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

1 The effect of drugs acting on beta-adrenoceptors on the absorption and excretion of paracetamol was studied in 26 volunteers and nine patients with mild hypertension, each subject acting as his/her own control. 2 Isoprenaline given 30 min before paracetamol significantly slowed absorption, the effect being dose related, and blocked by prior administration of propranolol. 3 When isoprenaline was given immediately before the paracetamol, absorption was not altered, although a cardiovascular response was seen. 4 Oral salbutamol also delayed paracetamol absorption. 5 Propranolol given alone increased the rate of paracetamol absorption. 6 These results with the changes in the rate of gastric emptying produced by these agents.
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PMID:The effect on paracetamol absorption of stimulation and blockade of beta-adrenoceptors. 625 20

In young subjects with normal blood pressure (N = 10) or with mild (n = 6) or moderate (n = 8) hypertension we assessed the effects of increasing doses of i.v. isoproterenol (each dose for 10 min) on systolic and diastolic blood pressure, heart rate, plasma renin activity (PRA), serum potassium and free fatty acids (FFA). Except for blood pressure, basal levels did not differ significantly between the groups. Isoproterenol induced dose-related increases in systolic blood pressure, heart rate and PRA, and dose-related decreases in diastolic blood pressure. Neither the threshold dose (i.e. the lowest dose significantly affecting these parameters), nor the changes induced by the higher doses differed between the normotensive and hypertensive subjects. Levels of serum potassium and FFA, obtained at the end of the infusion, also did not differ significantly between the groups. These results indicate, that in contrast to older and/or more severely hypertensive subjects, young subjects with mild to moderate hypertension have a peripheral beta-adrenoceptor responsiveness similar to that of normotensive controls.
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PMID:Peripheral beta-adrenoceptor responsiveness in young normotensive and hypertensive subjects. 626 69

Our previous studies, in vivo and in vitro, have shown reduced inotropic responsiveness to isoproterenol of hypertrophied hearts in renovascular hypertensive rats. In the present study, we have investigated, in the same model, the effects of treatment either by nephrectomy or captopril on the inotropic responsiveness to isoproterenol and on the number and affinity of ventricular beta-receptors. Isoproterenol infusion of isolated hearts from renovascular hypertensive rats 12-18 weeks post-clipping produced lower inotropic responses (delta peak dP/dt) than age-matched sham-operated normotensive rats (P less than 0.001). Quantitative assessment of beta-adrenergic receptors in the same hearts showed a significant decrease in renovascular hypertensive rats ventricular receptor numbers, whether calculated per milligram membrane protein (22.3 +/- 2.66 fmol/mg vs. 37.9 +/- 4.34, P less than 0.005) or per gram wet ventricular weight (1.43 +/- 0.14 pmol/g vs. 2.2 +/- 0.21, P less than 0.005), with no significant change in Kd. Control of hypertension by either nephrectomy or captopril led to regression of hypertrophy 6 weeks after stabilization of blood pressure (12-18 weeks post-clipping) and returned both the ventricular receptor density and inotropic responsiveness toward normal. The improvement in inotropic responsiveness to isoproterenol in regressed hearts correlated with both the reduction in ventricular weight and the decrease of blood pressure. Regression of hypertrophy did not alter the relationship between inotropic response, receptor density, and ventricular weight. These results indicate that the increase in cardiac mass associated with renovascular hypertension may interfere with adrenergic support to the heart, and that proper control of hypertension and regression of hypertrophy could reverse that impairment and restore its responsiveness to adrenergic stimulation.
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PMID:Reversal of changes in myocardial beta-receptors and inotropic responsiveness with regression of cardiac hypertrophy in renal hypertensive rats (RHR). 631 41

These studies were undertaken to clarify the role of the central and peripheral sympathetic nervous system and the renin-aldosterone system on the onset and maintenance of high blood pressure in essential hypertension (EH), and the following examinations were performed: 1) Urinary free norepinephrine and epinephrine excretion (UNEf and UEf), urinary conjugated norepinephrine and epinephrine excretion (UNEconj and UEconj), plasma norepinephrine and epinephrine concentration (PNE and PE), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were measured in 52 patients with EH, who were divided into two groups (borderline EH: b-EH, and sustained EH: s-EH), and fifteen normals (N). 2) Cardiac index (CI), total peripheral resistance index (TPRI), appearance time, mean transit time and stroke index (SI) were determined by the dye-dilution method in eight patients with b-EH, ten patients with s-EH and ten N. 3) Clonidine was administered orally in a single dose of 150 micrograms to seven patients with s-EH and three patients with b-EH, and PNE, PE and growth hormone (GH) were measured before and after the administration. 4) Isoproterenol was infused intravenously in a dose of 0.02 microgram/kg/min for 30 min to 18 patients with s-EH and six N, then plasma cyclic AMP (c-AMP) and PRA were determined before, during and after the infusion. 5) Methacholine was injected intramuscularly in a dose of 10 mg to seven N, and PNE, PE and PRA were measured before and after the injection. There were no significant differences of PNE, PE, UNEf and UEf among the three groups (b-EH, s-EH and N), but UNEconj in both b-EH and s-EH was higher than in N (b-EH: p less than 0.1, s-EH: p less than 0.05). PRA in s-EH was slightly lower not only in N but also in b-EH. PAC in b-EH and s-EH was slightly lower than in N. The difference of PAC between b-EH and s-EH was not found. CI and SI were higher than in N (p less than 0.05), but TPRI was normal. In s-EH, TPRI was slightly elevated as compared with b-EH (p less than 0.1). In s-EH, clonidine caused a significant lowering of both blood pressure and PNE with a simultaneously marked increment of GH; on the other hand, in b-EH blood pressure and PNE did not change significantly in spite of the distinct rise of GH. After the isoproterenol infusion, PRA and c-AMP increased, and there was a significant correlation between the initial level of PRA and the maximal increment of PRA after the infusion in both s-EH and N.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Studies on the role of the central and peripheral sympathetic nervous system and the renin-aldosterone system on the onset and maintenance of high blood pressure in essential hypertension]. 632 58

