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

The effect of a four weeks oral treatment with 100 mg isosorbide dinitrate (ISDN) daily on platelet function was evaluated in 40 patients (aged 40-65 years) with proven coronary artery disease. Isosorbide dinitrate decreased platelet reactivity to ADP (p less than 0.001), increased platelet sensitivity to PGI2 (p less than 0.01) while the production of TXB2 from exogenous arachidonic acid substrate and from endogenous substrate were both significantly reduced. Circulating platelet aggregates as measured by the Wu-test were markedly reduced (p less than 0.001) but there was little change in the plasma concentration of the platelet proteins beta-thromboglobulin and platelet factor 4. Overall, platelet activation correlated with smoking, hypertension and a family history of coronary artery disease. The reduced platelet activation seen during treatment with isosorbide dinitrate may contribute to the therapeutic benefit seen with this drug in patients with coronary artery disease.
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PMID:Modification of platelet function by isosorbide dinitrate in patients with coronary artery disease. 138 8

The enzymatic conversion of human big endothelins (1, 2, and 3) to their respective active metabolites (endothelin-1, -2, and -3) was investigated in the perfused rabbit kidney through the pressor- and eicosanoid-releasing properties of these peptides. Intra-arterial bolus injections of endothelin-1 and -2 (5-50 pmol), endothelin-3 (100-250 pmol), and big endothelin-1 and -2 (100-250 pmol) into the kidney produced dose-dependent increases of perfusion pressure, whereas big endothelin-3 was inactive at doses up to 1,000 pmol. Endothelin-1 and -2 (10 nM), endothelin-3 (100 nM), and big endothelin-1 and -2 (100 nM) are potent enhancers of prostacyclin release without inducing any release of thromboxane B2 in the perfused kidney. In contrast, big endothelin-3 did not trigger the release of eicosanoids. A metalloprotease inhibitor, phosphoramidon (100 microM, 60 minutes), reduced the prostanoid release and pressor responses induced by big endothelin-1 and -2 without affecting the response induced by endothelin-1, -2, and -3. These results suggest the presence of a phosphoramidon-sensitive endothelin converting enzyme that converts the precursors of endothelin-1 and -2, but not of endothelin-3, in the renal vasculature of the rabbit.
Hypertension 1992 Oct
PMID:Phosphoramidon-sensitive effects of big endothelins in the perfused rabbit kidney. 139 87

Researchers analyzed data on 47 black, pregnant women of more than 33 weeks gestation who had preeclampsia with diastolic blood pressure of at least 110 mm Hg and 1+ of proteinuria and were in the delivery department of King Edward VIII Hospital in Durban, South Africa to compare antihypertensive effects of dihydralazine infusion with that of epoprostenol sodium infusion. Overall, both treatments reduced the patient's systolic and diastolic blood pressures. No significant differences in the hypertensive effects existed between the 2 groups. Yet the reduction in blood pressures occurred much more quickly in the epoprostenol group than in the dihydralazine group (51.1 minutes vs. 86.8 minutes;p=.0072). Epoprostenol reduced high blood pressure in all 22 patients while dihydralazine did not adequately control blood pressure in 2 of 25 patients. Physicians had to perform a cesarean section in these 2 cases due to considerable deceleration of the fetal heart rate. They had to 1st administer the rapidly acting ganglion blocking agent, trimetaphan, before placing the women under general anesthesia. Their blood pressures returned to normal after delivery. Even though both groups experienced tachycardia after treatment, the pulse rate of dihydralazine patients was significantly higher than that of epoprostenol patients (102.68/minute vs. 88.36/minute; p=.0024). Only 2 women suffered from side effects. The epoprostenol patient experienced nausea and vomiting. The other patient received dihydralazine and experienced a severe headache. The researchers concluded that physicians should use epoprostenol in patients with severe hypertension and tachycardia and those who need acute control of severe hypertension on the operating table before endotracheal intubation (which tends to cause considerable increases in blood pressure) and administration of general anesthesia.
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PMID:A comparative study of the use of epoprostenol and dihydralazine in severe hypertension in pregnancy. 142 10

