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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the effects on blood pressure, plasma lipoproteins, and platelet function when marine oil supplements (rich in n-3 fatty acids) or vegetable oil supplements (rich in n-6 fatty acids) were added to the usual diets of patients with mild essential hypertension. In a randomized, double-blind, parallel-group study, patients received 50 g of either marine oil (n = 8) or vegetable oil (n = 8) daily for 6 weeks following a baseline observation period. Diastolic blood pressure declined during treatment with fish oil (mean +/- SEM, 96 +/- 2 v 89 +/- 2 mm Hg, P = .02), but did not change with vegetable oil (92 +/- 1 v 94 +/- 1 mm Hg). Systolic blood pressure did not change significantly during either treatment. Serum triglycerides declined (by approximately 30%) in patients receiving only marine oil, but total cholesterol, LDL-, HDL-, HDL2-, and HDL3-cholesterol-subfractions and apolipoproteins A-I and B were unchanged in both treatment groups. Bleeding time increased by 33% during treatment with marine oil but did not change with vegetable oil supplements. Marine oil did not alter in vitro platelet aggregation thresholds. The lack of a significant correlation between blood pressure changes and platelet membrane fluidity, plasma renin activity, aldosterone, norepinephrine, or epinephrine suggests that these variables did not mediate the antihypertensive effect of the marine oil. We conclude that large doses of marine oil reduce diastolic blood pressure, lower triglycerides, and increase bleeding time in patients with mild hypertension.
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PMID:Effects of n-3 fatty acids in essential hypertension. 222 42

The cholesterol:phospholipid ratio was measured in platelet plasma membrane, red blood cell (RBC) membranes, low density lipoprotein (LDL) and whole plasma in patients with primary hypertension and in matched normal controls. The cholesterol:phospholipid ratio was raised in the platelet membrane from hypertensive patients compared with that from normal controls (0.65 +/- 0.03 vs 0.53 +/- 0.02: mean +/- SEM; P less than 0.01). The ratio observed in RBC membranes, LDL and whole blood was similar in the two groups. If this abnormality in the lipid composition of platelet plasma membrane is present in other cells it could account for some of the changes in cell membrane function that have been described in hypertension.
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PMID:Cholesterol:phospholipid ratio is elevated in platelet plasma membrane in patients with hypertension. 236 60

To study the metabolism and production of angiotensin I, highly purified monoiodinated [125I] angiotensin I was given by constant systemic intravenous infusion, either alone (n = 7) or combined with unlabeled angiotensin I (n = 5), to subjects with essential hypertension who were treated with the angiotensin converting enzyme inhibitor captopril (50 mg b.i.d.). Blood samples were taken from the aorta and the renal, antecubital, femoral, and hepatic veins. [125I]Angiotensin I and angiotensin I were extracted from plasma, separated by high-performance liquid chromatography, and quantitated by gamma counting and radioimmunoassay. Plasma renin activity was measured at pH 7.4. The plasma decay curves after discontinuation of the infusions of [125I]angiotensin I and unlabeled angiotensin I were similar for the two peptides. The regional extraction ratio of [125I]angiotensin I was 47 +/- 4% (mean +/- SEM) across the forearm, 59 +/- 3% across the leg, 81 +/- 1% across the kidneys, and 96 +/- 1% across the hepatomesenteric vascular bed. These results were not different from those obtained for infused unlabeled angiotensin I. Despite the rapid removal of arterially delivered angiotensin I, no difference was found between the venous and arterial levels of endogenous angiotensin I across the various vascular beds, with the exception of the liver where angiotensin I in the vein was 50% lower than in the aorta. Thus, 50-90% of endogenous angiotensin I in the veins appeared to be derived from regional de novo production. The blood transit time is 0.1-0.2 minute in the limbs and in the kidneys and 0.3-0.5 minute in the hepatomesenteric vascular bed. This is too short for plasma renin activity to account for the measured de novo angiotensin I production. It was calculated that less than 20-30% in the limbs and in the kidneys and approximately 60% in the hepatomesenteric region of de novo-produced angiotensin I could be accounted for by circulating renin. These results indicate that a high percentage of plasma angiotensin I may be produced locally (i.e., not in circulating plasma).
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PMID:Metabolism and production of angiotensin I in different vascular beds in subjects with hypertension. 240 79

