ and endo- segments were exposed to adenosine 3',5'-cyclic monophosphate-dependent vasodilator papaverine (10(-8) to 10(-4) M), and no difference in EC50 was noted between endo+ and endo- segments. Thus endothelium attenuates NTG-mediated vasorelaxation, and this attenuation is abolished by inhibition of endothelial NO production with L-NMMA. These observations indicate that endothelium is a dynamic modulator of vascular smooth muscle relaxant effects of NTG. This modulation appears to result from a competitive interaction between endothelial NO and NTG.

Role of catalase in the smooth muscle relaxant actions of sodium azide and cyanamide

2002 ◽  
Vol 435 (1) ◽  
pp. 93-101 ◽  
Author(s):  
Mohammad Shahidullah ◽  
Andrew Duncan ◽  
Peter D Stracħan ◽  
Komel M Rafique ◽  
Sarah L Ball ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Sodium Azide ◽  
Muscle Relaxant ◽  
Smooth Muscle Relaxant

Historical and Recent Changes in Maternal Mortality Due to Hypertensive Disorders in the United States, 1979 to 2018

Hypertension ◽  
2021 ◽  
Vol 78 (5) ◽  
pp. 1414-1422
Author(s):  
Cande V. Ananth ◽  
Justin S. Brandt ◽  
Jennifer Hill ◽  
Hillary L. Graham ◽  
Sonal Grover ◽  
...  
Keyword(s):  
United States ◽  
Mortality Rate ◽  
Maternal Mortality ◽  
Birth Cohort ◽  
White Women ◽  
Gestational Hypertension ◽  
The United States ◽  
Chronic Hypertension ◽  
Maternal Deaths ◽  
Live Births

We evaluated the contributions of maternal age, year of death (period), and year of birth (cohort) on trends in hypertension-related maternal deaths in the United States. We undertook a sequential time series analysis of 155 710 441 live births and 3287 hypertension-related maternal deaths in the United States, 1979 to 2018. Trends in pregnancy-related mortality rate (maternal mortality rate [MMR]) due to chronic hypertension, gestational hypertension, and preeclampsia/eclampsia, were examined. MMR was defined as death during pregnancy or within 42 days postpartum due to hypertension. Trends in overall and race-specific hypertension-related MMR based on age, period, and birth cohort were evaluated based on weighted Poisson models. Trends were also adjusted for secular changes in obesity rates and corrected for potential death misclassification. During the 40-year period, the overall hypertension-related MMR was 2.1 per 100 000 live births, with MMR being almost 4-fold higher among Black compared with White women (5.4 [n=1396] versus 1.4 [n=1747] per 100 000 live births). Advancing age was associated with a sharp increase in MMR at ≥15 years among Black women and at ≥25 years among White women. Birth cohort was also associated with increasing MMR. Preeclampsia/eclampsia-related MMR declined annually by 2.6% (95% CI, 2.2–2.9), but chronic hypertension–related MMR increased annually by 9.2% (95% CI, 7.9–10.6). The decline in MMR was attenuated when adjusted for increasing obesity rates. The temporal burden of hypertension-related MMR in the United States has increased substantially for chronic hypertension–associated MMR and decreased for preeclampsia/eclampsia-associated MMR. Nevertheless, deaths from hypertension continue to contribute substantially to maternal deaths.

scholarly journals Future Directions: Analyzing Health Disparities Related to Maternal Hypertensive Disorders

2020 ◽  
Vol 2020 ◽  
pp. 1-5
Author(s):  
Margaret Harris ◽  
Colette Henke ◽  
Mary Hearst ◽  
Katherine Campbell
Keyword(s):  
United States ◽  
Gestational Hypertension ◽  
Treatment Strategies ◽  
Ethnic Disparities ◽  
Ethnically Diverse ◽  
The United States ◽  
Chronic Hypertension ◽  
Future Directions ◽  
Hypertensive Disorders ◽  
Maternal Morbidity And Mortality

Hypertensive disorders of pregnancy complicate up to 10% of pregnancies worldwide, constituting one of the most significant causes of maternal morbidity and mortality. Hypertensive disorders, specifically gestational hypertension, chronic hypertension, and preeclampsia, throughout pregnancy are contributors to the top causes of maternal mortality in the United States. Diagnosis of hypertensive disorders throughout pregnancy is challenging, with many disorders often remaining unrecognized or poorly managed during and after pregnancy. Moreover, the research has identified a strong link between the prevalence of maternal hypertensive disorders and racial and ethnic disparities. Factors that influence the prevalence of maternal hypertensive disorders among racially and ethnically diverse women include maternal age, level of education, United States-born status, nonmetropolitan residence, prepregnancy obesity, excess weight gain during pregnancy, and gestational diabetes. Examination of the factors that increase the risk for maternal hypertensive disorders along with the current interventions utilized to manage hypertensive disorders will assist in the identification of gaps in prevention and treatment strategies and implications for future practice. Specific focus will be placed on disparities among racially and ethnically diverse women that increase the risk for maternal hypertensive disorders. This review will serve to promote the development of interventions and strategies that better address and prevent hypertensive disorders throughout a pregnant woman’s continuum of care.

