Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In arterial hypertension, hyperviscosity with hemorheological disturbances and platelet dysfunction may play a role in the prognosis and complications of the disease. We studied the effects of Nicardipine (NIC) on these blood disturbances in a group of 21 untreated patients with essential hypertension, aged 25 to 70 years (SBP/DBP = 185 +/- 28/105 +/- 17 mmHg). During one hour before and 4 hours after the IV injection of single doses of 5, 7.5 or 10 mg NIC over 5 min, blood pressure was recorded automatically (Dinamap). Hemorheological variables and platelet function were studied before and 30 min, 3 h and 24 hours after the injection. NIC lowered blood pressure and increased heart rate significantly (At 5 min, SBP = -24 mmHg; DBP = -18 mmHg; HR = +22 b/min). These effects were dose-dependent with rapid onset and short duration (less than 2 hrs). NIC decreased plasma viscosity from 1.36 +/- 0.08 to 1.30 +/- 0.07 Cst; p less than 0.01, whole blood viscosity from 22.4 +/- 2.8 to 20.7 +/- 1.5 mPas; p less than 0.05 for gamma = 0.512 s-1, and erythrocyte filterability with the Ca++ ionophore A 23187 from 16.3 +/- 3.8 to 13.5 +/- 3.1; p less than 0.01. Platelet aggregation with ADP was unchanged, but aggregation with A 23187 decreased from 46.9 +/- 21.2 to 31.3 +/- 25.6; p less than 0.05, as well as plasma levels of beta-thromboglobulin (71.2 +/- 29.8 to 55.4 +/- 24.3 ng/ml; p less than 0.02) and platelet generated malonaldehyde (7.2 +/- 1.8 to 6.7 +/- 1.4 nM/10(9) platelets; NS).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Effects of intravenous nicardipine on blood pressure, hemorheology platelet function in arterial hypertension. Dose-effect relations]. 311 84

The inhibitory effect of high and low molecular weight native and synthetic rat atrial peptides on oxygen consumption in isolated rat kidney mitochondria and slices was measured. Oxygen consumption by mitochondria was measured in the presence of succinate and/or adenosine diphosphate, furosemide, and low and high molecular weight native and synthetic rat atrial peptides. After the addition of succinate, adenosine diphosphate limiting respiration (State 4) increased in the presence of low, but not high, molecular weight native rat atrial peptides. Furosemide caused a significant decrease in State 4 respiration (p less than 0.001). Angiotensin II and arginine vasopressin did not alter State 4 respiration. The rate of oxygen consumption after the addition of saturating adenosine diphosphate in the presence of saturating succinate (State 3 respiration) was reduced by low and high molecular weight native rat atrial peptides. Furosemide completely blocked oxygen consumption after the addition of adenosine diphosphate. Oxygen consumption was unchanged by trypsin treated (natriuretically inactive) low molecular weight rat atrial peptides and ventricular protein extracts of high and low molecular weight native rat atrial peptides. Synthetic and low molecular weight native rat atrial peptides had similar effects on mitochondrial oxygen consumption. Low molecular weight native and synthetic rat atrial peptides decreased the adenosine diphosphate to oxygen ratio, and these peptides, as well as furosemide, also induced mitochondrial swelling; none of the other rat atrial peptide combinations nor angiotensin II produced this effect. In kidney slices, basal oxygen consumption (without substrates) was stimulated by succinate.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Rat atrial natriuretic peptides inhibit oxygen consumption by rat kidney. 315 63

Twenty-three patients with essential hypertension and diabetes mellitus type II were treated with the calcium antagonist diltiazem (120 to 180 mg twice daily). The mean dose was 307 mg/day. The study was a double-blind, placebo-controlled, crossover design. All measurements were performed 12 to 14 hours after drug intake. Blood pressure, heart rate and forearm blood flow were measured noninvasively. Platelet function was studied by measuring adenosine diphosphate-induced platelet aggregation and the platelet specific proteins, beta thromboglobulin and platelet factor 4. Thromboxane B2 formation in serum and the plasma concentration of diltiazem and its metabolites N-demethyldiltiazem, deacetyldiltiazem and N-demethyldeacetyldiltiazem were measured both during placebo and diltiazem treatment. Diabetic control was evaluated by following HbA1C, fasting blood glucose and urinary glucose. Diltiazem reduced both systolic and diastolic (supine and standing) blood pressure significantly. Forearm blood flow was significantly increased by 32%, p less than 0.05. Supine heart rate decreased significantly, while no such change was seen in the standing position. No significant changes were observed in platelet function during diltiazem treatment. There was no relation between the observed blood pressure reduction and the plasma concentration of diltiazem or its metabolites. A positive correlation between the change in heart rate and the metabolite N-demethyldeacetyldiltiazem was observed (r = 0.647, p = 0.005). Three patients were excluded during diltiazem treatment (skin exanthema, headache and atrial fibrillation) and 1 during placebo treatment (angina pectoris). No negative effect on diabetes control was observed. Thus, diltiazem could be used for treatment of hypertension in diabetic patients.
 ...
PMID:Diltiazem in hypertensive patients with type II diabetes mellitus. 317 28