Age and elevated blood pressure are associated with blunted beta-adrenoceptor-mediated cardiovascular effects. To investigate a possible relationship between beta-adrenoceptor cardiovascular function and receptor density, beta-adrenoceptor binding capacity in mononuclear leucocytes and cardiac isoproterenol sensitivity were compared in 12 essential hypertensive and 17 normotensive subjects of comparable age. The bolus dose of isoproterenol which increased heart rate by 25 beats/min (CD25) as well as plasma norepinephrine, epinephrine, and renin activity were measured. In a radioreceptor assay using [3H]dihydroalprenolol, the antagonist binding capacity (Bmax) and the affinity constant (KD) of mononuclear leucocytes were determined. Bmax in patients was higher than in normotensive subjects (66.8 +/- 4.1 versus 48.0 +/- 3.8 SEM fmol/mg, p less than 0.05), and KD was identical in both groups. In hypertensive patients, Bmax correlated positively with age (r = 0.639, p less than 0.05) and CD25 (r = 0.593, p less than 0.05) and negatively with plasma renin activity (r = 0.679, p less than 0.05), while in normotensive subjects, Bmax correlated with CD25 only (r = 0.615, p less than 0.05). Thus, in patients with essential hypertension, a decrease in cardiac isoproterenol sensitivity and plasma renin activity is associated with an age-related increase in antagonist binding capacity. This suggests a defect in the membrane coupling of the beta-adrenoceptor effector system distal to the receptor recognition site in patients with essential hypertension.
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PMID:Increased beta-adrenoceptor binding capacity is associated with blunted beta-adrenoceptor-mediated cardiovascular responses in essential hypertension. 241 82

We have studied the acute effects of the serotonergic type-2 (5-HT2) antagonists ketanserin and ritanserin given as single oral doses to patients with essential hypertension. Ketanserin has alpha 1-antagonist properties, whereas ritanserin is largely devoid of alpha 1-receptor binding affinity. Ketanserin (40 mg orally) caused a significant reduction (p less than 0.03) of sitting mean arterial pressure over the 8-h period following drug administration by an average of 15.4 +/- 3.2 mm Hg (mean +/- SEM) as compared to a reduction of 8.5 +/- 2.2 following placebo. In contrast, ritanserin had no significant effect on blood pressure compared to placebo; sitting mean arterial pressure was reduced by 9.0 +/- 2.6 and 10.8 +/- 1.8 mm Hg after administration of 10 and 20 mg, respectively, of ritanserin. There were no significant differences in pulse rate among placebo, ketanserin, or ritanserin phases. Ritanserin caused a reduction in the hostility score (p less than 0.05) as measured by the Multiple Affect Adjective Check List; ketanserin had no significant effects. The highly selective 5-HT2 antagonist ritanserin, given in a dose which caused measurable alteration of psychological function tests, had no acute effects on blood pressure. The acute antihypertensive effects of ketanserin are not caused by 5-HT2 antagonism alone, but are likely to be dependent on its alpha 1-antagonistic properties.
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PMID:Does acute serotonergic type-2 antagonism reduce blood pressure? Comparative effects of single doses of ritanserin and ketanserin in essential hypertension. 244 81

