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

The influence of phenylephrine (PHE), methoxamine (MET) and ephedrine (EPH) on kininogen and prekallikrein level in plasma was investigated in male Wistar rats. Simultaneously the effect of these drugs on blood pressure was monitored. No changes in kininogenesis were observed during the hypertension period (2 h after ip injection). The significant decrease in kininogen level (by 20-30%) was found 4 h after PHE (5 mg/kg) or EPH (40 mg/kg) and 4-12 h after MET (40 mg/kg) injection. The reduction of kallikrein utilization, indicating an increase in prekallikrein level in plasma, was noted only after PHE (by 34%) or MET (by 44%) administration. Phentolamine (REG) in a dose of 20 mg/kg, which counteracted the hypertensive effect of investigated drugs, abolished the influence of these drugs on kininogen level. The results indicate that the hypertension induced by alpha-adrenoceptor agonists evokes the delayed activation of kininogenesis parallel to the secondary decrease in blood pressure. Such a reaction of kinin system seems to be related to primary alpha-adrenoceptor stimulation, not to the direct influence of hypertensive drugs on kinin system in rat plasma.
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PMID:Hypertensive drugs and plasma kinins in rats. 287 49

A brief analysis is presented of the large recorded numbers of swimmers who have been stung by the "Irukandji" (Carukia barnesi) jellyfish during the 1985-1986 summer season in north Queensland, and the results are discussed. Many of the victims may suffer from symptoms of overstimulation of the sympathetic system, and hypertension is shown to be another complication of this syndrome. This hypertension seems to respond well to intravenously-administered phentolamine, an alpha-adrenergic receptor blocking drug. Phentolamine also reduces the excessive shaking and sweating that appears to be part of the "Irukandji syndrome". Diazepam relieves the anxiety which is part of the syndrome, but antihistamine agents and hydrocortisone seem to have no beneficial effect.
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PMID:Further understanding of, and a new treatment for, "Irukandji" (Carukia barnesi) stings. 287 13

Phentolamine (Phe) prevents the induction by epinephrine (E: 1800 nmol/kg, i.v.) of lung edema (LE) in urethane-anesthetized and bivagotomized rats in a dose-related manner (from 246 to 3933 nmol/kg, i.v.). Since Phe blocks and E activates both alpha 1- and alpha 2-adrenoceptors, the evidence does not allow us to link LE to selective (alpha 1 or alpha 2) or non-selective (alpha 1 + alpha 2) alpha-adrenoceptor activation. Accordingly, we tried to find out whether: phenylephrine (PE), a selective alpha 1-adrenoceptor agonist, and B-HT 920, a selective alpha 2-adrenoceptor agonist, would cause LE; prazosin (Praz), a selective alpha 1-adrenoceptor antagonist, and yohimbine (Yoh), a selective alpha 2-adrenoceptor antagonist, would protect rats against LE caused by E or PE. We found that: 1) PE (from 736 to 5892 nmol/kg, i.v.), but not B-HT 920 (from 190 to 12200 nmol/kg, i.v.), caused LE, while both drugs increased arterial blood pressure; 2) Praz prevented induction of LE, whether by E (1800 nmol/kg, i.v.) or by PE (5892 nmol/kg, i.v.), in a dose-related manner (from 15 to 119 nmol/kg, i.v.). In contrast, Yoh was ineffective at doses up to 7675 nmol/kg, i.v. We conclude, therefore, that E-induced LE in urethane-anesthetized and bivagotomized rats strictly depends on alpha 1-adrenoceptor activation. The outcome of E-induced LE is usually rat death, the incidence of which depends on the dose. Since alpha 1-adrenoceptor agonists rank in the same order of potency for the induction of death as for that of LE, and since Phe and Praz protect from death at LE-preventing doses, there seems to be some link between LE and death, even though protection against death is obtained with doses of antagonists lower than those abolishing induction of LE. Finally, alpha 1-agonists cause maximum arterial hypertension at all doses used, irrespective of induction of LE and of protective pretreatment against LE.
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PMID:Studies on epinephrine-induced lung edema in the rat. I. Selective alpha 1-adrenoceptor involvement. 301 61