A model in which partial ligation of the left external iliac artery results in a decrease in mean arterial blood pressure to the ipsilateral femoral artery (70 mmHg; protected) while mean pressure increases in the contralateral femoral artery (125 mmHg; unprotected) was used to determine the effect of high blood pressure stress on vascular adrenergic responsiveness. Age-matched (5 week old) male Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) were used in the study. Partial ligation was performed at 6 weeks of age and vascular reactivity studies undertaken at 10 weeks of age when the SHR were considered hypertensive (indirect systolic blood pressure greater than 150 mmHg). Force-tension analysis of femoral arterial rings revealed that all tissues contracted maximally at 1.0 gram of preload force. This value was used in subsequent studies on adrenergic responsiveness. Isoproterenol-induced relaxation was significantly attenuated in rings of vascular smooth muscle from unprotected femoral arteries of the SHR, however, the response of rings from protected arteries of the SHR was similar to that of the protected and unprotected arteries of the WKY animal. Unprotected arteries of the SHR exhibited a greater response to norepinephrine stimulation when compared to protected arteries of the SHR as well as unprotected and protected arteries of the WKY animal. This study suggests that alterations in vascular alpha- and beta-adrenergic responsiveness in the SHR are most probably due to the increase in blood pressure.
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PMID:Effect of high blood pressure stress on vascular adrenergic responsiveness in the spontaneously hypertensive rat. 646 41

The influence of isoproterenol, norepinephrine, and dopamine on the cardiomoderator effects of moderate vagal stimulation was studied in anesthetized dogs. The drugs were administered at increasing doses in successive perfusions. Stimulation of the vagus nerve, the parameters of which remained constant throughout each experiment, was performed immediately before each sequence of perfusion and after 10-min perfusion. Isoproterenol at 0.025, 0.05, 0.1, and 0.2 microgram X kg-1 X min-1 raised heart rate dose relatedly but did not alter heart rate under vagal stimulation. Thus the amplitude of vagal bradycardic effects increased dose relatedly. Norepinephrine at 0.125, 0.25, 0.5, and 1 microgram X kg-1 X min-1 lowered heart rate through reflex hypertension. Heart rate under vagal stimulation remained constant. Thus the effects of vagal stimulation decreased as dose increased, finally becoming null. Dopamine at 0.5, 1, 2.5, and 5 micrograms X kg-1 X min-1 did not significantly alter heart rate, but at 10 and 20 micrograms X kg-1 X min-1, like norepinephrine, it raised blood pressure, causing a reflex fall in heart rate. At all doses, heart rate under vagal stimulation remained stable. Consequently, at the highest doses, the net effects of vagal stimulation were slight. These results suggest the simultaneous involvement of sympathetic-parasympathetic interactions both post- and prejunctionally. In the latter case, different mechanisms of regulation of neurotransmitter release are involved during vagal stimulation according to the sympathomimetic used. With isoproterenol, norepinephrine release seems more particularly affected, whereas with norepinephrine and dopamine, acetylcholine release is apparently inhibited.
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PMID:Effects of catecholamines on cardiac chronotropic response to vagal stimulation in the dog. 663 96