In six hospitalized subjects with mild or moderate and untreated essential hypertension, we measured mean blood pressure (MBP, brachial artery catheter), heart rate (HR, electrocardiogram), cardiac output (CO, thermodilution), and total peripheral resistance (TPR, MBP divided by CO) at rest and during a cold pressor test (CPT, 60 s), a hand-grip exercise (HG, 40% maximum strength for 90 s), and a cyclette exercise (CE, 50 W for 5 min). The study was performed in a no-drug condition, 1 h after 20 mg oral nitrendipine (aN) and 1 week after daily administration of 20 mg oral nitrendipine (pN). Compared with the no-drug condition, aN reduced resting MBP from 137.3 +/- 7.3 (mean +/- SEM) to 112.3 +/- 9 mm Hg (p less than 0.05), increased resting HR from 72.3 +/- 6.9 to 85.3 +/- 8.8 beats/min) (p less than 0.05), increased resting CO from 6,191 +/- 508, to 8,700 +/- 1,050 ml/min (p less than 0.05), and reduced resting TPR from 1,807 +/- 119 to 1,140 +/- 228 dynes/s/cm5 (p less than 0.05). The reduction in resting MBP and TPR were unchanged by pN, whereas the increase in HR and CO were attenuated by 47 and 42%, respectively (p less than 0.05). Neither aN nor pN altered the hemodynamic responses to CPT, HG, and CE. As a result, the peak MBP and TPR values that were measured during these maneuvers were always lower (p less than 0.05) during aN and pN than in the no-drug condition. Thus, nitrendipine exerts marked antihypertensive and vasodilatatory effects that are evident at rest and during conditions elevating BP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic effects of acute and prolonged administration of nitrendipine in essential hypertension. 245 12

Fourteen patients with mild to moderate essential hypertension were randomized, after a baseline placebo period of 4 weeks, to receive the angiotensin converting enzyme (ACE) inhibitor quinapril or a placebo. During a 12 week, double-blind phase, the dosage of quinapril was increased from 10 to 40 mg twice daily being doubled every 4 weeks. At the end of the baseline period and of each month of the double-blind phase, 12 h overnight urine collections were made and morning blood samples were taken about 12 h after the last dose of medication. During the double-blind phase, blood pressure in the quinapril group (n = 7) decreased from 159 +/- 3/105 +/- 1 to 141 +/- 6/94 +/- 2 mm Hg (mean +/- SEM). Serum ACE activity and plasma angiotensin II concentration were reduced to 4 +/- 1% and 14 +/- 1% of the pretreatment values, respectively. Neither the plasma concentrations nor the urinary excretions of prostaglandin E2, 6-keto-prostaglandin F1 alpha (a prostacyclin metabolite), or thromboxane B2 (a metabolite of thromboxane A2) were affected by quinapril. In the placebo group, blood pressure tended to decline but the biochemical variables remained essentially unchanged. These results indicate that prostanoids are not involved in the antihypertensive action of quinapril, the principal effect of which seems to be inhibition of the renin-angiotensin system.
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PMID:Effects of the converting enzyme inhibitor quinapril (CI-906) on blood pressure, renin-angiotensin system, and prostanoids in essential hypertension. 245 40

We measured the ouabain- and bumetanide-resistant Na+ efflux in Mg2+-sucrose medium (passive Na+ leak) in erythrocytes from 30 normotensive controls and 72 essential hypertensive patients. The mean values (+/- SEM) of the rate constant of Na+ leak (kpNa) were not significantly different between normotensives and hypertensives. Nevertheless, using the 95% confidence limits of the kpNa (in 10(-3).h-1) in the normotensive group as a cut-off point, 7 (9.7%) essential hypertensives exhibited increased values (58.96 +/- 10.12) when compared with the other 65 patients (23.86 +/- 0.74). revealing increased passive Na+ permeability in the former (leak "+" hypertensives). Na+ fluxes depending on the Na+-K+ pump, outward Na+-K+ cotransport, and Na+-Li+ countertransport were also measured in fresh erythrocytes from the same 72 patients. Three of them (4.2%) exhibited decreased values of ouabain-sensitive Na+ efflux and 6 (8.3%) of bumetanide-sensitive Na+ efflux, while 8 patients (11.1%) showed increased values of Li+-stimulated Na+ efflux and, finally, 48 patients (59.7%) did not present any evident abnormality in these Na+ transport systems. No differences were observed between leak "+" hypertensives and the remaining 65 patients when both basal erythrocyte Na+ content and clinical parameters of hypertension were compared. However, Na+ efflux depending on the outward Na+-K+ cotransport was significantly higher in the leak "+" hypertensive subset (299.43 +/- 43.18 vs 181.52 +/- 10.76 mumol.(l cells.h)-1; P = 0.0078), suggesting a compensatory phenomenon. Enhancement of Na+ permeability detected in 3% to 16% of essential hypertensives may be implicated in the pathogenesis of primary hypertension.
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PMID:Abnormal erythrocyte sodium leak in a subset of essential hypertensive patients. 246 45