We have assessed the benefit of separate or combined alpha- and beta-receptor blockade in the treatment of 33 patients suffering from acute (less than 48 hr) myocardial infarction complicated by sustained (greater than 6 hr) systolic hypertension (systolic blood pressure greater than 150 mm Hg). Eight patients have been treated with metoprolol, 7 with phentolamine and 18 with labetalol. We evaluated the effects of these drugs on hemodynamics and arterial and mixed venous blood gases. The patients were divided into two groups on the basis of the pulmonary wedge pressure. The first group had a pressure greater than 15 mm Hg. It included 9 patients treated with labetalol (1.8 mg/min for 1 hr) and 7 others with phentolamine (0.6 mg/min for 1 hr). The wedge pressure in the second group was less than 13 mm Hg. Nine patients in this group had been treated with labetalol (2.1 mg/min for 1 hr) and 8 others with metoprolol (0.2 mg/kg in 15 min). Labetalol normalized the blood pressure in both groups within 1 hr as did phentolamine. Metoprolol did not significantly reduce either the systolic or the diastolic pressures. The high wedge pressures in the first group were reduced by both labetalol and phentolamine. The cardiac index was increased following phentolamine administration while it was reduced by labetalol. In the group with low wedge pressure, labetalol and metoprolol induced a slight but significant reduction in cardiac index but the pulmonary wedge pressures were significantly increased for metoprolol only. The rate-pressure product was very significantly decreased by labetalol and metoprolol but not by phentolamine. The emergency treatment of systemic hypertension occurring in the setting of acute myocardial infarction would thus appear to be best achieved by combined alpha- and beta-blockade rather than with either pure alpha- or pure beta-blockade. Phentolamine, however, would be a good drug in the presence of a reduced cardiac index.
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PMID:A comparison of the effects of combined or separate alpha- and beta-blockade in the treatment of hypertension in the acute stage of myocardial infarction. 308 Mar 79

Propranolol is a commonly used drug; of new and refilled prescriptions, it ranked no. 1 in 1984 and no. 2 in 1985. Medical conditions for its use include angina pectoris, myocardial infarction, hypertension, cardiac dysrhythmias, hypertrophic subaortic stenosis, migraine headache, hyperthyroidism, and pheochromocytoma. Almost all dental practitioners will treat a patient receiving propranolol for one of these conditions. The following recommendations seem appropriate at this time: The patient should continue to receive propranolol during dental treatment. Sudden withdrawal of the beta-blocker will cost the patient the benefit of propranolol therapy and may lead to acute myocardial ischemia. Acute stress should be minimized, as hypertensive responses may also be caused by endogenously released epinephrine. Short appointments scheduled in the morning, possibly with conscious sedation, should be considered. The dosage of adrenergic vasoconstrictors should be limited and gingival retraction cord containing epinephrine avoided entirely. The blood pressure should be taken approximately 5 minutes after local anesthesia is administered to determine if a systemic response has occurred. In the unlikely event of a hypertensive emergency, a rapidly acting, short-duration antihypertensive drug, such as the alpha-blocker phentolamine (Regitine, 5 mg intravenously) should be administered. Sublingual nitroglycerin (Nitrostat, 0.4 mg) may be useful as a nonparenteral alternative. These recommendations apply to other nonselective beta-blockers, including nadolol (Corgard) and timolol (Blocadren). They may also apply to labetalol (Normodyne, Trandate), a nonselective beta-antagonist with some alpha-blocking activity and to pindolol (Visken), a beta-blocker with some intrinsic beta 2-agonistic activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypertensive response to levonordefrin in a patient receiving propranolol: report of case. 327 28

In conscious instrumented normotensive and two-kidney, one clip Goldblatt hypertensive dogs, we compared the effects of the alpha-receptor blocking agent, urapidil, on blood pressure, renal vascular resistance, heart rate, and plasma renin activity with those of prazosin and phentolamine. Urapidil (2 mg/kg) and prazosin (0.25 mg/kg) decreased blood pressure and renal vascular resistance in both groups of animals, and urapidil caused a small increase in renal blood flow. Heart rate, but not plasma renin activity, was increased at the peak of the hypotension. Phentolamine had no significant effect on any of these parameters. All three agents markedly inhibited the renal vasoconstrictor responses to intraarterially administered phenylephrine and norepinephrine, and thus exhibited an alpha 1-receptor blocking action. Only urapidil significantly antagonized the response to B-HT 933, a selective alpha 2-receptor agonist, indicating that it also interacts at alpha 2-receptor sites. Since both normotensive and hypertensive animals exhibited similar hypotensive responses after both urapidil and prazosin, the degree of alpha-receptor blockade achieved did not reveal greater sympathetic tone in renal hypertension.
Hypertension
PMID:Relationship of alpha receptor types to hypotension and renal vasodilation caused by alpha blockers in conscious dogs. 613 Oct 31

The present study was conducted to measure norepinephrine release during sympathetic nerve stimulation and to evaluate vascular reactivity in the isolated perfused mesenteric vasculature of normotensive and Doca-salt hypertensive rats. Significantly greater vasoconstrictor responses to periarterial nerve stimulation, norepinephrine, and vasopressin, but not to barium chloride, were observed in the mesenteric vasculature of the hypertensive rats in comparison with the control normotensive group. Norepinephrine release, measured as total tritium overflow, during periarterial nerve stimulation at 4 Hz for 2 min, was identical in both normotensive and hypertensive animals. Phentolamine (5.3 micro M) significantly increased tritium overflow, but to the same extent in the normotensive and the hypertensive mesenteric vasculature, suggesting that the negative feedback presynaptic alpha-adrenoceptor mechanism, which has been proposed to modulate transmitter release, was unaltered in this form of hypertension. These results indicate that hyperresponsiveness of the mesenteric vasculature to periarterial nerve stimulation in the hypertensive rats is due to increased sensitivity of the vascular alpha-adrenoceptor and not facilitation of the transmitter release. The increased vascular reactivity to norepinephrine and vasopressin may be involved in the maintenance of Doca-salt hypertension.
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PMID:Sympathetic nerve function and vascular reactivity in Doca-salt hypertensive rats. 625 76

