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

Autoregulation of blood flow denotes the intrinsic ability of an organ or a vascular bed to maintain a constant perfusion in the face of blood pressure changes. Alternatively, autoregulation can be defined in terms of vascular resistance changes or simply arteriolar caliber changes as blood pressure or perfusion pressure varies. While known in almost any vascular bed, autoregulation and its disturbance by disease has attracted particular attention in the cerebrovascular field. The basic mechanism of autoregulation of cerebral blood flow (CBF) is controversial. Most likely, the autoregulatory vessel caliber changes are mediated by an interplay between myogenic and metabolic mechanisms. Influence of perivascular nerves and most recently the vascular endothelium has also been the subject of intense investigation. CBF autoregulation typically operates between mean blood pressures of the order of 60 and 150 mm Hg. These limits are not entirely fixed but can be modulated by sympathetic nervous activity, the vascular renin-angiotensin system, and any factor (notably changes in arterial carbon dioxide tension) that decreases or increases CBF. Disease states of the brain may impair or abolish CBF autoregulation. Thus, autoregulation is lost in severe head injury or acute ischemic stroke, leaving surviving brain tissue unprotected against the potentially harmful effect of blood pressure changes. Likewise, autoregulation may be lost in the surroundings of a space-occupying brain lesion, be it a tumor or a hematoma. In many such disease states, autoregulation may be regained by hyperventilatory hypocapnia. Autoregulation may also be impaired in neonatal brain asphyxia and infections of the central nervous system, but appears to be intact in spreading depression and migraine, despite impairment of chemical and metabolic control of CBF. In chronic hypertension, the limits of autoregulation are shifted toward high blood pressure. Acute hypertensive encephalopathy, on the other hand, is thought to be due to autoregulatory failure at very high pressure. In long-term diabetes mellitus there may be chronic impairment of CBF autoregulation, probably due to diabetic microangiopathy.
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PMID:Cerebral autoregulation. 220 48

An increased platelet-vessel wall interaction plays an important role in most forms of cardiovascular disease. In healthy arteries, the vascular endothelium prevents platelet adhesion and aggregation. As a mediator of this protective function, the endothelium produces prostacyclin, endothelium-derived nitric oxide and tissue plasminogen activator. Cardiovascular risk factors such as hypertension, hyperlipidemia and diabetes are associated with an increased platelet activation and with decreased antithrombotic properties of the blood vessel wall. The available inhibitors of platelet function interfere only with one of various mechanisms of platelet activation and of the platelet-vessel wall interaction. Prostaglandin inhibitors, such as aspirin and newer, more specific inhibitors, prevent the production and/or the effect of thromboxane A2 on platelets and the blood vessel wall. Other drugs interfere with the effect of adenosine diphosphate on platelets, or they increase intracellular concentration of cyclic GMP or AMP in platelets and vascular smooth muscle cells. The protective effects of platelet inhibitors in primary and particularly in secondary prevention of cardiovascular diseases have been documented in numerous studies. The successful clinical use of these substances, however, requires a selective prescription of the drugs in patients with cardiovascular disease.
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PMID:[Thrombocyte inhibitors in cardiovascular therapy]. 221 49

The author gives a definition of the term "vasculitis". Histopathological modifications are the result of a disturbance in the barrier function exerted by the vascular endothelium. The disturbances observed are characterized by piles of endothelial or intimal debris associated with a perivascular inflammatory reaction of the connective tissue and the appearance of a resorption granuloma. Whether superficial or deep, vasculitis can become "nodular" in appearance and is then characterized by "nodules" or "patches". In order to implement aetiological treatment, it is necessary to look for the causative agent: an infectious, drug or bacterial allergen, or hypertension is frequently involved.
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PMID:[Deep vasculitis]. 229 Aug 64