The Role of the Legal System in the Cesarean Childbirth Controversy

1980 ◽  
Vol 1 (10) ◽  
pp. 1-8
Author(s):  
Judy Miller
Keyword(s):  
Birth Rate ◽  
Nursing Practice ◽  
Fetal Monitoring ◽  
Fetal Distress ◽  
The United States ◽  
Cesarean Birth ◽  
Threefold Increase ◽  
Cesarean Births ◽  
Patient Advocates

The threefold increase in the cesarean birth rate in the United States during the last ten years has caused much concern among the general public and some medical professionals. Nurses particularly have shared this concern as the scope of nursing practice has expanded and nurses increasingly see themselves as patient advocates. Obviously, not all cesarean births are unwarranted. The procedure may be indicated if there is maternal or fetal risk during labor, if attempted induction of labor fails, and/or if an emergency mandates immediate delivery which is not possible or suitable vaginally.A recent review of over 1,000 U.S. and foreign research articles cites three general reasons for the increasing cesarean birth rate: use of the operation for breech presentations and for repeat sections; the need for early intervention due to fetal distress as determined by the increasing use of fetal monitoring; and physicians' fear of malpractice suits. The first two reasons are matters of medical controversy.

Role of vasoconstrictors in the systemic hypertension of rats acclimatized to hypoxia

1995 ◽  
Vol 79 (5) ◽  
pp. 1657-1667 ◽  
Author(s):  
Y. Moue ◽  
P. G. Smith ◽  
R. L. Clancy ◽  
N. C. Gonzalez
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Sodium Nitroprusside ◽  
Barometric Pressure ◽  
Systemic Hypertension ◽  
Ang Ii ◽  
Arterial Blood ◽  
Smooth Muscle Relaxant

Exposure to hypoxia (2–5 wk) results in systemic hypertension in rats and in humans. The possible mechanism(s) was investigated in rats acclimatized for 3 wk to barometric pressure of approximately 370 Torr (A) and in nonacclimatized littermates (NA) by administration of alpha-adrenergic [phentolamine (PHLM)], angiotensin II (ANG II), and arginine vasopressin (AVP V1) receptor antagonists. Both A and NA rats were studied in hypoxia (inspiratory O2 fraction = 0.10). Baseline mean arterial blood pressure (MABP) was higher in A than in NA rats: 126 +/- 4 vs. 101 +/- 2 mmHg (P < 0.05). Neither ANG II nor AVP V1 receptor antagonist influenced baseline MABP; however, both contributed to MABP recovery after PHLM. After simultaneous blockade of ANG II and AVP V1, PHLM lowered MABP by 65 +/- 2 and 45 +/- 3 mmHg in A and NA rats, respectively (P < 0.05). After combined blockade of the three systems, the smooth muscle relaxant sodium nitroprusside did not further modify MABP, which remained higher in A rats. It is concluded that 1) the hypertension in A rats is partly due to a higher alpha-adrenergic tone, 2) neither ANG II nor AVP contributes to the hypertension, but ANG II and AVP participate in MABP control after PHLM, 3) no other vasoconstrictor agents operate in either group, and 4) the higher MABP in A rats after sodium nitroprusside may reflect additional hypertensive mechanisms.

Mechanisms of protein kinase C regulation of airway contractility

1989 ◽  
Vol 66 (4) ◽  
pp. 1935-1941 ◽  
Author(s):  
C. M. Schramm ◽  
M. M. Grunstein
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Functional Activity ◽  
Phorbol Esters ◽  
Isometric Tension ◽  
Channel Blockers ◽  
Kinase C ◽  
Higher Doses

To elucidate the role of protein kinase C (PK-C) in regulating airway contractility, the effects of PK-C activation with phorbol esters, 12-deoxyphorbol 13-isobutyrate (DPB), and phorbol 12-myristate 13-acetate (PMA), and with the diacylglycerol analogue 1-oleoyl-2-acetate-rac-glycerol (OAG) were separately evaluated in isolated rabbit tracheal smooth muscle (TSM) segments. The latter agents produced dual and opposing contractile effects, with DPB being the most potent. Lower doses of DPB (less than or equal to 10(-6) M) elicited significant increases in isometric tension in both untreated TSM, as well as in TSM half-maximally precontracted with methacholine. These potentiated TSM contractions were inhibited by the Ca2+ channel blockers, nifedipine (10(-4) M) and diltiazem (10(-5) M). In contrast, higher doses of DPB (greater than or equal to 10(-6) M) induced airway relaxation, which was ablated by preinhibition of the electrogenic Na+-K+ pump with ouabain (5 x 10(-6) M) or K+-free buffer. Indeed, in separate experiments DPB (10(-7) M) was found to significantly potentiate the functional activity of the Na+-K+ pump, an effect occurring independent of inhibition of Na+-H+ exchange with amiloride (10(-4) M) or extracellular Ca2+ influx with nifedipine (10(-4) M).(ABSTRACT TRUNCATED AT 250 WORDS)

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