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

Increases in the water pressure (PW) around the trunk of the sea raven (Hemitripterus americanus Gmelin) were used to evaluate the effects of vascular compression on cardiovascular variables. Cardiac output (Vb), heart rate (fH) and blood pressures in the ventral aorta, dorsal aorta and ductus Cuvier (Pva, Pda and Pdc, respectively) were measured. A 20 cm H2O increase in PW decreased vascular conductance by up to 25%. During vascular compression, a reflex bradycardia reduced Vb and attenuated the accompanying rise in arterial blood pressure. Pretreatment of the fish with the sympathetic antagonist, propranolol, further attenuated the hypertension by accentuating the reflex bradycardia. Subsequent pretreatment with papaverine, a vascular smooth muscle poison, potentiated these effects and did not reveal any autoregulatory vasodilation in the periphery. Atropine pretreatment completely abolished the reflex bradycardia, indicating that the bradycardia resulted from increased vagal cholinergic tone. The fish also exhibited cardiovascular compensation during the 2 min vascular compression. An accommodation of the barostatic reflex (reduced vagal tone) and a sympathetic tachycardia raised Vb and passively increased vascular conductance. The set point for the barostatic bradycardia was apparently temperature-sensitive.
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PMID:Cardiovascular responses in the sea raven, Hemitripterus americanus, elicited by vascular compression. 372 76

Prophylactic ephedrine was administered to healthy parturients undergoing elective cesarean section under spinal anesthesia. The methods of ephedrine administration were as follows: intramuscular injection of 0.3 mg/kg, 15 minutes before the block (20 cases: group M), infusion of 0.02% solution immediately after the block (20 cases: group D), premedication with atropine 0.5 mg and infusion immediately after the block (20 cases: group AD). The mean ephedrine dosage was 18.8 +/- 2.2 gm (SD) in group M, 12.6 +/- 6.2 mg in group D and 5.2 +/- 0.7 mg in group AD, and there were significant differences among the three groups. The base line (a), the minimal postanesthetic (b) and the maximal postpartum systolic blood pressures (c) revealed no significant difference among the three groups, and 'b' was significantly higher than 'a' and lower than 'c' in all groups. Only one case (group M) was transiently hypotensive, while hypertension was not found in any of the subjects. One- and 5-minute Apgar scores were 8 or more in all, and umbilical acid-base values were within normal limits in all of them, though the base deficit in group AD was significantly lower than that in group M. Atropine premedication makes it possible to retrench the ephedrine dosage without any harmful effect on either mother or fetus, and ephedrine infusion makes it easy to cope with changes in maternal blood pressure. Consequently, for healthy parturients receiving elective cesarean section under spinal block, we recommend atropine premedication and minimal infusion of ephedrine immediately following the block.
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PMID:[Ephedrine administration for cesarean section under spinal anesthesia]. 381 18

The hypothesis that neurally mediated coronary vasodilation occurs as part of the carotid baroreceptor reflex was investigated. The left main coronary artery was cannulated and perfused at constant pressure (100 mm Hg) in closed-chest, chloralose-anesthetized dogs. The heart was paced at a constant rate between 60 and 70 beats/min after atrioventricular heart block. Propranolol (1 mg/kg) was given to prevent beta-receptor-mediated alterations in contractility. Aortic blood pressure was stabilized with a blood reservoir. The aortic depressor nerves were cut bilaterally to prevent the buffering influence of aortic arch baroreceptors on the carotid baroreceptor reflex. The carotid sinuses were vascularly isolated and perfused with arterial blood at controlled pressures. Under these conditions, a step change in carotid sinus pressure from 70 to 210 mm Hg produced a 0.29 ml/min per g increase in coronary flow above control and a 10 mm Hg increase in coronary sinus blood oxygen tension. A step in carotid sinus pressure from 70 to 150 mm Hg resulted in a flow increase of 0.13 ml/min per g and a coronary sinus oxygen tension increase of 5.3 mm Hg relative to prestimulation values. Atropine (0.5 mg/kg, iv) blocked most of the reflex coronary vasodilation, indicating a parasympathetic component, and the addition of adrenergic alpha-receptor blockade with phenoxybenzamine (0.25 mg/kg, ic) abolished the remaining response, demonstrating sympathetic participation. The reflex nature of the coronary response was confirmed with carotid sinus denervation and vagotomy. It is concluded that carotid sinus hypertension results in a graded reflex neural coronary vasodilation independent of myocardial metabolic factors. The major component is due to activation of parasympathetic coronary vasodilator fibers, but there is also inhibition of sympathetic vasoconstrictor fibers.
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PMID:Carotid baroreceptor reflex coronary vasodilation in the dog. 397 70

