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

1. Vascular reactivity was studied in Tyrode solution perfused kidneys from young (7 weeks) and mature (4-6 months) spontaneously hypertensive rats (SH rats). 2. The response to nerve stimulation was greater in the kidneys from young SH rats than in those from young control rats, both in control solution and after inhibition of the disposition of noradrenaline; both groups exhibited the same sensitivity to noradrenaline, angiotensin II and barium chloride. 3. The response to nerve stimulation was normal in kidneys from mature SH rats, but responses to noradrenaline, angiotensin II and barium chloride were greater than the control. 4. Cocaine potentiated the response to nerve stimulation more in the kidneys from mature SH rats than in those from the control rats. 5. The results suggest that renal sympathetic nerves release more noradrenaline than normal in the young SH rats, which could be an important factor in causing hypertension. 6. In the established phase of spontaneous hypertension the vascular reactivity to exogenous agonists is increased, probably as a consequence of high blood pressure; the more efficient neuronal uptake causes normalization of the response to sympathetic nerve stimulation.
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PMID:Neuronal and vascular reactivity in isolated perfused kidneys during the development of spontaneous hypertension. 28 59

Cardiovascular complications are among the most common and dangerous complications of cocaine abuse, ranging from episodic arrhythmias to myocardial infarction, strokes, cardiomyopathy, and sudden death. The central nervous system-mediated action of cocaine triggers an increase in circulating catecholamines, resulting in arterial vasoconstriction, increase in myocardial oxygen demand, myocardial ischemia, tachycardia, and other arrhythmias. The peripheral cardiovascular action of cocaine involves the inhibition of reuptake of catecholamines at adrenergic nerve terminals, with local release of epinephrine, direct stimulation and vasospasm of the coronary arteries, coronary intimal hyperplasia, inhibition of baroreceptors, interference with the electrical conduction through the myocardium, and direct myocardial toxicity. The cardiovascular complications of cocaine include cardiac dysrhythmias and hypertension, acute myocardial infarction, myocarditis, infectious endocarditis, ventricular dysfunction, dilated cardiomyopathy, hypotensive shock, and cerebral strokes. Cocaine-related vascular changes in the pregnant woman and fetus have been related to an increased incidence of abortion, abruptio placentae, and congenital anomalies of the fetus.
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PMID:Cardiovascular complications of cocaine abuse. 158 6

Intramural sympathetic neuroeffector responses and presynaptic regulation of neurotransmission by amine uptake and alpha 2-adrenergic receptors were examined in young (5-week-old) and mature (12-week-old) spontaneously hypertensive rats (SHR) and were compared with those of age-matched Wistar-Kyoto (WKY) control rats. Electrical field stimulation (20 V, 0.2-msec pulse width, 3-second pulse train each minute, 5-100 Hz) elicited contractile responses from isolated mesenteric arteries mounted in a myograph. There was a significant difference between the sensitivity of arteries to electrical field stimulation in the two age groups, with arteries from 12-week-old rats being more sensitive than arteries from 5-week-old animals. Also, there was a significant age-strain interaction: the sensitivity of arteries from SHR to electrical field stimulation increased dramatically with age compared with that of WKY rat arteries. Cocaine significantly increased the sensitivity to electrical field stimulation after inhibition of presynaptic alpha 2-adrenergic receptors, and had a significantly greater effect in arteries from 5-week-old SHR compared with WKY controls. This would reflect an overactive neuronal amine uptake mechanism in young SHR. At 12 weeks there was no significant interstrain difference in the effect of cocaine. Yohimbine increased the sensitivity to electrical field stimulation both before and after inhibition of neuronal amine uptake, but there was no difference in its effect with age or strain. Therefore, although sensitivity to sympathetic nerve stimulation varies with age in the SHR, there is no evidence that this can be ascribed to alpha 2-adrenergic receptor function.
Hypertension 1991 Nov
PMID:Arterial neuroeffector responses in early and mature spontaneously hypertensive rats. 165 71

Frequency-responses curves for nerve stimulation and dose-response curve for norepinephrine, 5-hydroxytryptamine potassium chloride, vasopressin and acetylcholine (ACh) were determined in isolated, perfused mesenteric vascular beds from young (approximately 5 weeks) spontanelouly hypertensive (SHR) and Wistar Kyoto rats. Although mean systolic blood pressure (measured by tail cuff plethysmography) was slightly higher in the SHR, this difference was not significant. Slopes and maximum responses were increased significantly for nerve stimulation and all agonists. The basal perfusion pressure was also significantly elevated in the SHR. These differences are consistent with existing evidence that structural changes occur in blood vessels of SHR at an early stage and probably precede development of hypertension. Such structural changes could therefore contribute to development of the hypertension. Cocaine (1 microM) markedly increased responses to nerve stimulation and bolus injections of norepinephrine in preparations from SHR with little or no effect on such responses in Wistar Kyoto preparations, a result consistent with the known greater density of noradrenergic nerves in SHR vasculature. In the presence of cocaine, there was unmasked a selective super-sensitivity (significantly lower ED50) to norepinephrine in the SHR. Thus SHR mesenteric vessels may possess an alteration in adrenoreceptors or their coupling to other cellular mechanisms. Responses to ACh revealed no indication of a deficient endothelial mediated relaxation. An altered media:lumen ratio of small arteries, hypernoradrenergic innervation and supersensitivity to the transmitter may contribute to development of hypertension.
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PMID:Mesenteric vascular responses of young spontaneously hypertensive rats. 207 89