Arterial blood pressure, serum fibrin/fibrinogen degratory products, plasma thromboxane B2, in vitro platelet aggregation, and platelet ultrastructure were studied in ten gravid ewes during fast-triggered ovine pregnancy-induced hypertension and subsequent administration of the thromboxane synthetase inhibitors CGS13080 and CGS12970. During the hypertensive period, blood pressure (p less than 0.005) and plasma thromboxane B2 levels (p less than 0.005) were significantly altered. Collagen-induced in vitro platelet aggregation lag times increased (p less than 0.01), and percent aggregation (p less than 0.05), primary (p less than 0.01), and secondary (p less than 0.005) aggregatory slopes decreased. Collagen also failed to induce aggregation in some ewes. Primary slopes of ADP-induced in vitro platelet aggregation decreased (p less than 0.01) during hypertension. Degranulation and open canalicular tubule system swelling were observed in platelets which produced abnormal or no aggregation response. However, these ultrastructural abnormalities did not necessarily correspond to hypertensive periods. Thromboxane synthetase inhibitor administration lowered blood pressure (p less than 0.005) and plasma thromboxane B2 levels (p less than 0.005). Abnormalities in collagen and ADP-induced platelet aggregation curves were also corrected, and ultrastructural abnormalities were not detected. Marked elevations in plasma thromboxane levels during ovine pregnancy-induced hypertension may have had an "exhaustive" effect on thrombocytes which was reversed by thromboxane synthetase inhibition.
 ...
PMID:Effect of thromboxane synthetase inhibition on platelet function and morphology during ovine pregnancy-induced hypertension. 323 44

Although it has been known for many years that prolonged ingestion of ethanol may be associated with numerous side effects, among them cardiovascular alterations, e.g., hypertension, cardiac arrhythmias, strokes, and cardiomyopathy, a direct cause and effect between alcohol and injury to the cardiovascular system has only been accepted recently. However, what mechanism is responsible for these cardiovascular alterations remains to be determined. Since it is well known that chronic alcohol consumption leads to hypophosphatemia and hypomagnesemia, we designed experiments to determine if controlled depletion of either phosphorous or magnesium (Mg2+) lead, in themselves, to cardiovascular disturbances and what effects these mineral depletions exert on myocardial cellular bioenergetics. Biochemical studies were carried out on left ventricular muscle, including mitochondrial and myofibrillar preparations. With respect to phosphate depletion, myocardial creatine phosphate, ATP, and ADP levels were reduced. Phosphate depletion also reduced mitochondrial and myofibrillar creatine phosphokinase activities; significant alterations in mitochondrial oxygen consumption, acid-extractable phospholipid precursors, and mitochondrial oxidation of long chain fatty acids were noted. With respect to magnesium depletion, significant reductions in inorganic oxygen consumption was also reduced. Utilizing these data, we have proposed several schemes for possible alcoholic-induced myocardial and vascular injury.
 ...
PMID:Hypophosphatemia and hypomagnesemia result in cardiovascular dysfunction: theoretical basis for alcohol-induced cellular injury. 329 28

The effects of a dihydropyridine calcium channel antagonist, nitrendipine 20 mg orally, have been investigated in 24 women in the first trimester human pregnancy in a double-blind, placebo controlled study. The effects on systemic arterial pressure, pulse rate (PR), blood loss at termination of pregnancy (TOP), plasma renin, renin substrate and aldosterone concentrations and platelet aggregation to adenosine diphosphate 0.5 microM, adrenaline bitartrate 0.1-1.0 microM, thrombin 0.05 u ml-1 and sodium arachidonate 0.1-0.2 mM were studied. Administration of nitrendipine was associated with a statistically-significant fall in diastolic pressure (BPD) the magnitude of which was directly related to the individual peak concentrations of the drug (P less than 0.02). No significant effects were observed on systolic pressure (BPS);PR rose slightly. Baseline variability of all three parameters fell in the nitrendipine-treated group over the first 2 h but then increased significantly (BPS, P less than 0.05; BPD, P less than 0.025; PR, P less than 0.005). There was a positive association in both placebo and treated groups between the rates of change of BPD and PR (P less than 0.005 for both); nitrendipine exerted a highly significant (P less than 0.001) effect on this association compatible with its effect as a vasodilator. Blood loss consequent on TOP did not differ in the two groups (nitrendipine 104 +/- 16 ml; placebo 114 +/- 20 ml). There were no significant differences in basal or stimulated hormone concentrations in the two groups. The ex vivo platelet aggregatory response in whole blood to 0.1 mM sodium arachidonate was inhibited by nitrendipine (P less than 0.05); responsiveness to the other aggregatory agents studied was not changed. There was a wide individual variation in both time to peak concentration of nitrendipine and the size of the peak, making classical pharmacokinetic analysis impossible. The median time after ingestion to peak concentration was 105 min; the median concentration was 7.8 ng ml-1. These data suggest that, in the context of the severe vasoconstriction and platelet aggregability of pregnancy-induced hypertension, further studies of this drug in pregnancy are warranted.
 ...
PMID:Some observations on the effects of a calcium channel blocker, nitrendipine, in early human pregnancy. 330 Jul 58

