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)

Beta-Blockers are used in pregnancy-associated hypertension and in postnatal cardiac arrhythmias, and the neonate may get them in breast milk. We therefore studied the effects of beta-adrenergic medication on interrelations between heart rate (HR), respiration, and arterial blood pressure (aBP) in newborn lambs. The influence of sleep state on these cardiorespiratory interrelations was also examined. HR, aBP, and respiration (based on transthoracic electrical impedance) were recorded and the sleep state was visually documented in five healthy chronically instrumented newborn lambs before the age of 30 d. Propranolol was given (1 mg/kg). Two-min stationary segments of the three signals were analyzed using a multivariate autoregressive model, which yields oscillations of the signals and intersignal relationships as source contributions. The variabilities of aBP and HR were greatest at the low frequencies (less than 0.25 Hz) and so were their intersignal relationships (including baroreflex). The respiratory variability was greatest at the frequencies corresponding to the respiratory rate. During quiet sleep, the variabilities in HR, aBP, and respiration were lowest. The impact of respiratory oscillations on other signals increased but the impact of aBP variability decreased during quiet sleep. beta-Blockade and sleep state affected separately the cardiovascular and respiratory variables and their interrelations. beta-Blockade reduced HR and increased pulse pressure. The overall heart rate variability and the respiratory low-frequency contribution to heart rate variability decreased due to the beta-blockade. We postulate that the beta-adrenergic system is an important regulator of HR and HR variability in neonatal lambs and also of the low-frequency components of the respiratory sinus arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Do beta-adrenergic blockade and sleep state affect cardiorespiratory control in neonatal lambs? Multivariate autoregressive modeling approach. 203 75

Certain decerebrate lesions of brain stem or hypothalamus induce pharmacologically reversible hypertension and hyperthermia in animals. We observed three young patients with episodic decerebration, hyperthermia, hypertension, and hyperventilation during recovery from comas of different etiologies. The shared pathology on neurologic examinations and computed tomographic scans was hypothalamic-mesencephalic dysfunction, suggesting a diencephalic-brain-stem disconnection syndrome or brain-stem release mechanism. Propranolol was the most effective drug tested, but only two patients responded, one dramatically. This novel clinical syndrome may have localizing and therapeutic significance in pediatric coma that needs to be further defined in future studies.
 ...
PMID:Hypothalamic-midbrain dysregulation syndrome: hypertension, hyperthermia, hyperventilation, and decerebration. 155 45

Forty-seven male patients with mild essential hypertension were randomly allocated to three subgroups. After a run-in period of 4 weeks, the first subgroup (n = 16) received propranolol (80 mg/day) for 36 weeks followed by a placebo period of 4 weeks. The second subgroup (n = 15), after a run-in period of 4 weeks, was given a supplement of encapsulated fish oil (9 g/day) for 36 weeks with a subsequent period of 4 weeks in which fish oil placebo was given. The third subgroup (n = 16), after a run-in period of 4 weeks, was given propranolol (80 mg/day) for 12 weeks, propranolol (80 mg/day) plus fish oil capsules (9 g/day equivalent to 1.8 g/day of eicosapentaenoic acid and 1.1 g/day of docosahexaenoic acid) for 12 weeks, propranolol plus fish oil placebo (same doses for 12 weeks) with a subsequent period of 4 weeks when propranolol placebo was administered. The results indicate a blood pressure-lowering effect of fish oil, which was comparable with that of propranolol. The simultaneous intake of fish oil plus propranolol was more effective than propranolol or fish oil alone. Propranolol treatment resulted in a decrease of plasma norepinephrine, plasma renin activity, and thromboxane B2 formation. After fish oil supplementation, plasma norepinephrine and thromboxane B2 formation were likewise reduced, whereas plasma renin activity appeared increased. The decrease of serum triglycerides, total and low density lipoprotein cholesterol as well as the rise of high density lipoprotein cholesterol are concomitant beneficial effects, which justify the consideration of fish oil alone or in combination with antihypertensive drugs for the treatment of mild hypertension.
Hypertension 1990 Dec
PMID:Fish oil amplifies the effect of propranolol in mild essential hypertension. 214 75