It has been reported that atrial natriuretic peptide (ANP) concentrations are elevated in pregnancy and further elevated in pregnancy-induced hypertension. Atrial stretch and volume expansion appear to be important stimuli for ANP release. During normal pregnancy, a striking change in hemodynamics occurs that may increase plasma ANP concentrations. ANP has potent natriuretic, diuretic, and smooth muscle relaxant activities. The biological effects of ANP during pregnancy may play an important role in the physiology and pathophysiology of pregnancy. Because of possible interactions during pregnancy due to secondary effects of maternal cardiovascular changes and physiological adaptation, the present study sought to evaluate and characterize the local effects of atriopeptin II on the uterine vascular bed of the nonpregnant sheep. Ewes with catheters in the femoral artery, femoral vein, and uterine artery and electromagnetic flow probes on the middle uterine arteries were monitored for blood pressure (BP), heart rate (HR), and uterine blood flow before and after the administration into the uterine artery of bolus injections of 2, 4, 20, and 40 x 10(-9) M (5, 10, 50, and 100 micrograms) of the synthetic ANP (atriopeptin II). For comparison purposes, the effects of prostaglandin I2 in doses of 1.2, 2.5, 12, and 25 x 10(-8) M (5, 10, 50, and 100 micrograms), vasoactive intestinal polypeptide in doses of 3, 9, 30, 90, 300, and 900 x 10(-11) M (0.1, 0.3, 1, 3, 10, and 30 micrograms), and bradykinin in doses of 9.4, 28, 94, 280, 940, and 2800 x 10(-11) M (0.1, 0.3, 1, 3, 10, and 30 micrograms) were also tested. Appropriate vehicles were tested and found to be without effect. All four compounds were found to be vasodilators of the nonpregnant uterine vasculature. ANP administered into the uterine artery decreased BP (87 +/- 4 mm Hg to 79 +/- 4 mm Hg with 50 micrograms [20 x 10(-9) M]), increased HR (90 +/- 5 bpm to 105 +/- 4 bpm), and significantly increased uterine blood flow (from 14 +/- 3 to 37 +/- 4 ml/min with a dose of 100 micrograms [40 x 10(-8) M, P < 0.05]). Prostaglandin I2 failed to alter BP, but caused significant increases on HR (100 +/- 4 to 124 +/- 13 bpm, P < 0.05) and uterine blood flow (17 +/- 4 to 73 +/- 10 ml/min, P < 0.05). Vasoactive intestinal polypeptide caused a significant tachycardia (97 +/- 10 to 158 +/- 9 bpm, P < 0.05) at the highest dose.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effect of atrial natriuretic peptide and other vasoactive compounds on the uterine vascular bed of the nonpregnant sheep. 143 42

Fourteen normotensive and 14 hypertensive black men with mild essential low-renin hypertension were examined during two protocols producing sodium depletion (less than 40 mmol sodium diet per day) for 5 days, followed by sodium loading (300 mmol sodium diet per day) for another 5 days. Changes in plasma renin activity, urinary aldosterone excretion, and excretion rates of stable breakdown products of thromboxane A2 (thromboxane B2) and prostacyclin (6-keto PGF1 alpha) were simultaneously assessed by radioimmunoassay. On the basis of low-renin status and paradoxically normal aldosterone excretion in both normotensives and hypertensives, thromboxane B2 excretion was increased by 14% (not significant); 6-keto PGF1 alpha was significantly decreased by 47% in the hypertensives compared to the normotensives. As a result, thromboxane B2/6-keto PGF1 alpha ratio was significantly increased from 1.29 +/- 0.10 in the normotensives to 2.78 +/- 0.12 in the hypertensive patients. The same ratio increased significantly after sodium loading in both groups, but more distinctly in the hypertensives (40%). Prostacyclin is a vasodilator, a natriuretic, and a potent inhibitor of platelet aggregation. Thromboxane A2 has opposite effects. The impaired prostacyclin biosynthesis we found in the hypertensive patients could account for the increased vascular resistance and some complications typical for hypertensive state.
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PMID:Renin-angiotensin-aldosterone system and thromboxane A2/prostacyclin in normotensive and hypertensive black Zimbabweans. 145 13