The effect of Cd2+ and related metals (Ni2+, Hg2+, Pb2+, Co2+, Sn2+ Cu2+ and Zn2+) on vascular tension was studied using isolated rings of endothelium-free, smooth muscle from the ventral aorta of the shark, Squalus acanthias. Both Cd2+ and Ni2+ produced significant vasoconstriction at concentrations at or above 10(-6) M (112 and 59 ppb, respectively); the other metals were either marginally constrictive (Hg2+ and Sn2+) or were without effect (Pb2+, Co2+, Cu2+, and Zn2+). We suggest that previously published vascular effects of Hg2+ and Pb2+ may have been secondary to responses of the vascular endothelium, and that the role of Ni2+ in hypertension should be investigated further. Our data indicate that the effects of metals on this vascular smooth muscle are specific and not generic. Moreover, this system could be utilized to investigate the mechanisms of metal-induced vasoconstriction.
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PMID:The effect of cadmium and other metals on vascular smooth muscle of the dogfish shark, Squalus acanthias. 233 May 99

Serotonin has several effects on vascular smooth muscle. In most vascular beds it causes vasoconstriction, but under the proper conditions it can cause vasodilatation. The constrictor response is a result of activation of specific receptors on the vascular smooth muscle, whereas the vasodilator response is mediated in part by the vascular endothelium. In addition to these direct effects on the vascular wall, serotonin can potentiate contractile responses to several other vasoactive agents (norepinephrine, angiotensin II, histamine, etc.). This indirect sensitizing action of the monoamine is probably mediated by activation of the S2 subclass of serotonergic receptors. These complex actions of serotonin on vascular smooth muscle may be altered in disease states such as hypertension.
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PMID:Direct and sensitizing effects of serotonin agonists and antagonists on vascular smooth muscle. 241 57

There are four humoral substances which are synthesized in the vascular endothelium: Endothelium Derived Relaxing Factor (EDRF); Endothelium Derived Hyperpolarizing Factor (EDHF); Endothelium Derived Contracting Factor (EDCF) and Prostacyclin. EDRF is identical with nitric oxide (NO), and, under physiological conditions is synthesized in the body from l-arginine. I the release of EDHF muscarinic M1 and M2 receptors are involved (implicated). EDCF (endothelin) is a 21 amino acid peptide (or series of peptides). The authors discuss the role and importance of the endothelum derived factors in different processes under physiological and pathophysiological conditions such as: regulation of the vascular tone, inflammation, trauma, hypertension, arteriosclerosis and aggregation.
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PMID:[The role of blood vessel endothelium in vascular smooth muscle reactivity to biologically active substances and drugs]. 249 Sep 97

The recent discovery of endothelium-derived relaxation factor (EDRF) has altered the traditional classification of vasodilators used in angina pectoris and heart failure. If a vasodilator induces release of EDRF from the epithelium it is classified as endothelium-dependent, if not it is independent. Sodium nitroprusside and SIN-1 (active metabolite of molsidomine) are the main independent vasodilators since the endothelium relaxation factor appears to be principally a nitric oxide radical in these synthetic vasodilators. In contrast, calcium-channel blockers and a good number of endogenous chemical mediators (acetylcholine, bradykinin, serotonin, etc.) are endothelium-dependent. Furthermore, simple increase in blood flow through the large vessels can result in endothelium-dependent vasodilation (flow rate-dependence) the extent of which depends on the drug examined. The fact that the pharmacologic response of a vasodilator can be altered under certain pathologic conditions (atherosclerosis, hypertension, diabetes, etc.) further increases the importance of the role of the vascular endothelium in the action of vasodilators since endothelial modulation may then be completely diverted to secretion of endothelium-derived contracting factors (EDCFS).
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PMID:[Vasodilator agents and the vascular endothelium]. 262 13

