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)

Intravenous and intracarotid injections of nicotine were delivered to cats anesthetized with pentobarbital. Low doses of nicotine were found to induce reflex hyperventilation and hypertension, mainly due to excitation of carotid body chemoreceptors. The frequency of discharge of carotid nerve chemosensory fibres was increased by nicotine in doses as low as 1 mug/kg when injected intravenously and 50 ng when injected into the carotid artery. Nicotine also activates vagal afferent fibres; some of them produce reflex excitation of the respiratory and vasomotor centres, but others provoke reflex inhibition. High doses of nicotine can act directly upon the medulla provoking acceleration or arrest of ventilation. Nicotine can also induce 'late' changes of b.p. (delay 5 sec or more) which are not mediated by the carotid or vagus nerves.
 ...
PMID:Respiratory and circulatory reflexes induced by nicotine injections: role of carotid body chemoreceptors. 126 36

Cigarette smoking is the most preventable cause of cardiovascular morbidity and mortality. Smoking has been associated with a two-to fourfold increased risk of coronary heart disease, a greater than 70% excess rate of death from coronary heart disease, and an elevated risk of sudden death. These risks are compounded in the presence of hypertension, hypercholesterolemia, glucose intolerance, and diabetes, all of which exhibit a synergistic effect with smoking. The relationship between smoking and the risk of peripheral vascular disease has also been well documented. Smokers account for approximately 70% of patients with atherosclerosis obliterans and virtually all those with thromboangiitis obliterans. An association between smoking and cerebrovascular disease remains a matter of debate, although a higher risk of stoke and stroke-related mortality has been observed in smokers than in nonsmokers. Smoking has also been implicated in the development of cor pulmonale, but a direct association with congestive heart failure has not been established. Nicotine and carbon monoxide appear to play major roles in the cardiovascular effects of smoking. Both components adversely alter the myocardial oxygen supply/demand ratio and have been shown to produce endothelial injury, leading to the development of atherosclerotic plaque. Adverse effects on the lipid profile have been noted as well, but the relationship between these changes and the risk of cardiovascular disease remains to be confirmed. Notably, smoking cessation results in a dramatic reduction in the risk of mortality from both coronary heart disease and stroke. In light of the fact that the incidence of smoking has declined primarily among educated sectors of the U.S. population, future efforts must focus on providing effective education, including smoking cessation techniques, to the less-educated groups.
 ...
PMID:Smoking and cardiovascular disease. 149 5

Smoking exacerbates the increase in arterial pressure in hypertension. The effect of nicotine on the baroreceptor-mediated reflex responses of renal nerve activity (RNA), heart rate, and respiratory activity (minute diaphragmatic activity [MDA]) after bolus injections of phenylephrine was compared in deoxycorticosterone acetate (DOCA)-salt sensitive and normotensive rats. Osmotic minipumps that dispensed either nicotine (2.4 mg/kg/day) or saline were implanted in DOCA and normotensive rats for 18 days. Anesthetized DOCA-nicotine, DOCA-saline, control-nicotine, and control-saline rats had mean arterial pressures (MAP) of 117 +/- 3, 110 +/- 9, 90 +/- 3, and 89 +/- 5 mm Hg, respectively. Nicotine decreased the sensitivity (p less than 0.05) of baroreceptor reflex control of RNA (% delta RNA/delta MAP) in the DOCA-nicotine rats (-0.92 +/- 0.08) compared with the DOCA-saline (-1.44 +/- 0.16), control-nicotine (-1.45 +/- 0.08), or control-saline (-1.45 +/- 0.21) rats. The reflex decrease in respiratory activity (% delta MDA/delta MAP x 100) was impaired (p less than 0.01) in both control-nicotine (-24.5 +/- 3.3) and DOCA-nicotine (-18.2 +/- 4.6) rats compared with control-saline (-59.2 +/- 9.1) and DOCA-saline (-52.5 +/- 9.9) rats. The reflex decrease in heart rate (absolute delta HR/delta MAP) in both DOCA-nicotine (1.56 +/- 0.17) and control-nicotine (1.54 +/- 0.24) rats was augmented compared with DOCA-saline and control-saline rats (0.91 +/- 0.12 and 0.97 +/- 0.14).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Feb
PMID:Nicotine impairs reflex renal nerve and respiratory activity in deoxycorticosterone acetate-salt rats. 199 50

