Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Dibutyryl cyclic AMP (Db cAMP, 75-500 microgram/kg), injected into the lateral ventricle of the brain of the cat increased blood pressure, heart rate and splanchnic discharge rate. 2. ATP, but not AMP, induced similar changes; GMP in small doses increased blood pressure. 3. A number of drugs are known to activate adenylate cyclase-induced hypertension, tachycardia and increase splanchnic discharge rate. This was shown for TRH, tetracosactide and a new beta2-adrenoceptor stimulant, NAB 365. 4. Injection into the lateral ventricle of theophylline or Ro 7/2956, both inhibitors of phosphodiesterase, similarly increased blood pressure. 5. Histamine administered by the same route induced similar reactions; it is not known if this action was exerted by activation of H1- or H2-receptors. 6. Somatostatin, known to reduce cAMP levels, induced a small but significant decrease in blood pressure. Melanocyte stimulating hormone release inhibiting factor (MIF) and TSH were ineffective. 7. These results provide evidence for the possibility of a role for cAMP in the central regulation of blood pressure at suprabulbar levels.
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PMID:Cyclic 3'5'-adenosine monophosphate and central circulatory control in cats and dogs. 2 Feb 56

Central activity, antihypertensive action and antiulcerogenic actions of Neurotropin (NSP), an extract isolated from vaccinia virus-innoculated skin or tissues of rabbits were investigated herein. When actions of NSP were examined in isolated muscle preparations by the Magnus-method, peristalsis and ACh-induced contraction in the small intestine isolated from crayfish were not influenced, peristalsis and ACh-induced contraction in the small intestine from mice were slightly accelerated, but adrenaline-induced relaxation in the small intestine from mice was not affected. Histamine-induced contraction in the small intestine and tracheal muscles isolated from guinea pigs was antagonized slightly, or not at all by NSP in a high concentration. NSP had no direct action nor anti-ACh action on abdominal muscles from frogs. NSP had no influence on E1-mice-convulsions. Both spontaneous motor activities and exploratory movements in mice were depressed. Sleeping time induced by hexobarbital-Na was prolonged in mice. Tremorine-induced tremor in mice was inhibited by NSP, while perphenazine-induced catalepsy in rats was not. Normal blood pressure in Wistar rats was not influenced, but high blood pressure in SHR (spontaneously hypertensive rats) decreased close to normal levels after NSP. NSP had antiulcerogenic effects on Takagi's restraint-plus-water-immersing ulcers in rats and histamine-induced duodenal ulcers in guinea pigs, but no influence on Shay ulcers in Wistar rats. From the data obtained herein, it may be concluded that NSP has many central depressant-like activities.
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PMID:[Central activity, antihypertensive action and antiulcerogenic effects of neurotropin]. 103 90

A potential physiological role for cardiac histamine and its interaction with norepinephrine were investigated in isolated left ventricles from spontaneously hypertensive rats (SHR). Prior to drug administration, left ventricle-to-body weight ratios and spontaneous firing rates (beats per min) were significantly increased in SHR ventricles vs. age- and sex-matched controls (WKY). Also, action potential duration was significantly prolonged in SHR at all levels of repolarization. In all hearts, norepinephrine (10(-7)-10(-4) M) increased spontaneous rate and the percent incidence of arrhythmias. The H2-receptor antagonist cimetidine (10(-5) M) potentiated the rate and arrhythmogenic effects of norepinephrine in SHR and, to a lesser extent, in WKY preparations; propranolol (10(-6) M) reduced them. Histamine (10(-7) M) also inhibited the norepinephrine-induced increase in arrhythmias in SHR, but not in WKY. The attenuation of adrenergically induced rhythm disturbances by histamine and their potentiation by cimetidine in hypertensive hearts support the hypothesis that histamine plays a role as a postjunctional modulator of adrenoceptor function in a setting of hypertension and myocardial hypertrophy.
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PMID:Histamine attenuates the arrhythmogenic effects of norepinephrine in hearts of spontaneously hypertensive rats. 253 44

Histamine levels, histidine decarboxylase and histamine-N-methyltransferase activities were determined in various brain areas of young (9-week old) and adult (18-week old) normotensive rats (WKY) and hypertensive rats (SHR). When compared with WKY, histamine levels were increased in the anterior and posterior hypothalamus of young and adult SHR, as well as in the brainstem of young SHR. Histidine decarboxylase activity was unchanged in the posterior hypothalamus and in the medulla oblongata of young and adult SHR as well as in the anterior hypothalamus of young SHR, but it was slightly decreased in the anterior hypothalamus of adult SHR. Histidine decarboxylase activity was enhanced in the cortex-midbrain of young, as well as adult SHR, histamine-N-methyltransferase in the cortex-midbrain of young SHR. The following differences were found between young and adult rats: histamine levels were elevated in the cortex-midbrain of adult WKY and SHR. In the cortex-midbrain and brainstem of adult WKY and SHR histidine decarboxylase activity was also increased, while histamine-N-methyltransferase activity was elevated in the cortex-midbrain of adult WKY. The findings show changes in histamine levels, histidine decarboxylase and histamine-N-methyltransferase activities in SHR and suggest involvement of histaminergic neurons in hypertension. The activity of histaminergic neurons of adult rats seems to be higher than that of young animals.
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PMID:Histamine, histidine decarboxylase and histamine-N-methyltransferase in brain areas of spontaneously hypertensive rats. 324 96