This review discusses the role of three mediators synthesized by the vascular endothelium, which are involved in maintaining the surface of the endothelial cells in a non-thrombogenic state. Prostacyclin, discovered in 1976, is a product of arachidonic acid metabolism. This labile prostanoid, with a chemical half life of approximately three minutes, relaxes vascular smooth muscle and inhibits the aggregation of blood platelets. Endothelium-derived relaxing factor (EDRF), discovered in 1980, is even more labile than prostacyclin with a half life counted in seconds. It also relaxes smooth muscle and inhibits the aggregation and adhesion of platelets. Recently, it has been identified as nitric oxide. Prostacyclin and EDRF are released together following stimulation of receptors on endothelial cells and cooperate to inhibit platelet aggregation and adhesion. 13-HODE, acts from inside the cell to make the endothelial surface less adhesive and is not released. These mediators act together to form the endothelial defence mechanism against adhering blood cells. Underproduction can lead to diseases such as hypertension or atherosclerosis. A mainly fish diet, rich in eicosapentaenoic acid alters the prostacyclin/thromboxane balance in favour of prostacyclin-like activity. This type of diet may provide protection against atherosclerosis and myocardial infarction.
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PMID:Mediators and the anti-thrombotic properties of the vascular endothelium. 264 8

The responsiveness of acetylcholine (ACh), nitroglycerin (NG) and norepinephrine (NE) (aorta only) in both basilar arteries (BA) and thoracic aortic (TA) rings from coarctation hypertensive rats (CHR) were studied and compared to their sham-operated normotensive control rats (SNR). The effects of these agents were also evaluated in TA or BA with and without endothelium from naive normotensive rats (NNR). Blood pressure (BP) and plasma renin activity (PRA) of CHR were significantly higher than their time-matched SNR. Endothelium removal from TA of NNR significantly enhanced NE and NG sensitivity and reduced the maximum ACh relaxation. Removal of BA endothelium of NNR abolished ACh-induced relaxation but had no effect on NG-induced relaxation. In BA from CHR at any stage of hypertension studied, the sensitivity and maximum relaxation induced by ACh or NG were not significantly different than their respective time-matched SNR. ACh sensitivity of TA did not change in 1 Day CHR but decreased in 4 and 14 Day CHR. NG sensitivity increased, did not change and decreased in 1, 4 and 14 Day CHR, respectively. NE sensitivity increased in all stages of hypertension. These data suggest that in coarctation-induced hypertension there is a complex progression of events in TA which is modulated by different mechanisms as evidenced by the changes in the effects of NE, ACh and NG at various stages of hypertension. The results also suggest that the vascular endothelium of TA but not of BA may provide an acute protective mechanism to counteract the imbalance created by the increased sensitivity of smooth muscle cells to contractile agonists in the early stage of hypertension. However, persistent hypertension appears to override this mechanism.
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PMID:Endothelium-dependent basilar and aortic vascular responses in normotensive and coarctation hypertensive rats. 267 67

Extrarenal renin has been identified in a number of tissues, including the brain, the submaxillary gland, uterus, ovary, vascular endothelium, testes, pituitary gland, and the adrenal cortex. In some tissues, including the adrenal cortex, all of the components of the renin-angiotensin system have been identified; however, no specific physiologic role has been clearly demonstrated for these extrarenal renin-angiotensin systems. We have studied the role of the renin-angiotensin system in the adrenal cortex of the rat and have found that renin is localized and synthesized in the zona glomerulosa cells. Its production can be influenced by alterations in electrolyte balance, as well as the genetic background of the rat. In adrenal capsular explant cultures, a converting enzyme inhibitor can lower angiotensin II production and reduce the stimulation of aldosterone by potassium, suggesting that this system is involved in the aldosterone response to potassium. In addition to rat adrenals, renin has been identified in human adrenal tissue and human adrenal tumors, including aldosteronomas, and a patient with hypertension has been reported to have an adrenal tumor that appeared to be secreting renin into the circulation.
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PMID:Adrenal renin: a possible local regulator of aldosterone production. 269 84


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