Toxic injury is one of the many ways by which the functional integrity of the heart may become compromised. Any of the subcellular elements may be the target of toxic injury, including all of the various membranes and organelles. Understanding the mechanisms underlying cardiotoxicity may lead to treatment of the toxicity or to its prevention. Doxorubicin and its analogs are very important cancer chemotherapeutic agents that can cause cardiotoxicity. Other agents which are cardiotoxic and which have profound public health implications include the alkaloid emetine in ipecac syrup, cocaine, and ethyl alcohol. The most important cardiotoxic mechanisms proposed for doxorubicin include oxidative stress with its resultant damage to myocardial elements, changes in calcium homeostasis, decreased ability to produce ATP, and systemic release of cardiotoxic humoral mediators from tissue mast cells. Each of the first 3 mechanisms can lead to each of the other 2, and the causal relationships between all of these mechanisms are not clear. New evidence suggests that doxorubicinol, one of the metabolites of doxorubicin may be the moiety responsible for cardiotoxicity. Several other potential mechanisms also have been proposed for doxorubicin. Emetine in ipecac syrup is the first aid treatment of choice for many acute toxic oral ingestions and the alkaloid, itself, is used to treat amebiasis. Cardiotoxicity occurs following chronic exposure, such as occurs therapeutically in amebiasis and with ipecac abuse by bulemics. A number of mechanisms are proposed for emetine cardiotoxicity, but the current mechanistic literature is quite scarce. Cocaine abuse recently has caught the public interest, in particular because of the drug-related sudden deaths of certain athletes. Cocaine can cause hypertension, arrhythmias, and reduced coronary blood flow, each of which can contribute to its lethality. However, it may be possible that cocaine sudden death episodes are more related to hyperthermia and convulsive seizures, rather than to cardiovascular toxicity. Chronic alcohol use leads to dilated cardiomyopathy and failure as part of the general physical degeneration that occurs with alcoholism. Several mechanisms are proposed for the cardiomyopathy, but only 2 things seem clear. The cardiotoxicity is due to an intrinsic effect of alcohol, rather than to malnutrition or co-toxicity, and abstinence is the only effective treatment for the cardiomyopathy. Recent articles indicate that very moderate use of alcohol may be beneficial and protect against cardiovascular-related morbidity. One explanation for these findings seems to be that the non-drinking groups, against whom the moderate drinking comparisons were made, were enriched in former drinkers with significant alcohol-related cardiovascular pathology.
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PMID:Toxic mechanisms of the heart: a review. 209 Dec 37

The effects of beta-adrenoceptor agonists and antagonists on pressor responses of the isolated perfused mesenteric arteries to periarterial nerve stimulation (PNS) in the prehypertensive 4-week-old spontaneously hypertensive rat (SHR) and the age-matched Wistar Kyoto rats (WKY) were examined. The systolic arterial blood pressure (SBP) of SHR and WKY were not significantly different at this young age. The pressor responses of the mesenteric arteries to PNS at various stimulating frequencies, however, were significantly greater in SHR than WKY. Cocaine, isoproterenol (a nonselective beta-adrenoceptor agonist) and salbutamol (a selective beta 2-adrenoceptor agonist) significantly enhanced the pressor responses to PNS in SHR and WKY, with significantly greater increase in SHR than WKY. The nonselective beta-adrenoceptor antagonist (propranolol) and the selective beta 2-adrenoceptor antagonist (ICI 118,551) significantly inhibited the pressor response to PNS in SHR without affecting that in WKY. The selective beta 1-adrenoceptor antagonist (practolol) was without effect on the PNS-induced pressor responses in both SHR and WKY. These results demonstrate that the presynaptic beta 2-adrenoceptor-mediated facilitation of neurogenic pressor response in mesenteric arteries already are enhanced in 4-week-old SHR. In view of the higher concentration of circulating epinephrine (Epi) in prehypertensive SHR, the enhanced facilitatory modulation via presynaptic beta 2-adrenoceptors in prehypertensive SHR may be involved in development of hypertension.
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PMID:Enhanced presynaptic beta 2-adrenoceptor-mediated facilitation of the pressor responses in the prehypertensive SHR. 248 Nov 88