Low-caloric diet is one of the non-pharmacological methods of treatment of hypertension. The study was performed to assess the efficacy of such a regimen in overweight patients with hypertension. 30 patients (17 female, 13 male mean age 46 +/- 7.23) were studied. They were divided into two groups each consisting of 15 patients. The first group was treated with a low-caloric diet (1000-1100 kcal per day), the second with propranolol 120 mg daily. At the beginning and at the end of the treatment clinical and echocardiographic investigations were performed. In the patients treated by a low-caloric diet blood pressure and left ventricular hypertrophy significantly decreased. Propranolol treatment lowered blood pressure but did not reduce left ventricular hypertrophy.
 ...
PMID:[The effect of a low caloric diet on blood pressure and left ventricular hypertrophy in overweight hypertensive patients]. 215 82

Left ventricular hypertrophy is an adaptation of the cardiac fibre to the imposed mechanical overload. This adaptation is quantitative; increased numbers of contractile units with decreased wall stress. Qualitative changes in genomic expression allow the hypertrophied cardiac fibre to develop a normal active tension at the expense of its maximal shortening velocity. These changes are preceded by the temporary expression of proto-oncogenes, of genes of the proteins of thermal shock and by reorganisation of the cytoskeleton, all possible candidates of the regulation of the gene expression in cardiac hypertrophy. In the long-term, the hypertrophy becomes harmful: inadequate subendocardial vascular development; the lowering of the Vmax is beneficial at cellular level but eventually affects cardiac output; ventricular compliance decreases with the development of fibrosis; changes in calcium metabolism are arrhythmogenic. Modifying, prolonging and improving the natural process of adaptation is clearly the first therapeutic objective in order to decrease the hypertension and cause the hypertrophy to regress. Propranolol acts by reducing the cardiac work load. However, betablockers have the disadvantage of increasing the relative density of the subendocardial collagen. Rilmenidine decreases the quantity and density of the collagen. Vasodilators and diuretics induce regression of the myocytic hypertrophy by lowering the threshold of adaptation of these cells, but they have no effect on collagen synthesis. Angiotensin converting enzyme inhibitors which have been shown to be beneficial in controlling hypertension, induce a decrease in the hypertrophy of the myocytes and reduce fibrosis.
 ...
PMID:[Remission of left ventricular hypertrophy of hypertensive origin. Experimental data]. 215 Apr 72

The effect of the selective 5-HT2 agonist (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI) on arterial pressure (AP), heart rate (HR), renal blood flow (RBF) and plasma renin activity (PRA) was determined in conscious rats. DOI increased AP and PRA, but decreased HR and RBF. All responses to DOI were abolished by central (LY 53857) or peripheral (xylamidine) 5-HT2 antagonists. Prazosin did not alter the AP or HR response to DOI. Chlorisondamine abolished the bradycardia but slightly increased the hypertension produced by DOI, while enalapril attenuated the pressor response. No further reduction was produced by the combination of enalapril and prazosin. Propranolol attenuated but did not eliminate the renin response, and blocked the bradycardia elicited by DOI. The data suggest that DOI activates 5-HT2 receptors located on vascular smooth muscle and/or the circumventricular organs of the brain to: (1) increase AP and reflexly decrease HR, (2) decrease RBF and (3) increase PRA. The hypertension is mediated by angiotensin II and direct vascular effects whereas the increase in PRA is mediated by an interaction of increased sympathetic nerve activity and decreased renal perfusion pressure.
 ...
PMID:Hemodynamic and renin responses to (+-)-DOI, a selective 5-HT2 receptor agonist, in conscious rats. 218 26