Male and female, normotensive, Sprague-Dawley (S-D) rats, and spontaneously hypertensive rats (SHR) were subjected to acute and massive myocardial infarction with isoproterenol. Some of the animals were pre-treated (7 days) with the prolactin-lowering drug, bromocryptine. SHR survived in greater numbers than S-D but developed massive congestive heart failure of late onset. The adrenal glands and hearts became greatly hypertrophied in parallel with severely involuted thymus glands. ECG tracings demonstrated intense tachycardia and myocardial ischaemia. Bromocryptine reduction of prolactin (PRL) showed no effect on ECG tracings but reduced triglyceride, free fatty acid, total cholesterol and glucose levels. Isoproterenol caused dynamic increase in glucose, free fatty acids and triglycerides. CPK levels demonstrated greater cardiac damage in S-D vs SHR; greatly elevated SGOT and SGPT levels confirmed the presence of fatty liver in S-D and SHR. Myocardial infarction caused marked increase in circulating PRL in females only and sustained increases in aldosterone and corticosterone. SHR survivors had a high incidence of atrial and ventricular thrombi, left ventricular aneurysms, and intense fibroplasia and cartilaginous metaplasia in areas adjacent to damaged myocardium. It is suggested that adrenal steroidogenesis during an acute myocardial infarct favours survival and more complete myocardial repair in females vs males, and preexisting hypertension in SHR is associated with hormonal and metabolic response patterns different from normotensive S-D rats.
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PMID:Hormonal and metabolic changes during acute myocardial infarction in normotensive vs hypertensive rats. 684 10

1 Labetalol at a dose of 800 to 1600 mg daily inhibited isoprenaline-induced tachycardia and phenylephrine-induced elevation in arterial pressure in hypertensive subjects. The beta-adrenoreceptor effect was four times more potent than the alpha-adrenoreceptor effect. 2 Isoprenaline-induced tachycardia was more effectively blocked than isoprenaline-induced inotropism, thereby raising the possibility of a subselective effect on cardiac beta-adrenoceptors. 3 Labetalol reduced blood pressure in hypertensive subjects with no change in cardiac output in the supine or upright position and with marked inhibition of the heart rate and blood pressure response to treadmill exercise. 4 Labetalol administered in single doses to patients with stable, treated congestive heart failure impaired blood pressure support during exercise. 5 The unique adrenoceptor and haemodynamic effects of labetalol make it a potentially attractive drug for management of hypertension and other cardiovascular disorders.
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PMID:A review of the haemodynamic effects of labetalol in man. 709 99

1. Whole body trans-section at the level of the first or second lumbar vertebra of stress-susceptible or normal Poland China swine provided a preparation of isolated perfused caudal muscle that was without nervous or hormonal influences. Metabolic responses to halothane anaesthesia were exaggerated in the susceptible preparation. 2. Carbachol (10(-4) M) increased O2 consumption threefold and elevated blood lactate levels from 3 to 8 mumole/ml. in susceptible but not in normal muscle preparations. 3. Isoprenaline in a continuous infusion (2.5 micrograms/kg caudal wt. per min for 12 min, subsequently diminished to 1.2 microgram/kg per min) did not increase O2 consumption of susceptible or normal muscle but did increase blood lactate by 2 mumole/ml. in both. 4. Simultaneous administration of carbachol and isoprenaline resulted in additive increases in blood lactate. 5. Incremental increases in temperature above 41 degrees C initiated exaggerated increases in O2 consumption and blood lactate in susceptible but not normal muscle; these were similar to whole body responses. 6. Phenylephrine (0.2-25 micrograms/kg per min continuous) produced (i) hypertension, (ii) no observed effects upon aerobic or anaerobic metabolism and (iii) progressive tissue oedema; these effects were similar in susceptible and normal muscle. 7. Skeletal muscle from stress-susceptible swine is evidently inherently capable of metabolic responses to cholinergic agonists and increased temperature; these responses are greater than those in normal muscle. This suggests that initiation of stress responses in intact swine is related to somatic motor and sympathetic stimulation of abnormal skeletal muscle, and not to a disorder of the somatic or sympathetic nervous system.
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PMID:Porcine muscle responses to carbachol, alpha- and beta-adrenoceptor agonists, halothane or hyperthermia. 720 67

1. Using the electromagnetic flow probe and the radioactive microsphere technique, systemic and regional haemodynamic variables were measured in conscious normotensive and hypertensive rabbits. The rabbits were made hypertensive by unilateral nephrectomy combined with cellophane-wrapping of the remaining kidney and systemic and regional haemodynamic effects of isoprenaline infusions (0.5 micrograms.kg-1 .min-1) were compared in the two groups of animals. 2. Isoprenaline evoked increases in heart rate and cardiac index while the total peripheral resistance decreased. In the hypertensive rabbits the effects were similar, except for a significantly more pronounced decrease in blood pressure. 3. Isoprenaline increased the fraction of the cardiac output delivered to the heart, skin and fat, at the expense of the fractions to the brain, stomach, small intestine, pancreas, liver and kidney(s) in both normotensive and hypertensive animals. Local peripheral resistance was decreased, most prominently, in the heart, skin, skeletal muscle and fat. 4. In the normotensive rabbits pretreatment with propranolol (4 mg.kg-1 infused in 1 h) effectively blocked the cardiovascular responses following isoprenaline infusion. 4. Since the systemic and regional haemodynamic effects of isoprenaline were not less (if anything, slightly more) in the hypertensive than in the normotensive rabbits, our results provide no evidence for subsensitivity of beta-adrenoceptors as a contributory factor in the development of hypertension in this model.
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PMID:Systemic and regional haemodynamic responses to isoprenaline in conscious renal hypertensive rabbits. 724 10


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