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

Nicotine evokes the release of catecholamines from bovine adrenal glands perfused with oxygenated Krebs-bicarbonate solution. Two 2-min pulses of 5 microM nicotine, at 40-min intervals (S1 and S2), gave net catecholamine outputs of 45.2 +/- 3.6 and 29.1 +/- 3.5 micrograms/8 min, respectively. Apomorphine (1 or 10 microM) markedly inhibited catecholamine release during S2 to 9.1 +/- 2.2 and 0.5 micrograms/8 min, respectively. Haloperidol (0.5 microM) reversed the inhibitory effects of apomorphine. Haloperidol alone enhanced catecholamine release induced by nicotine to 67.9 +/- 7.9 micrograms/8 min. [3H]Spiperone binds to adrenomedullary membranes with a KD of 0.24 nM and a Bmax of 117 fmol/mg of protein. Whereas spiperone and haloperidol potently displaced such binding, 3,4-dihydroxyphenylethylamine (dopamine) and sulpiride were poorer displacers, and SCH23390, prazosin, phenoxybenzamine, propranolol, BAY-K-8644, and nitrendipine did not displace [3H]spiperone bound. These data strongly suggest that, as in the cat, the bovine adrenal medulla chromaffin cell contains a dopaminergic receptor that modulates the catecholamine secretory process triggered by stimulation of the nicotinic cholinoceptor. Such a receptor seems to be of the D2 type and might be involved in a sympatho-adrenal cooperative mechanism contributing to the maintenance of cardiovascular homeostasis during stressful situations as well as to the pathogenesis of hypertension. If so, selective dopaminergic agonists might prove clinically useful in the treatment of hypertension.
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PMID:Characterization of a dopaminergic receptor that modulates adrenomedullary catecholamine release. 373 85

The tissue contents of catecholamines (CAs) and methionine-enkephalin-like immunoreactivity (Met-enk) were examined in 8 patients with phaeochromocytomas (Phs). In 6, Ph cells were cultured, and the modes of secretion of CAs and Met-enk were examined. Tissue contents of CAs and Met-enk varied from patient to patient, but larger amounts of Met-enk were found in medullary Phs than extramedullary ones, regardless of the secreting CA type. Three patients with extramedullary Phs had clinically showed a sustained hypertension, whereas five with medullary Phs were normotensive or had occasional paroxysmal hypertension. Nicotine (10(-7) M to 10(-4) M) stimulated simultaneous secretion of CAs and Met-enk from the cultured human Ph cells. Met-enk, however, was not secreted in proportion to either epinephrine (E), norepinephrine (NE) or total CAs (E + NE). Met-enk, FK33-824 (FK) (Met-enkephalin analogue), and dynorphin 1-13 (Dyn) significantly suppressed the secretion of CA evoked by 10(-5) M nicotine. The 50% inhibitory concentrations (IC50) of Met-enk, FK, and Dyn were 5 X 10(-6) M, 9.9 X 10(-5) M, and 9.0 X 10(-8) M, respectively, in one patient and 9.0 X 10(-6) M, 1.5 X 10(-7) M, and 1.4 X 10(-7) M in another. In one patient, 10(-5) M naloxone inhibited the CA secretion evoked by 10(-5) M nicotine and did not reverse the 10(-5) M FK-induced suppression of CA secretion in the presence of 10(-5) M nicotine. These results suggest that human Phs may be heterogeneous with regard to storage and secretion of CAs and opioid peptides.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Catecholamines and opioid peptides in human phaeochromocytomas. 378 13