These studies were undertaken to examine the contribution of central nervous system mechanisms to the cardiovascular and sympathoadrenal effects of cocaine. Changes in systolic and diastolic blood pressure, heart rate and plasma catecholamine concentrations were determined in response to cocaine injected i.a. or i.c.v. in conscious unrestrained rats. Systemically administered cocaine produced brisk, transient dose-related increases in systolic and diastolic pressure at doses of 0.05 to 5 mg/kg i.a. Plasma catecholamine concentrations increased in a dose-related manner, reaching peak levels at 5 to 10 min after i.a. cocaine injection. Only the higher doses of cocaine induced reflex vagal bradycardia that was blocked by atropine (0.4 mg/kg i.a.). Propranolol (1 mg/kg i.a.) prolonged the duration of cocaine-induced hypertension and bradycardia. Ganglionic blockade with chlorisondamine (7.5 mg/kg i.a.) antagonized completely the cardiovascular and sympathoadrenal effects of cocaine, indicating that intact ganglionic transmission is required for full expression of the autonomic responses. Antagonist drugs selective for the D-1 or D-2 dopamine receptors attenuated effects of cocaine on plasma catecholamine concentrations but not on cardiovascular parameters. Intracerebroventricular injection of cocaine (50-250 micrograms) increased systolic pressure and plasma catecholamine concentrations, providing direct evidence for an action of cocaine in the central nervous system. These results demonstrate that cocaine acts centrally to increase sympathetic outflow leading to hypertension and reflex bradycardia in conscious rats.
 ...
PMID:Role of the central nervous system in hemodynamic and sympathoadrenal responses to cocaine in rats. 221 51

The powdered bark of Maquira sclerophylla is consumed as snuff in north Brazil. Both the crude and the purified hydrosoluble extract (WP) injected i.p. in the dose range of 0.05-0.5 g/kg induced hyperexcitability, tremors, motor incoordination, ataxia, quietness and muscle relaxation in rats. The effects were progressive, dose-related and reversed after 30 min. Anesthetized rats, guinea-pigs and dogs injected with the purified extract (10-50 mg/kg, i.v.) showed a biphasic change of carotid blood pressure. The early and transient hypotension was blocked by atropine but not by vagotomy: the secondary hypertension was long lasting and sustained for over 30 min. The hypertension was shortened but not blocked after ganglionic blockade or reserpine treatment. Either pithing or alpha receptor blockade with yohimbine reduced both effects of the extract. Guinea-pigs and dogs were more responsive than rats and died by heart arrest. Incubation of WP (20 micrograms/ml) increased both the rate and force of contraction of isolated guinea-pig right atria by 2 and 5 times, respectively. Propranolol (4 micrograms/ml) blocked the chronotropic effect but did not decrease the inotropic effect. In electrically driven guinea-pig left atria, WP (10 micrograms/ml) increased the force of contraction by 80% and the maximum rate of force development by 60%, but did not change the time to peak tension, the time to 50% relaxation, or the rate of relaxation. These cardiovascular effects resemble those of digitalis-like drugs. Cardenolides were detected in WP by phytochemical screening.
 ...
PMID:Pharmacology of an Indian-snuff obtained from Amazonian Maquira sclerophylla. 221 23

This was a prospective, randomized, double-blind, placebo-controlled trial to establish whether beta blockers or calcium-channel blockers limit exercise capacity and training responses in men with mild hypertension. Circuit weight and aerobic training was used to assess the effects of drugs on cardiovascular fitness and muscle strength. Fifty-two sedentary men, ages 25-59 yr, with a diastolic blood pressure of 90-105 mm Hg off drugs, without significant ST depression during maximal stress testing, received diltiazem, propranolol, or placebo. Maximal oxygen uptake (VO2max) and exercise duration during treadmill testing, as well as one-repetition maximal strength, were assessed on eight weight machines after a single-blind placebo baseline, after 2 wk of drug run-in, and after 10 wk of exercise training. Total daily doses were 240 mg for propranolol and 360 mg for diltiazem. Propranolol decreased VO2max after drug run-in (P less than 0.05). Exercise training increased VO2max (P less than 0.05) in the diltiazem and placebo groups. After training VO2max in the propranolol group increased (P less than 0.05) from run-in but not beyond baseline levels. Thus, the reduction of VO2max consequent to propranolol therapy limited the overall benefits of training. Exercise duration did not change with run-in and increased (P less than 0.05) with training by 22%, 19%, and 10% for the diltiazem, placebo, and propranolol groups, respectively. Strength after run-in was unchanged, and exercise training increased strength (P less than 0.0001) on all weight machines in all groups. The results show an advantage of diltiazem to propranolol, particularly among physically active patients engaged in aerobic exercise who require antihypertensive therapy.
 ...
PMID:Effects of diltiazem or propranolol during exercise training of hypertensive men. 235 13

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


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