Reduced vascular histamine content is postulated to contribute to increased peripheral vascular resistance in experimental hypertension in rats. Experiments were conducted to examine histamine content, in vitro uptake ability and in vitro catabolism of histamine in blood vessels from 12-week-old spontaneously hypertensive rats (SHR) and age-matched normotensive controls. Histamine content of mesenteric artery and abdominal aorta from SHR was significantly reduced (P less than .05) when compared to Wistar-Kyoto normotensive controls. This finding confirms a similar observation of reduced vascular histamine content in deoxycorticosterone acetate salt hypertensive rats reported from our laboratory. This reduction in histamine content may be more prevalent in arteries because the decrease was not observed in the portal vein from SHR. Uptake of [14C]histamine into mesenteric artery and abdominal aorta was unchanged in SHR compared to Wistar-Kyoto controls. No significant differences between slopes for uptake regression lines were observed for either mesenteric artery or abdominal aorta. Mesenteric artery exhibited a greater capacity of [14C]histamine accumulation than aorta and significant reductions in accumulation of labeled histamine after 20 and 60 min were found in this vessel from SHR. Because metabolism of histamine was inhibited by aminoguanidine, this reduction may reflect diminished retention by histamine storage sites. In vitro I-[14C]histidine uptake was significantly increased in abdominal aorta and iliac artery but not mesenteric artery from SHR. These differences were also present at the later accumulation periods of 20 and 60 min.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Studies on uptake and catabolism of vascular histamine in spontaneously hypertensive rats. 399 26

Histamine (HA) turnover rate in the brain of spontaneously hypertensive rats (SHR) was determined by the accumulation of telemethylhistamine after pargyline treatment. The values in these SHR were lower than in the Wistar Kyoto rats, particularly in the hypothalamus and brainstem. However, chronic treatment with L-histidine had no effect on the development of hypertension in the SHR. The functional significance of the decreased HA turnover in SHR is discussed in relation to the pathogenesis of hypertension.
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PMID:Decrease in histamine turnover in the brain of spontaneously hypertensive rats. 404 52

1. Acute systemic anaphylaxis in calves was characterized by marked systemic hypotension; hypertension in the pulmonary arteries and abdominal vena cava, and transient apnoea. Calves responded with a second reaction to antigen, but a third anaphylactic response could not be evoked.2. Suppression of systemic anaphylaxis could not be effected with mepyramine, whereas methysergide or diethylcarbamazine each suppressed anaphylaxis by 50%. Disodium cromoglycate alone did not inhibit anaphylaxis: however, when disodium cromoglycate was combined with diethylcarbamazine almost total suppression (85%) was achieved. Sodium meclofenamate also was a powerful inhibitor of anaphylaxis (80%). It is tentatively suggested that slow reacting substance (SRS-A) may be an important mediator of bovine anaphylaxis.3. Bilateral vagotomy did not modify the circulatory responses to injected histamine, 5-hydroxytryptamine (5-HT) or antigen, whereas the effects of these agents on ventilation (apnoea) were abolished by vagotomy.4. Plasma histamine concentration was increased during anaphylaxis, whereas plasma 5-HT was not. Whole blood histamine concentration fell sharply and remained depressed during 20 min of anaphylactic shock. Reduced whole blood histamine levels probably reflect the severe leucopoenia in the calves.5. Histamine concentrations in six tissues taken from calves subjected to anaphylaxis were not different from those in control calves; mast cells were of similar numbers to controls, but showed some swelling, granular spilling and metachromasia.6. Histamine, 5-HT, bradykinin and antigen caused increased pulmonary artery perfusion pressure and ventilation resistance in isolated lungs from sensitized calves. However, there was no difference in histamine and 5-HT concentration in perfusates obtained during antigen infusion of sensitized and control lungs.7. Systemic anaphylaxis of calves may result from the interaction of histamine, 5-HT and SRS-A. The present data implicate (by indirect measurement) SRS-A as an important mediator of anaphylaxis in this species.
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PMID:Acute systemic anaphylaxis in the calf. 414 91