The chemistry, pharmacology, and pharmacokinetics of cocaine are described, and the medical complications of illicit cocaine use are reviewed. Cocaine is readily absorbed from mucous membranes, the gastrointestinal tract, and the vascular beds of the lungs. Thus there are a number of routes for illicit cocaine administration, with the most popular one being intranasal. The most prevalent problems associated with the use of cocaine appear to be route and dose independent and are cardiovascular in nature; they include myocardial infarction and ischemia, sudden death, cardiac arrhythmias, and hypertension. Seizures, cerebrovascular accidents, hepatotoxicity, rhabdomyolysis, pulmonary complications, and obstetrical complications have also been reported. Gastrointestinal complications and acute toxicity may occur in cocaine smugglers who ingest cocaine-filled packets. Route-dependent complications of cocaine use are also of concern. The mechanism underlying the medical complications has not been fully elucidated but appears to be an extension of the drug's pharmacological properties. The treatment of cocaine-related toxicities is supportive and is based on the organ system affected. Drugs such as propranolol, labetalol, and nitrendipine have been advocated for treating the cardiovascular complications, and measures such as maintaining arterial blood pH, monitoring core body temperature, and diazepam therapy have been used to manage seizures. As the number of case reports of cocaine toxicity increases and the underlying mechanism is conclusively defined, management of the medical complications will improve.
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PMID:Medical complications of illicit cocaine use. 266 29

The isolated tail artery when exposed to 0.14-2.80 microM tityustoxin (a purified peptide from the venom of the scorpion Tityus serrulatus) underwent a transient contraction which was followed by a long lasting period of unresponsiveness to further additions of the toxin. Reserpine pretreatment, the addition of phentolamine, tetrodotoxin, verapamil or lowering the sodium concentration abolished the responses to the toxin. Cocaine potentiated it. Tityustoxin caused a slight leftward shift of the dose-response curves to adrenaline and norepinephrine and a large potentiation of the frequency-response curves to electrical stimulation. The latter effect was greater within the lower range of frequencies assayed, which coincide with those of the physiological discharge of sympathetic nerves. These data indicate that in the tail artery the tityustoxin acts indirectly on the smooth muscle through the release of endogenous catecholamines. Most likely, changes of the properties of the sodium channels and calcium influx are involved in this effect at the nerve endings. The potentiation of the frequency-response curves suggests that the arterial hypertension produced by the scorpion sting may result mainly from an abnormally elevated overflow of sympathetic transmitters.
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PMID:Effects of tityustoxin on the rat isolated tail artery. 293 87

Cocaine use has increased rapidly over the past few years. This has led to an increase in the number and variety of cocaine-related conditions for which medical attention is sought. Among these have been several cases of intracranial hemorrhage. Four cases reported in the literature and 6 from our own institution are presented here. They represent different diagnoses including hemorrhage from aneurysms and arteriovenous malformations, hemorrhage into a tumor, and spontaneous hemorrhage with no underlying lesion with and without preexisting hypertension. Analysis of these cases suggests that the hypertension induced by cocaine secondary to sympathetic stimulation may be the common factor. Cocaine may also cause arterial spasm. Although the pathophysiology has not been entirely resolved, the clinical significance of this association is clear. Intracranial hemorrhage should be considered in the differential diagnosis whenever a patient presents with an acute alteration in neurologic examination associated with cocaine use.
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PMID:Intracranial hemorrhage and cocaine use. 360 97

Epinephrine has been implicated in the genesis of some forms of hypertension. We have investigated the effects of epinephrine on vasoconstrictor responses evoked by adrenergic stimuli in the isolated perfused rat kidney. Low concentrations of epinephrine (2.5 - 5 X 10(-9) M) increased the amplitude of vasoconstrictor responses evoked by electrical stimulation of the renal adrenergic nerves. These concentrations of epinephrine had no effect on the basal perfusion pressure of the kidney or on the amplitude of vasoconstrictor responses evoked by exogenous norepinephrine. The potentiating effect of epinephrine persisted after infusion of the amine had ceased. Kidneys that had been perfused with 3H-epinephrine accumulated radioactivity, which could then be released by renal nerve stimulation. Cocaine (3 X 10(-5) M) reduced the renal accumulation of 3H-epinephrine and abolished both the persistent potentiating effect of the amine and the release of radioactivity evoked by subsequent nerve stimulation. The potentiating effect of epinephrine infusion was abolished by the beta 2-selective adrenergic receptor antagonist ICI 118,551 (3 X 10(-8) M), but not by the beta 1-selective adrenergic receptor antagonist atenolol (10(-6) M). These results indicate that concentrations of epinephrine that can be achieved during acute stress can enhance the amplitude of neurogenic vasoconstrictor responses. This effect appears to be mediated via a prejunctional beta 2-adrenergic receptor. The persistent nature of this effect may be due to the neuronal accumulation and subsequent release of epinephrine.
Hypertension
PMID:Epinephrine enhances neurogenic vasoconstriction in the rat perfused kidney. 398 58


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