This multicenter study evaluated nitrendipine, a dihydropyridine calcium antagonist, alone or in combination with hydrochlorothiazide and/or propranolol in severe essential hypertension (baseline supine diastolic BP greater than or equal to 115 mm Hg). After an initial 3- to 7-day drug-free run-in, a 2- to 5-week titration phase, and a 4- to 6-week maintenance period, patients with supine diastolic less than or equal to 90 mm Hg entered long-term maintenance. Four centers enrolled 57 patients initially; 43 qualified for the extended therapy trial, and 30 had completed greater than 2 years of therapy (mean duration of 756 days) at the time of analysis. Supine BP fell from 186/122 +/- 5/2 mm Hg at baseline (group mean +/- SEM) to 139/89 +/- 3/2 mm Hg after 2 years (p less than 0.001/0.001). Standing BP fell from 185/126 +/- 5/2 to 138/90 +/- 3/2 mm Hg (p less than 0.001/0.001). Supine pulse rate changed from 82 beats/min at baseline to 74 beats/min (p less than 0.01) and standing pulse rate from 88 to 78 beats/min (p less than 0.01). Seventeen patients received nitrendipine alone, 4 received nitredipine plus HCTZ, 2 received nitrendipine plus propranolol, and 7 patients received all three drugs. Response was similar in patients less than 50 years old and in those greater than or equal to 50 years, and also in black and nonblack patients. Three patients were lost to follow-up, six were terminated for inadequate BP control, and four terminated for side effects. Twenty-four patients completed greater than 2.5 years treatment (mean duration of 933 days).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term efficacy and safety of nitrendipine in severe essential hypertension. 246 63

Several abnormalities in Na metabolism have been implicated in the pathogenesis of essential hypertension. In addition, recent work by several investigators has showed that some Na transport systems in red cell membranes may be altered in those patients. In order to confirm such abnormalities we evaluated simultaneously four different and clearly defined Na transport systems in red cell membranes: the ouabain sensitive Na pump (P) and the Na-K cotransport (Co) in nystatin loaded cells, the maximal rate of Na-Li countertransport (CTT) in lithium loaded cells and the rate constant of Na passive permeability (pp) in 58 normotensive control subjects with no family history of hypertension (N), 19 normotensive subjects with family history of hypertension (NH) and 34 essential hypertensive patients (HE). The mean (mean +/- SEM microns/lc/h) value of the P and pp was found to be comparable in the three groups. Co was found significantly decreased in both HE (241 +/- 28) and in NH (227 +/- 42) when compared to the control group (290 +/- 10). Although NH also showed CTT values (377 +/- 87) higher than controls, the difference did not reach statistical significance. Our results indicate that approximately 90.9% of both HE and NH presented abnormalities in one or more of the various Na transport systems studied. Normotensive patients with a positive family history and alterations in some of the Na transport systems in red cell membranes may prove an interesting experimental model to assess the importance of such alterations for the development of hypertension.
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PMID:[Sodium transport in red blood cell membranes in essential arterial hypertension]. 248 32


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