We wished to determine if nicotine exaggerates the blood pressure increase in deoxycorticosterone (DOCA)-salt hypertension. Uninephrectomized, male Sprague-Dawley rats were implanted with DOCA pellets (75 mg) and placed on a 5.2% salt diet for sixteen days and then infused with nicotine (DOCA-Nicotine; 2.4 mg/kg/day) or vehicle (DOCA-Sham). Control animals were treated with vehicle (Control) or nicotine (Control-Nicotine). The DOCA-Nicotine group had significantly greater tail-cuff blood pressures than the DOCA-Sham group by one week of nicotine infusion. At 2.5 weeks of nicotine infusion the DOCA-Nicotine rats had significantly greater tail-cuff blood pressures, direct arterial blood pressures, and cardiac outputs compared to the DOCA-Sham animals. Renal blood flows were similar in the two groups. Control-Nicotine animals demonstrated no response to nicotine during 2.5 weeks of infusion. We conclude that in the DOCA-salt rat nicotine induces an exaggerated rise in blood pressure and that the mechanism involves an increase in cardiac output.
 ...
PMID:Cardiac output and the blood pressure increase in deoxycorticosterone acetate-salt hypertension after nicotine infusion. 202 74

Cigarette smoking is associated with an increased risk and extent of advanced atherosclerotic vascular disease in peripheral as well as coronary arteries. The likelihood of claudication, amputation, stroke, abdominal aortic aneurysm, and failure of vascular reconstruction is higher in smokers than nonsmokers. Smoking exerts its deleterious effects through many interactive mechanisms. Nicotine and carbon monoxide produce acute cardiovascular consequences, including altered myocardial performance, tachycardia, hypertension, and vasoconstriction. Smoking injures blood vessel walls by damaging endothelial cells, thus increasing permeability to lipids and other blood components. Among metabolic and biochemical changes induced by smoking are elevated plasma, free fatty acids, elevated vasopressin, and a thrombogenic balance of prostacyclin and thromboxane A2. Chronic smoking is associated with a tendency for increased serum cholesterol, reduced high density lipoprotein, and other lipid effects that contribute to atherosclerosis. In addition to rheologic and hematologic changes from increased erythrocytes, leukocytes, and fibrinogen, smokers have alterations in platelet aggregation and survival that produce thrombosis. Considering the ubiquitous repercussions of this menace, vascular surgeons should play an active role in motivating their patients to quit smoking.
 ...
PMID:The peripheral vascular consequences of smoking. 206 25

Nicotine poisoning is a rarely reported toxicosis. The clinical signs and symptoms are complex and are mostly of central nervous system derangement. In addition, animals may have hypersalivation, vomiting, diarrhea, tachycardia, tachypnea, hypertension and hyperthermia. Some animals are presented in total collapse with slow and shallow respirations, hypotension, dilated pupils, and a weak, rapid and irregular pulse. Treatment is directed toward removing the unabsorbed poison and diluting, and counteracting or controlling the animal's signs. This report emphasises the comparative ease with which a dog would readily ingest chewing tobacco, which is sweet in taste, and come down with nicotine poisoning, as compared to cigarette tobacco which is nonpalatable and therefore less of a threat. The report further discusses clinical nicotine toxicosis, its incidence, clinical manifestations, diagnosis, prognosis and treatment.
 ...
PMID:Nicotine poisoning in a dog. 226 69

To investigate the mechanisms of action of nicotine we studied the effect of muscarinic and adrenergic receptor antagonists on nicotine-induced changes in the lungs and circulation. Nicotine increased mucus secretion from tracheal submucosal glands and caused bronchocon-striction. Cardiovascular effects were a bradycardia followed by tachycardia, hypertension and a biphasic increase in cardiac output. All of these effects were completely blocked by prior administration of hexamethonium. Propranolol and phentolamine prevented the increase in heart rate, and reduced the increase in blood pressure. Only atropine inhibited nicotine-induced hypersecretion and bronchocon-striction.
 ...
PMID:[Effect of repeated nicotine administration on mucus secretion, bronchodilation and circulatory variables: inhibitory effect of autonomic antagonists]. 236 68