Ten patients have been studied for lipidic behaviour during hemodialysis using as anticoagulant heparin and prostacyclin. Hearing has been administered at infusion rate of 2000 U/h and prostacyclin in 5 ng/kg/min. Lipidic behaviour (before and after hemodialysis) has been studied for apolipoproteins A and B, total serum cholesterol and serum triglycerides, HDL-cholesterol, lipoprotein. Total serum cholesterol/HDL-cholesterol, apolipoproteins A/apolipoproteins B, apolipoproteins A/HDL-cholesterol ratios have been also studied. Our findings show that heparin produces acute changes in lipidic behaviour after hemodialysis and suggest that administrations may contribute to lipidic derangement of uremic dialytic patient while heparin free dialysis (prostacyclin infusion) doesn't show lipidic derangement after dialytic treatment. Prostacyclin infusion suggests that may be a useful anticoagulant and therapeutic drug especially in uremic dialytic subject with high atherosclerosis involvement, dyslipidemia and arterial hypertension.
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PMID:[Lipid behavior during hemodialysis using heparin and prostacyclin]. 149 59

In one third of patients who suffered an infarction NIDDM and arterial hypertension are present. In the absolute majority of patients with IHD, as apparent from the IRI and C-peptide response after a glucose load, hyperinsulinism is present. The blood sugar response can have the character of diabetes or of impaired glucose tolerance, the curve may be very flat or normal while the IRI and C-peptide response are excessive. Hyperinsulinism has a hypersecretory origin as suggested by the concurrently elevated C-peptide level but also reduced insulin utilization in the liver and peripheral target organs. Hyperinsulinism is thus a regular associated phenomenon of IHD and is a special risk factor independent on hyperglycaemia and associates with the other main risk factors of IHD such as arterial hypertension, HPLP (android obesity), hyperglycaemia (NIDDM) and hirsutism as a manifestation of a hyperandrogenic state in the female organism with the syndrome of polycystic ovaries. Hyperinsulinism plays an indirect role in the pathogenesis of coronary syndrome via the main risk factors (5H syndrome--hyperinsulinism, hypertension, HPLP, hyperglycaemia, hirsutism) and also directly by its action on endothelial paracrine mechanism of the coronary circulation where in the early stage vasoconstrictor factors predominate (endothelin-1, PGF2-alpha) over physiological vasodilatating factors (EDRF-NO, PGE2, PGI2) and this leads then to functional spasms. It seems that also the coronary X syndrome develops very frequently on the background of the hormonal metabolic X syndrome or the 5H syndrome.
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PMID:[Hyperinsulinism and the coronary syndrome]. 149 68

Prostacyclin (PGI2) is known to cause vasorelaxation and inhibit platelet aggregation by receptor-mediated mechanisms. While cyclic (c) AMP is known to act as a second messenger for inhibition of platelet aggregation, vasorelaxation by hyperpolarization has been described only recently and may provide an explanation, in addition to stimulation of cAMP for the PGI2 mechanism of action on blood vessels. When PGI2 is infused into healthy volunteers it reduces blood pressure only at infusion rates that also cause significant side-effects, primarily, nausea, emesis, flushing, diaphoresis, and restlessness. In hypertensive patients blood-pressure responses are complex and are influenced to some extent by renin secretion. PGI2 stimulates renin secretion by a direct effect on the juxtaglomerular apparatus, and it also has an indirect effect by activating the sympathetic nervous system. Thus, it is useless as an antihypertensive agent even apart from its debilitating side-effects. Vascular PGI2 is synthesized endogenously by both the endothelial cells and the muscularis of arteries. While the endothelial cells undoubtedly synthesize large amounts of PGI2, the muscularis comprises a much larger tissue mass so that the overall synthesis is about equally distributed between the endothelial and muscle cells. In patients with pregnancy-induced hypertension and some patients with essential hypertension endogenous synthesis of PGI2 has been evaluated by measuring 2,3-dinor-6-keto-PGF1 alpha and has proved to be greatly reduced. Some drugs (thiazides, propranolol) have been shown to stimulate PGI2 synthesis, and inhibition of cyclooxygenase has been shown to reduce their antihypertensive effects. The effects of low- and high-dose aspirin on prostacyclin and thromboxane synthesis are discussed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prostacyclin in hypertension]. 149 51