Electrical stimulation of the dorsal periaqueductal gray matter (DPAG) eliciting flight behavior in awake rats caused an increase in arterial blood pressure (BP), heart rate (HR) and respiration in rats anesthetized with urethane. The hypertension was markedly reduced by 5 mg/kg of intravenously injected hexamethonium or bretylium, virtually abolished by 5 mg/kg of phentolamine and partially antagonized by 0.1 mg/kg of the alpha 1-adrenoceptor blocker, prazosin. The tachycardia induced by DPAG stimulation was partially antagonized by hexamethonium or bretylium and abolished by propranolol (5 mg/kg, IV) or practolol (5 mg/kg, IV), but not affected by N-butylscopolamine (10 mg/kg, IV). Phentolamine increased basal HR and abolished the tachycardic response caused by either brain stimulation or intravenous noradrenaline. Prazosin moderately decreased the response to noradrenaline, but did not affect basal HR or the tachycardia induced by brain stimulation. The increase in respiratory amplitude occurring during brain stimulation was abolished by phentolamine as well as by prazosin, while the increase in respiratory rate was moderately reduced by phentolamine and propranolol. These results demonstrate that the cardiovascular component of the defense reaction of the rat is almost entirely due to a sharp increase in sympathetic tone. They also suggest that the hyperventilation induced by aversive brain stimulation is modulated by central and peripheral adrenergic mechanisms.
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PMID:Neuroeffector mechanisms of the defense reaction in the rat. 665 64

Treatment of severe arterial hypertension associated with neuroblastoma is not well discussed in the literature. A six-month-old boy was referred for evaluation of an abdominal mass which proved to be neuroblastoma stage IV. Arterial hypertension of 26/16 kPa (190/110 mmHg) was also found. Because of the degree of malignancy and the risk of intra-tumoral haemorrhage, urgent management of the hypertension was required before proceeding to surgery. Phentolamine, a short-acting alpha-blocking agent, was administered as a continuous infusion of a 0.01 per cent solution, at a rate of 1 to 4 microgram X kg-1 X min-1 titrated according to the arterial blood pressure (BP), central venous pressure and urinary output. BP was rapidly controlled and the child went to surgery within 48 hours. The operation was uneventful but only 80 per cent of the tumour could be resected. Phentolamine was discontinued intraoperatively but was reinstituted postoperatively when hypertension recurred. With the return of normal intestinal function five days after surgery, phenoxybenzamine was begun p.o. and phentolamine was tapered over 24 hours and discontinued. A continuous infusion of phentolamine provided satisfactory control pre- and post-operatively with no significant hypotension. We consider this technique to be potentially very useful in the management of severe arterial hypertension associated with neuroblastoma, as it permits early surgical intervention under optimal conditions.
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PMID:[Continuous phentolamine perfusion in the treatment of severe arterial hypertension associated with neuroblastoma]. 670 85

Topical chemical irritants induce an acute reaction in the eye, consisting of an increased intraocular pressure (IOP), breakdown of the blood-aqueous barrier, anterior uveal vasodilation and miosis. In the present study these effects were studied in the rabbit eye after topical application of neutral formaldehyde by measuring IOP continuously using electromanometrical equipment. The protein content of the aqueous humour was measured and miosis as well as anterior hyperemia were analyzed. Intravenously injected sodium fluorescein was used to visualize the site of the disruption of the blood-aqueous barrier in freeze-dried specimens. Iridectomies were performed to study the mechanisms of hypertension and disruption of the blood-aqueous barrier. In iridectomized rabbits the acute irritative response was very similar to that of normal eyes. Breakdown of the blood-aqueous barrier, miosis and anterior hyperemia occurred. However, the increase in IOP was only partially reduced. This indicates that a pupillary block due to the intense miosis plays a minor role in the hypertensive reaction or in the breakdown of the barrier. The effect of three autonomic receptor blocking agents: phentolamine (alpha-adrenergic antagonist), timolol (beta-adrenergic antagonist) and biperiden (cholinergic antagonist) on the irritative ocular response caused by formaldehyde was studied. Phentolamine proved to be an efficient inhibitor of the hypertensive reaction. It also effectively prevented the breakdown of the blood-aqueous barrier. Biperiden inhibited only slightly the increase in IOP caused by formaldehyde. Timolol had no significant effect. None of these three antagonists was able to prevent the miosis or hyperemia. The present findings indicate that a part of the irritative response is mediated by a phentolamine-sensitive neuronal pathway.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of autonomic receptor blockers on the ocular response to topical chemical irritation. 674 78


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