This case-control study assessed the relation of cigarette smoking during pregnancy to the risk of preeclampsia and gestational hypertension. All subjects were primiparous women without a history of high blood pressure who gave birth in Quebec City or Montreal, Canada, hospitals between 1984 and 1986. Cases (172 women with preeclampsia and 251 with gestational hypertension) and 505 controls were interviewed at the hospital after delivery. Adjusted relative risks were estimated by polychotomous logistic regression. Compared with women who had never smoked, women who were smokers at the onset of pregnancy had a reduced risk of preeclampsia (relative risk = 0.51, 95% confidence interval 0.34-0.77). Relative risks of preeclampsia decreased with increases in the number of cigarettes smoked daily at the onset of pregnancy: Relative risks among smokers of less than 11, 11-20, and more than 20 cigarettes per day were 0.79, 0.56, and 0.38, respectively (test for trend: p = 0.0002). The protective effect of smoking on preeclampsia was stronger for women who continued to smoke after 20 weeks of pregnancy. While smoking tended to reduce the risk of gestational hypertension, this effect was less evident than that for preeclampsia. Relative risks varied little with severity of disease as based on gestational age at the onset of hypertension, maximal blood pressure and, for preeclampsia, amount of proteinuria. The reduction in mean birth weight attributable to smoking during pregnancy was similar among cases and controls. Nicotine inhibition of thromboxane A2 production might explain the decreased risk of pregnancy-induced hypertension among smokers. Despite these findings, the harmful consequences of smoking on pregnancy outcome outweigh its protective effect against pregnancy-induced hypertension.
 ...
PMID:The effect of cigarette smoking on the risk of preeclampsia and gestational hypertension. 281 2

Nicotine administration, using mini-osmotic pumps, to male guinea pigs (31 micrograms/h for 10 days) resulted in a significant elevation of plasma epinephrine and enkephalin-like peptides but not norepinephrine. The increase in plasma epinephrine and enkephalin-like peptides was not accompanied by corresponding alterations in either adrenal medullary synthesis or blood pressure and heart rate. These findings may provide a partial explanation for the observation that chronic smoking does not induce hypertension.
 ...
PMID:Plasma enkephalin-like peptide response to chronic nicotine infusion in guinea pig. 356 35

We recently reported that the vagal cardiopulmonary baroreceptor reflex inhibition of renal nerve traffic is impaired in rabbits with renal hypertension. The purpose of this study was to determine if the locus of the abnormality is mainly in the brain or in the afferent limb of the reflex. Experiments were done in alpha-chloralose-anesthetized rabbits with (n = 10) or without (n = 10) hypertension induced 6 to 8 weeks before study by wrapping the left kidney in cellophane followed by removal of the right kidney. The left side of the chest was opened, and a pericardial cradle was made. Nicotine was applied to the epicardial surface of the heart in concentrations of 10 to 500 micrograms/ml, and changes in arterial pressure and renal nerve traffic were measured. Dose-dependent decreases in traffic and arterial pressure resulted that were significantly smaller in hypertensive than in normotensive rabbits. After sinoaortic baroreceptor denervation, a similar impairment in the responses of hypertensive rabbits was observed. Vagotomy nearly abolished the responses of the renal nerves to epicardial nicotine. The responses of the lumbar sympathetic nerves to epicardial nicotine also were impaired in renal hypertensive (n = 8) compared with normotensive rabbits (n = 8). If the behavior and number of chemically sensitive endings are assumed to be unaltered in hypertension, then these findings are explained best by an abnormality in the central nervous system. These results support the view that the previously reported impairment in the vagal cardiopulmonary baroreceptor reflex control of renal nerve traffic is due mainly to a central abnormality, although they do not exclude an abnormality in the afferent limb of the reflex.
Hypertension 1987 May
PMID:Impaired responses of sympathetic nerves to cardiac receptor stimulation in hypertension. 357 Apr 23


1 2 3 4 5 6 7 Next >>