The literature points out the meaning of risk factors causing stroke as well as their therapy or elimination as an effective prevention of cerebrovascular disease. Hypertension increases the risk of apoplexy by 4-fold, with regard to the diastolic values of blood pressure by the 5-fold up to the 10-fold. Consistent hypertension therapy decreases significantly the incidence of cerebral apoplectic attacks. Manifested diabetes mellitus and even reduced glucose tolerance raise the risk of stroke by the 3-fold, even though factors frequently associated with diabetes are taken into consideration. Hyperlipidemia, hypercholesteremia, and hypertriglyceridemia stipulate an increase of stroke incidence by the 2-fold to the 3-fold. Morbidity rate rises if these abnormalities coincide with further risk factors, up to the 6-fold. Nicotine consumption alone increases the risk of cerebral apoplectic attacks in relation to age, by the 3-fold up to the 5-fold. In combination with the use of hormonal contraceptive drugs, the risk of morbidity rate in women rises to the 7-fold. Overweight of more than 30% aggravates twice the risk of stroke. Heart diseases of different kind increase the risk of apoplectic attacks by the 2-fold, in combination with hypertension by the 5-fold. The intake of oral contraceptives (OCs) causes an increase of cerebral thromboembolic attacks by the 3-fold up to the 5-fold, whereby a relation to estrogen content and to hemorheology disturbances is proven. Blood coagulation disturbances, especially hypercoagulability with increase of blood level of fibrinogen, fibrin, and enhanced adhesiveness of thrombocytes in cerebrovascular disease are proven to be valid. By combination of various risk factors apoplexy risk is additionally increased. The possibility of surgical and neurosurgical prophylactic treatment in all stages of cerebral ischemia, caused by occlusive disease of the cartoid, vertebral, and intracranial arteries, exists in 75% of patients. With regard to the longterm results of patients with extraintracranial bypass surgery, due to stenosis or occlusion of the carotid artery in its high cervical or intracranial course, or of the middle cerebral artery, the operated group clearly was better than the nonoperated group in frequency of cerebral ischemia recurrence. The therapeutic effect of inhibitors of thrombocytic aggregates and of anticoagulants for the chemotherapeutic prevention of cerebral ischemia, is proven for acetylsalicylic acid and derivatives of coumarin. Both diminish significantly the rate of cerebral ischemia when compared with placebo-treated control groups.
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PMID:[Prevention of cerebrovascular circulatory disorders]. 404 14

Chronic smoking in humans and continuous nicotine application in animals do not induce hypertension, although the acute effects of nicotine are sympathoadrenal activation and elevation of blood pressure. In conscious dogs with a carotid artery loop preparation, we studied whether chronic nicotine application induced tolerance to the acute effects of nicotine test infusions. Nicotine was applied as salicylate via subcutaneously implanted osmotic minipumps at a dosage of 1 microgram/kg/min = 1.44 mg/kg/day, corresponding to heavy smoking in humans. Chronic treatment in eight dogs for 5-8 weeks did not modify resting heart rate and plasma levels of free catecholamines, but significantly increased plasma levels of conjugated dopamine by 100%. Mean arterial pressure at rest was elevated in the 2nd week by 6mm Hg, but did not increase further. Sham treatment (n = 8, sodium salicylate in equivalent dosage) was without effect. Acute test-infusions of nicotine (3 and 10 micrograms/kg/min i.v.) caused acute rises in mean arterial pressure (by 12 and 28 mm Hg), heart rate (by 9 and 18 bpm), plasma norepinephrine (by 36 and 68%), plasma epinephrine (by 110 and 180%) and led to plasma nicotine levels of 31 and 95 ng/ml. Chronic nicotine treatment attenuated the hemodynamic and partially abolished the hormonal effects without affecting the nicotine plasma levels obtained with these test infusions, but it did not modify the hemodynamic effects of a norepinephrine test infusion. The data demonstrate the development of a specific, reversible tolerance to the acute sympathoadrenal activation by nicotine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Development of specific tolerance to nicotine infusions in dogs on chronic nicotine treatment. 648 27