Serotonin content and accumulation in platelets and its release from them, as well as changes in thrombus formation in mesenteric arterioles and venules of the small intestine have been investigated in control rats and rats with spontaneous hypertension (SHR). Serotonin accumulation in platelets was determined upon its incubation with platelets. Disodium ADP salt was used as an inductor of release. Laser-induced thrombosis was caused by microvessels exposure to impulse laser irradiation. The control animals revealed a significant difference between the initial serotonin platelet level and serotonin level upon incubation and release; in values, the values of basic thrombus-forming parameters were higher than in arterioles. In SHR there is a decrease in biogenic amine content in platelets, a depression in its accumulation and release, an increase in the time of thrombus growth, its size up to the separation of the first embolus and its length along the vascular wall. It is concluded that spontaneous hypertension is characterized by decreased functional activity of platelets and depressed resistance of arterioles and venules to thrombus formation.
 ...
PMID:[Serotonin metabolism in thrombocytes and microvascular hemostasis in spontaneous arterial hypertension]. 334 66

Prolactin may play an important role in the pathogenesis of pregnancy-induced hypertension (PIH) and preeclampsia. In 105 normotensive nulliparous women at 28 to 32 weeks of gestation, the relationship between serum prolactin concentration (PRL) and blood pressure behaviour was examined under standardized conditions. Neither postural change from left lateral to supine recumbency nor the infusion of low doses of angiotensin-II-amide had an effect on PRL levels. Similar mean PRL levels were found in pregnant women with a low angiotensin pressor dose (ADP less than 10 ng x kg-1 x min-1) or "angiotensin sensitivity", a positive supine pressor response (delta pd greater than or equal to 20 mmHg) or an increased serum uric acid concentration (greater than 3.6 mg/dl), which are criteria for an increased risk of developing hypertensive complications. However, in the group of subjects with angiotensin sensitivity, a significant correlation was found (a) between PRL levels and the APD and (b) between PRL levels and diastolic blood pressure increase after 5 min of supine recumbency. These results may reflect diminished dopaminergic activity in the central nervous system, which could influence both blood pressure and prolactin secretion.
 ...
PMID:Relationship between serum prolactin concentration, vascular angiotensin sensitivity and arterial blood pressure during third trimester pregnancy. 340 Oct 43

Thirteen men, age 60 +/- 2 years (mean +/- SEM) with mild hypertension, 151 +/- 4/95 +/- 3 mm Hg, completed a randomized, double-blind, placebo-controlled crossover trial of ketanserin therapy. In comparison to placebo, ketanserin treatment at 40 mg bid for 6 weeks lowered systolic and diastolic blood pressure, 148 +/- 4/92 +/- 3 vs. 140 +/- 6/86 +/- 3 mm Hg, P = 0.19/0.02. The rate of platelet aggregation in response to ADP and epinephrine was unchanged while the response to serotonin was greatly diminished. Neither the systemic pressor response nor the pupillary mydriatic response to phenylephrine was significantly altered. Plasma norepinephrine concentration declined significantly. Ketanserin reduced blood pressure, particularly the diastolic component, in elderly men with mild hypertension. While antagonism of serotonin's effects on platelet aggregation was evident, blockade of alpha 1-receptor-mediated events was not apparent. The results suggest that during chronic therapy the antihypertensive effects of ketanserin were mediated by serotonergic blockade and a possible lytic effect on sympathetic drive. The dual effects of ketanserin on blood pressure and platelet aggregation may be beneficial in reducing cardiovascular complications in hypertensive patients.
 ...
PMID:Effects of ketanserin on blood pressure and platelet aggregation in elderly men with mild hypertension. 341 5

Platelet aggregation was studied in patients with high and stable arterial hypertension that was mostly associated with the malignant syndrome, and the effect of PGE2 introduced into the blood flow as repeated intravenous infusions on platelet activity was assessed. The addition of low-dose inductor produced the greatest changes in platelet aggregation following platelet exposure to different ADP doses in the patients, as compared to normal subjects. Stimulation with 0.1 mumol ADP produced a 7-fold increase in platelet aggregation in hypertensive patients, as compared to the controls. Repeated administration of 1.2-1.5 mg PGE2 normalizes cell sensitivity to ADP. Mean arterial BP dropped by 15-45 mm Hg during the infusions and remained low for several days afterwards.
 ...
PMID:[Platelet aggregation in severe and malignant forms of hypertension: effect of treatment with prostaglandin E2]. 347 7


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>