Seven days after sinoaortic denervation (SAD), mean blood pressure (MBP) and heart rate measured in conscious rats were not significantly different from sham-operated animals. A high dose of atropine, 8 mg kg-1, reduced MBP only in SAD rats. Atropine, 0.08-0.8 mg kg-1, or methylatropine, 0.8 mg kg-1, induced tachycardia in sham rats. This effect was reduced after sinoaortic denervation and it involves peripheral muscarinic receptors. The hypertension and tachycardia provoked by physostigmine were more marked in SAD than in sham rats. The cardiovascular responses induced by physostigmine were abolished by atropine and were not affected by methylatropine. The hypertension caused by physostigmine in SAD animals was more sensitive to the antagonism of atropine than in sham rats. Our results show that baroreceptor deafferentation affects peripheral parasympathetic tone to the heart and changes the cholinergic pathways involved in the modulation of cardiovascular response.
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PMID:Participation of cholinergic pathways in sinoaortic denervated rats. 399 83

Salivary flow was studied in normotensives and in subjects with hypertension. Salivary flow rate was lower in borderline hypertensives than in normotensives. Propranolol, phentolamine and noradrenaline had no influence on salivary flow. Atropine decreased this parameter. The stimulating effect of neostigmine on saliva production was more pronounced in normotensives than in borderline hypertensives. The data support the assumption that in subjects with borderline hypertension the parasympathetic influence on the salivary glands is reduced.
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PMID:Salivary flow in borderline hypertension. 399 34

Heart output, arterial pressures, and heart rate were measured directly in conscious unrestrained eels (Anguilla australis) and responses to intra-arterial injection of adrenaline monitored. Adrenaline increased systemic vascular resistance, heart output, and cardiac stroke volume in all animals. In some cases small transient decreases in stroke volume and hence heart output were seen at the peak of the pressor response: These probably reflect a passive decrease in systolic emptying due to increased afterload on the heart. In most cases, adrenaline produced tachycardia; but two animals showed consistent and profound reflex bradycardia, which was accompanied by a concomitant increase in stroke volume such that heart output was maintained or increased slightly. The interaction of changes in heart output and systemic vascular resistance produced complex and variable changes in arterial pressure. There was no consistent pattern of changes in branchial vascular resistance. Atropine treatment in vivo revealed vagal cardio-inhibitory tone in some animals and always blocked the reflex bradycardia seen during adrenaline induced hypertension. In some animals, adrenaline injection after atropine pretreatment led to the establishment of cyclic changes in arterial pressure with a period of about 1 min (Mayer waves).
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PMID:Adrenergic responses of the cardiovascular system of the eel, Anguilla australis, in vivo. 405 85

1. The effects of bradykinin (1-5 mug) injected into the cannulated lateral cerebral ventricles were studied in unanaesthetized rabbits before and after intravenous atropine, diphemanil and morphine.2. The intraventricular injections of bradykinin produced a short-lasting phase of behavioural excitation with vocalization followed by sedation. The behavioural excitation was associated with desynchronization in the electrocorticogram (e.co.g.), bradycardia and hypotension followed by tachycardia and hypertension. Tachypnoea was also observed. The subsequent phase of sedation was more prolonged and associated with synchronization of the e.co.g. and signs of catalepsy. Intense miosis was present during both phases.3. With repeated intraventricular injections of bradykinin, excitation, miosis, cardiovascular responses and tachypnoea diminished and eventually disappeared but the sedation did not exhibit tachyphylaxis.4. Atropine abolished the e.co.g. desynchronization, vocalization and bradycardia, reduced the duration of the excitatory and sedatory phase, diminished the tachycardia and hypotension, enhanced the hypertension, but did not affect the miosis and tachypnoea.5. Diphemanil affected only the cardiovascular effects produced by intraventricular bradykinin. They were affected in the same way as by atropine.6. Morphine did not affect the excitatory phase, but enhanced the cardiovascular effects produced by intraventricular bradykinin.7. The intraventricular injection of bradykinin (50 mug) caused a reduction in the amount of noradrenaline but not of 5-hydroxytryptamine (5-HT) in the brain stem; the amount of dopamine in the caudate nuclei was not affected.8. It is suggested that central cholinergic and adrenergic systems are activated by intraventricular bradykinin.
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PMID:Behavioural and somatic effects of bradykinin injected into the cerebral ventricles of unanaesthetized rabbits. 538 83