Cigarette smoking has been associated with increased upper body fat deposition, as estimated by the waist to hip ratio, which has been shown to be associated with glucose intolerance and dyslipidemia in nonsmoking subjects. Whether smoking is at the origin of central adiposity and its related metabolic disturbances is unclear. Moreover, it is controversial whether smoking influences fuel metabolism. Therefore, young healthy male volunteers smoking more than 10 cigarettes/day for more than 5 yr (n = 14) were compared with nonsmokers (n = 13) matched for age, sex, body mass index, alcohol consumption, physical activity, as well as family history for hypertension, diabetes, obesity, and coronary heart disease. After an overnight fast, blood was drawn for chemistry, body composition was assessed by dual energy x-ray absorptiometry, and fuel metabolism was determined by indirect calorimetry. Nicotine uptake was estimated by 24-h urinary excretion of cotinine. Lean and fat body mass as well as their respective segmental distribution (i.e. arms, trunk, legs, and head), total bone mineral content, resting energy expenditure, and fat, carbohydrate, and protein oxidation were similar between smokers and nonsmokers. In contrast, 24-h urinary cotinine excretion (72.0 +/- 11.4 vs. 0.8 +/- 0.2 mumol/L.24 h; P < 0.001), plasma glucose (4.62 +/- 0.09 vs. 4.25 +/- 0.1 mmol/L; P < 0.01), total cholesterol (4.87 +/- 0.15 vs. 4.27 +/- 0.16 mmol/L; P < 0.02), low density lipoprotein cholesterol (3.05 +/- 0.19 vs. 2.43 +/- 0.16 mmol/L; P < 0.02), and apolipoprotein B concentrations (1.09 +/- 0.11 vs. 0.83 +/- 0.03 mmol/L; P < 0.03) were all higher in smokers than in nonsmokers. In smokers, 24-h urinary cotinine excretion positively correlated with the waist to hip ratio (r = 0.58; P = 0.03) and negatively with hip circumference (r = 0.87; P < 0.001). Moreover, 24-h cotinine excretion positively correlated with fat oxidation (r = 0.57; P = 0.03), but was independent of the other metabolic parameters studied. These results suggest that the dyslipidemia and glucose intolerance observed in smokers are not related to either central obesity or the amount of nicotine inhaled, but, rather, are due to some other component in cigarette smoke. In contrast, in smokers, fat oxidation increases with increasing nicotine uptake, a fact that might account for the often observed weight gain after cessation of smoking, thus suggesting different mechanisms of action of tobacco consumption on cholesterol and glucose metabolism on one side and fat oxidation on the other.
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PMID:Impact of chronic cigarette smoking on body composition and fuel metabolism. 760 76

Nicotine abuse may cause severe nephrourologic diseases such as nephrosclerosis, hypertension and tumour of the bladder. The major factors for urinary tract diseases are hypoxaemia and cancerogenic substances. Aetiology and prophylaxis of malignant bladder tumour is discussed.
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PMID:[Adverse effects of smoking from the nephrologic viewpoint]. 770 40

The in vitro effect of nicotine (10(-7) mol l-1) on red blood cell (RBC) deformability in essential hypertension, efficacy of antihypertensive treatment (with the combination of enalapril, nifedipine and indapamid) on hypertension-induced decrease in RBC deformability and interaction between nicotine and efficacy of antihypertensive treatment were investigated in the blood samples obtained from 16 patients with untreated hypertension (UH) and 18 patients with treated hypertension (TH). Fourteen healthy subjects served as normotensive (NT) group. RBC deformability was assessed by using a gravity-driven microfiltration technique. In the UH group, the RBC deformability was found to be significantly lower than those in NT (0.623 +/- 0.06 versus 0.753 +/- 0.078, p < 0.001) and in TH (0.623 +/- 0.06 versus 0.732 +/- 0.055, p < 0.001) groups. The RBC deformability in the TH group was not significantly different than that in the NT group (0.753 +/- 0.078 versus 0.732 +/- 0.055, p > 0.05). Nicotine, in vitro, decreased deformability in the NT (0.668 +/- 0.067 versus 0.753 +/- 0.078, p > 0.0001), UH (0.509 +/- 0.052 versus 0.623 +/- 0.06, p < 0.0001) and TH (0.651 +/- 0.046 versus 0.732 +/- 0.055, p < 0.001) groups. The effect on the UH group was significantly greater than those in the NT (p < 0.0001) and TH (p < 0.0001) groups. These results suggest that nicotine and hypertension independently and cumulatively decrease the RBC deformability and nicotine inhibits the efficacy of antihypertensive treatment on RBC deformability.
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PMID:In vitro effect of nicotine on red blood cell deformability in untreated and treated essential hypertension. 770 69