1. The responses of rabbits, anaesthetized with pentobarbitone sodium, to intravenous injections of histamine and phenyl diguanide have been studied. Total lung conductance, lung compliance, breathing frequency, tidal volume, end-tidal CO(2)%, systemic arterial and right atrial blood pressures and heart rate were measured. Some of the rabbits were first paralysed and artificially ventilated.2. The role of vagal afferent nerves was determined by observing the responses before and after bilateral vagotomy, and before and during cooling the vagus nerves to 8-10 degrees C; such cooling selectively blocks some vagal afferent pathways.3. Histamine decreased conductance (bronchoconstriction), in spontaneously breathing and in paralysed, artificially ventilated animals, and caused rapid shallow breathing. The responses were considerably reduced or abolished by vagal cooling and vagotomy and are thought to be mainly vagal reflexes due to stimulation by histamine of irritant receptors in the lungs.4. Phenyl diguanide also decreased conductance, in spontaneously breathing and in paralysed, artificially ventilated animals, and caused rapid shallow breathing. Vagotomy abolished the respiratory changes and considerably reduced the bronchoconstriction. Vagal cooling caused an equal reduction of the bronchoconstriction but an increase in minute volume persisted. This respiratory response to phenyl diguanide which persists during vagal cooling is thought to be due to stimulation of deflation receptors in the lungs; it was associated with vagal reflex hypotension and bradycardia.5. Both histamine and phenyl diguanide decreased lung compliance when vagal conduction was unimpaired. The effects were largely secondary to changes in the pattern of breathing, although histamine also had a weak direct action on lung tissue leading to a fall in compliance.6. Both histamine and phenyl diguanide decreased end-tidal CO(2)% and increased right atrial pressure by direct (non-vagal) actions on lung tissues. Histamine also caused a non-vagal hypertension.
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PMID:The role of the vagus nerves in the respiratory and circulatory responses to intravenous histamine and phenyl diguanide in rabbits. 578 May 44

The cardiovascular actions of tolazoline are poorly understood. Therefore, we administered tolazoline (2 mg kg-1, IV) to anesthetized adult dogs and puppies. Tolazoline induced transient pulmonary and systemic pressor responses, transient systemic vasoconstriction and pulmonary vasodilation, and transient hypoxemia and acidosis in pentobarbital anesthetized dogs. None of these responses were evident during a second injection of tolazoline, indicating either the development of tachyphylaxis or a secondary antagonistic property of tolazoline. These responses to tolazoline were also prevented by alpha adrenergic blockade. Histamine H1 - and H2-receptor blockade sustained the transient pulmonary and systemic pressor and systemic vasoconstrictor responses to tolazoline. Thus, tolazoline appears to activate both alpha and histamine receptors in the pulmonary and systemic vascular beds of the anesthetized dog. In anesthetized puppies, tolazoline induced a slight pulmonary pressor response, marked bradycardia, and systemic hypertension. The present findings confirm the pharmacological complexity of tolazoline and suggest that anesthesia, age, and pulmonary vascular tone are important factors in determining the cardiovascular responses to tolazoline.
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PMID:Pulmonary and systemic vascular actions of tolazoline in anesthetized dogs. 629 95

The respiratory and circulatory alterations induced by intravenous histamine in the pentobarbital anesthetized rabbit were examined and compared to those alterations associated with IgE anaphylaxis following antigen challenge. Histamine induced several graded alterations including an increase in total pulmonary resistance, a decrease in dynamic compliance, an increase in breathing frequency, a decrease in tidal volume, a rise in right ventricular systolic pressure and systemic hypotension. Qualitatively similar alterations occurred during the anaphylactic response, but a quantitative comparison of the two responses revealed that the respiratory alterations in systemic anaphylaxis corresponded to relatively low equivalent histamine doses, whereas the anaphylactic circulatory alterations exceeded the maximum response obtainable with histamine. Pretreatment with H1 antihistamine competitively blocked all of the ventilatory and lung mechanical changes induced by histamine, but it inhibited only the increase in pulmonary resistance induced by antigen. The right ventricular hypertension induced by histamine was also inhibited by H1 antihistamine but the antigen-induced change in this variable was not significantly attenuated. Inhibition of the histamine-induced systemic hypotension required pretreatment with both H1 and H2 histamine antagonists. Such pretreatment, however, did not attenuate the fall in systemic arterial pressure induced by antigen. H1 antihistamine pretreatment prevented histamine- but not antigen-induced lethality. We conclude that histamine is an important mediator of the increase in pulmonary resistance but is not the major mediator of the other physiological alterations of IgE systemic anaphylaxis in the rabbit.
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PMID:The role of histamine in the physiologic alterations of IgE anaphylaxis in the rabbit. 672 78


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