Functional tolerance was demonstrated to the antihypertensive effect of chlorisondamine Cl (Ecolid), a noncompetitive autonomic ganglion blocking agent, when administered chronically in increasing doses to spontaneously hypertensive rats (SHR), and normotensive Wistar-Kyoto (WKY) rats. Concomitant administration of atropine SO4 restored the hypotensive response to chlorisondamine without increasing its serum concentration. Atropine had no effect on the blood pressure of chlorisondamine-naive animals. No qualitative differences in therapeutic response were observed between the SHR and WKY rats. The results support the hypothesis that tolerance to the antihypertensive action of ganglionic blocking agents may be mediated by an activation of an alternate compensatory sympathetic ganglionic muscarinic pathway. It is speculated that this secondary pathway does not contribute to the hypertension in the SHR model.
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PMID:A mechanism of tolerance to the antihypertensive effect of ganglionic blocking agents in rats. 614 92

Cyclic analogs of bradykinin (CBK) and kallidin (CK) have a weak myotropic activity and a marked and prolonged hypotensive effect unlike linear bradykinin (BK) and kallidin (K) which produce a short-term hypotension and considerable contraction of rat uterus smooth muscles. Myotropic effects of BK and CK were significantly inhibited by phentolamine, methysergide, papaverine and verapamil. Atropine, diphenhydramine and propranolol have no influence on the kinin-induced myotropic responses. The prolonged decrease in blood pressure induced by CBK and CK is observed in un- and anesthetized normotensive, spontaneously hypertensive rats and rats with renovascular hypertension and is absent from anesthetized cats and guinea-pigs. This indicates the species specificity of cyclokinins. Indomethacin, diphenhydramine and methysergide failed to influence the BK- and CK-induced hypotensive effects on anesthetized rats. CaCl2 did not influence the magnitude of the hypotensive effect of BK and CK, however, it significantly shortened the duration of the CK-induced hypotensive effect. In vitro CBK and CK inhibited activity of kininase II in a similar manner (at a concentration range of 10(-5) M) but to a less extent than BK (10(-7)-10(-6) M). It is suggested that the hypotensive effect of CK is mediated at least partly via Ca2+-dependent systems and inhibition of kininase II.
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PMID:[Mechanism of action of cyclokinins]. 631 9

The purpose of this study was to investigate the nature of the serotonin-induced coronary chemoreflex in the conscious monkey. Ten chronically prepared and four acute monkeys were used in this study. Five chronically prepared animals had catheters in the left atrium, ascending aorta, descending aorta, and, bilaterally, in the common carotid arteries. In addition, Silastic catheters were placed next to both vagi to permit vagal block with 2% lidocaine. Serotonin was injected (12-200 micrograms/kg) into the left atrium, ascending aorta, descending aorta, or, bilaterally, into the carotid arteries while blood pressure, heart rate, and respiratory movements were recorded. Injections of serotonin were associated with hypertension and bradycardia followed by tachycardia, all of which were preceded by a cough response. Atropine blocked the bradycardia, whereas atropine and phentolamine eliminated the cardiovascular components of the reflex. Vagal blockade eliminated the bradycardia but otherwise did not alter the response to left atrial serotonin. Three monkeys were prepared with aortic and left atrial catheters. Subsequently, they were subjected to sinoaortic deafferentation. Serotonin injected into these animals did not alter blood pressure or respiration. The results of this study show that serotonin injected into the left atrium of the conscious monkey produces respiratory and cardiovascular alterations by its effect on aortic and carotid chemoreceptors, and that there is no coronary chemoreflex in the conscious monkey.
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PMID:Is there a serotonin-induced hypertensive coronary chemoreflex in the nonhuman primate? 640 20


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