The HELLP syndrome (haemolysis, elevated liver enzymes, low platelet count) was first referred to by Weinstein in 1982 as an extremely progressive form of gestosis. In addition to the more common gestotic symptoms, such as oedema, proteinuria and hypertension, the clinical picture is characterized by microangiopathic haemolysis, thrombocytopenia and, especially, impaired hepatic function. Within this clinical picture severe complications can occur, such as eclamptic attacks, renal dysfunction, intracranial haemorrhage, intrahepatic haemorrhage and coagulopathy. An imbalance in prostanoid metabolism has been implicated in the pathogenesis. A decrease in synthesis of the vasodilator and thrombocyte aggregation inhibitor prostacyclin leads to a preponderance of the vasoconstrictor thromboxane A2, which promotes thrombocyte aggregation. This results in local vascular spasms and endothelial lesions, which in the case of hypercoagulopathy are accompanied by the formation of fibrin deposits with resultant vascular constriction. Intravascular fibrin deposits indicate that the coagulation system has been compromised and can lead to consumption coagulopathy in approximately 10% of cases. In the majority of cases, however, one finds low-grade disseminated intravascular coagulation (DIC), i.e. mild hypercoagulopathy with thrombocytopenia, a tendency to thrombocyte aggregation and fibrinogen deficiency in the presence of usually normal plasmatic coagulation. These vascular changes occur particularly in organs that have high blood flow, such as liver, kidneys and placenta. In the liver, sinusoidal obstruction causes vascular congestion, leading to an increase in intrahepatic pressure, dilatation of Glisson's capsule, development of subcapsular hepatic haematomas and hepatic rupture. Hepatic haematoma virtually always requires surgical treatment, and otherwise the patient has hardly any chance of survival. Nevertheless, mortality is around 35%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Spontaneous liver rupture as a rare complication of the HELLP syndrome]. 149 26

To define the role of the renal eicosanoid system in sustaining renal homeostasis in hypertension, we investigated the alterations in urinary excretions of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), a stable metabolite of vasodepressor prostacyclin, and thromboxane B2 (TXB2), a stable metabolite of vasoconstrictor TXA2, when norepinephrine was continuously infused for 90 min in hypertensive (n = 13) and normotensive subjects (n = 14). There was no difference in plasma norepinephrine concentration after the infusion between the hypertensive and the normotensive subjects. Moreover, the percent changes in renal vascular resistance elicited by norepinephrine in the hypertensives were equal to those of the normotensive subjects. In the normotensive subjects, the norepinephrine infusion significantly increased urinary 6-keto-PGF1 alpha excretion and decreased urinary excretion of TX, both of which are beneficial for sustaining renal function. In fact, the greater the production of renal 6-keto-PGF1 alpha was, the less the reduction of renal blood flow and urinary sodium excretion was. In the hypertensive subjects, however, these normal responses of the renal eicosanoid system, seen in the normotensives, were abolished; urinary 6-keto-PGF1 alpha was unaltered and thromboxane generation was rather increased. Thus, the renal eicosanoid system dysfunctions in hypertensive subjects when the renal circulation is challenged by norepinephrine. These abnormal responses are likely to cause sodium retention and could contribute, in part, to the hypertensive mechanism in patients with essential hypertension.
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PMID:Abnormal response of urinary eicosanoid system to norepinephrine infusion in patients with essential hypertension. 150 57


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