We analyzed mechanisms underlying neurogenic vasodilatation in dog and Japanese monkey renal arteries. Isometric mechanical responses of the arterial strip to nerve stimulation by nicotine were recorded. Nicotine-induced contractions were abolished by hexamethonium and potentiated by NG-nitro-L-arginine, a nitric oxide synthase inhibitor. The potentiating effect was reversed by L-arginine. NG-Nitro-L-arginine did not potentiate the contraction caused by norepinephrine. The nicotine-induced contraction was reversed to a relaxation by prazosin. The relaxation was not influenced by indomethacin, timolol, or atropine but was abolished by NG-nitro-L-arginine, methylene blue (a guanylate cyclase inhibitor), oxyhemoglobin (a nitric oxide scavenger), and hexamethonium. In the strips treated with NG-nitro-L-arginine, the nicotine-induced relaxation was restored by L-arginine. Histochemical study demonstrated perivascular nerves containing NADPH diaphorase and nitric oxide synthase immunoreactivity in dog and monkey arteries. We conclude that renal arteries are innervated by nitric oxide-mediated vasodilator and adrenergic vasoconstrictor nerves, and depression of the vasodilator nerve function by nitric oxide synthase inhibition potentiates the contraction caused by adrenergic nerve excitation.
Hypertension 1995 May
PMID:Nitroxidergic innervation in dog and monkey renal arteries. 773 21

Hypertension, cigarette smoking, and nicotine augment the clinical significance of other risk factors associated with cardiovascular diseases by mechanisms which are poorly understood. Since altered trace element metabolism and antioxidant status have also been implicated in these diseases, the present study investigated the interaction of nicotine treatment and hypertension on tissue trace element concentrations and select indices of antioxidant status. Spontaneously hypertensive (SHR) and normotensive Wistar Kyoto (WKY) rats were treated with nicotine, via a time release tablet at an average rate of 75 micrograms/h for 6 weeks. Systolic blood pressure in nicotine-treated SHRs was significantly higher at weeks 3 and 6 of treatment than in the SHR-controls. Blood pressure in WKY rats was not affected by nicotine. Plasma and liver iron concentrations in the nicotine-treated SHR were higher than the SHR-controls and the WKY groups. Nicotine treatment did not affect plasma and liver zinc and copper concentrations or liver manganese (Mn) concentrations. Plasma ceruloplasmin activity was increased by nicotine treatment in the SHRs. Liver Mn superoxide dismutase (MnSOD) activities and glutathione concentrations, and liver and heart glutathione reductase activities, were higher in both groups of SHRs than in the WKY groups. Red cell SOD activity in the nicotine-treated SHR was lower than in the SHR-controls. In summary, blood pressure increased more rapidly in the nicotine-treated SHRs compared to the controls. The marked effects on antioxidant status observed were attributable more to hypertension than to the nicotine treatment.
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PMID:Comparative effects of 6-week nicotine treatment on blood pressure and components of the antioxidant system in male spontaneously hypertensive (SHR) and normotensive Wistar Kyoto (WKY) rats. 774 May 54

Epidemiological studies have shown that chronic tobacco smoking is associated with a significant increase in risks of coronary disease (chiefly myocardial infarction and sudden death), occlusive arteriopathy of the lower limbs and cerebral vascular accident. The risk is strongly augmented by the presence of other vascular risk factors such as arterial hypertension, hypercholesterolaemia, diabetes and oral contraception. Nicotine and carbon monoxide seem to play a major role in the effect of smoking on vessels. In addition to its acute haemodynamic effects, tobacco not only has an atherogenic effect (endothelial toxicity and changes in lipid profile), but it also facilitates thrombosis (by alteration of platelet functions and elevation of fibrinogen level, haematocrit level and blood viscosity) and spasm (by modification of prostaglandin metabolism and action on catecholamines). All these isolated or associated mechanisms account for clinical and evolutive manifestations or coronary or peripheral arterial lesions. The progression of female smoking partly explains the frequency of vascular pathology in young women. Recent experimental data and epidemiological studies have confirmed the responsibility of passive smoking for coronary pathology, thus justifying the measures enforced to limit the exposure of non-smokers. To cease smoking is probably the most efficient primary or secondary preventive measure, as it results in a relatively rapid decrease in the risk of complications, and notably thrombosis. No effort should be spared to obtain these results and at the same time correct other vascular risk factors.
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PMID:[Tobacco smoking and cardiovascular diseases]. 823 58


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