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)

In the case we have reported, there is a combination of factors that can be attributed to SLE and its associated complications, which may explain the transient hypodensities seen on cranial CT scan. Vasculitis and uncontrolled hypertension lead to arterial spasm, ischemia, and increased vascular permeability, all of which eventually cause cerebral edema. This edema may manifest itself clinically as profound but transient neurologic deficits.
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PMID:Reversible profound neurologic deficits associated with transient cranial CT abnormalities and systemic lupus erythematosus. 271 92

Experimental renovascular malignant arterial hypertension was produced by modified Goldblatt's procedures, in 60 rhesus monkeys, and various retinal arteriolar changes in hypertensive retinopathy were studied in detail (by serial ophthalmoscopy, and stereoscopic color fundus photography and fluorescein fundus angiography on long-term follow-up). The retinal arteriolar changes, in ophthalmoscopically visible arterioles, consisted of arteriolar sclerosis and associated changes, e.g., increased arteriolar tortuosity, arteriolar narrowing and in some animals occlusion and sheathing of the fine arterioles; we could find no evidence of localized or generalized 'spasm' in these retinal arterioles. Eyes in animals with accelerated arterial hypertension revealed focal dilatation and leakage of the retinal precapillary terminal arterioles (resulting in development of focal intraretinal periarteriolar transudates), and also occlusion of the terminal retinal arterioles (producing cotton-wool spots and associated intraretinal microvascular abnormalities). We discuss the controversial subjects of narrowing (particularly 'spasm') of ophthalmoscopically visible retinal arterioles and of fibrinoid necrosis in malignant hypertension.
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PMID:Retinal arteriolar changes in malignant arterial hypertension. 274 97

Morphological changes of the renal blood vessels were studied in 143 patients with different nephropathies and hypertensive disease. Vessels wall changes proper included: fibroelastosis, hyalinosis as well as antibodies to smooth muscle cells observed exclusively in the development of arterial hypertension. The changes were more pronounced in severe and durable hypertension. Perivascular sclerosis was found almost in all hypertensive patients and in some normotonic patients with aggravated heredity for arterial hypertension. The obtained data allow to frame a hypothesis on the role of formation of perivascular sclerosis as a reflection of repeated vascular spasm, subsequent increase of the peripheral resistance in the pathogenesis of development of arterial hypertension.
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PMID:[Structural changes in the kidney vessels in nephropathies and hypertension]. 275 Jan 16

Ca2+ channel blocking agents have proven to be one of the most exciting groups of drugs for management of many cardiovascular diseases and as potentially first-line agents for treatment of angina pectoris and hypertension. Unlike beta blockers, they can directly relax coronary and peripheral arteries and, therefore, reduce total peripheral resistance and improve tissue perfusion. Ca2+ channel blockers are drugs of choice for patients with Prinzmetal's angina and should be first-line drugs for mixed angina, and can be used alone or with beta blockers for classic angina. These drugs as a group have many potential clinical indications, especially in diseases in which vascular or smooth muscle spasm seems to cause the disease. Although all three Ca2+ channel blockers have a common mechanism of action, their cardiac and hemodynamic effects are different, nifedipine being the least depressant to cardiac function. In choosing the right agent, careful consideration should be given to the patient's characteristics in order to derive maximum benefit with minimal risks.
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PMID:Clinical indications for calcium channel blockers. 285 25

Apart from the generally known functions, the heart has also an endocrine function. Atrial cardiocytes, being typical secretory cells, release peptide hormones into the blood stream: atrial natriuretic peptide containing 28 amino acids and cardiodilatin. The structure of atrial peptides was determined. It was shown that both peptides were derived from their common precursor, a protein containing 151 amino acids. The presence of specific receptors is demonstrated on plasmatic membranes of cells of kidney epithelium, arterial smooth muscle, arterial endothelium, kidney cortex and hypophysis. The interaction of atrial peptides with these receptors activates the guanylate cyclase system. The biological action of atrial peptides manifests itself in the quick, massive and instantaneous increase of diuresis and electrolyte excretion, elevated clearance of creatinine, decrease of kidney vascular resistance, intensification of glomerular filtration, inhibition of stimulated secretion of aldosterone, relaxation of blood vessels, elimination of arterial and intestinal spasm induced by various endogenous and exogenous vasoconstrictors and in correction of kidney hypertension. Various radioimmunoassays for the presence of atrial peptides in human plasma were developed; it was shown that in patients with congestive heart failure the content of atrial peptides is increased.
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PMID:[Endocrine function of the heart. Structure and biological properties of peptides secreted by the heart atrium]. 295 15

Besides generally known functions, the heart has also an endocrine function. Atrial cardiocytes, being typical secretory cells, released peptide hormones into the blood stream: atrial natriuretic peptide containing 28 amino acids and cardiodiolatin. The structure of atrial peptides was determined. It was shown that both derived from their common precursor, a protein containing 151 amino acid. The presence of specific receptors was demonstrated on plasmatic membranes of cells of kidney epithelium, arterial smooth muscle, arterial endothelium, kidney cortex and hypophysis. The interaction of atrial peptides with these receptors activated the guanylate cyclase system. The biological action of atrial peptides manifested itself in the quick, massive and instantaneous increase of diuresis and electrolyte excretion, elevation of clearance of creatinine, decrease of kidney vascular resistance, intensification of glomerular filtration, inhibition of stimulated secretion of aldosterone, relaxation of blood vessels, elimination of arterial and intestinal spasm induced by various endogenous and exogenous vasoconstrictors and correction of kidney hypertension. Various radioimmunoassays for detection of atrial peptides in human blood plasma were developed; it was shown that in patients with congestive failure the atrial peptide content was increased.
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PMID:[A new approach to the problem of cardio-vascular regulation: the endocrine function of the heart (review of the literature)]. 295 52

Calcium channel blockers have an important role in the pharmacotherapy of cardiovascular disorders. These agents act by inhibiting the slow inward current into excitable cells, exert direct negative inotropic, chronotropic, and dromotropic activity, and are potent vasodilators. These direct effects are modified by reflex autonomic stimulation and by pathologic states. Serious adverse effects of the calcium channel blockers are most frequently observed in patients with ventricular dysfunction, conduction system disease, or concomitant beta blockade. Calcium channel blockers are indicated in the treatment of angina pectoris, supraventricular arrhythmias, and hypertension. The use of these agents in patients with hypertrophic cardiomyopathy, congestive heart failure, and pulmonary hypertension is investigational. The calcium channel blockers are gaining increased importance in the management of patients undergoing cardiac surgery. Verapamil is indicated for the treatment of post-cardiac-surgical atrial flutter and fibrillation; however, the calcium antagonists are not effective as prophylaxis against postoperative supraventricular arrhythmias. Laboratory studies have shown that drug interactions exist between calcium channel blockers and inhalational anesthetics and nondepolarizing neuromuscular blocking agents; clinical studies have demonstrated that these interactions are rarely significant. Perioperative coronary spasm can be effectively treated with the calcium channel blockers. The timing of calcium antagonist withdrawal prior to surgery is controversial, but continuation of therapy until surgery is usually safe. The clinical significance of platelet function inhibition by the calcium antagonists is unknown. Protection of ischemic myocardium by calcium channel blockers has been demonstrated. Important interactions between the calcium antagonists, hypothermia, and the ionic constituents of cardioplegia require further study before the role of these agents as adjuncts to clinical cardioplegia is defined. Expanded indications and the introduction of new calcium channel blockers will result in increased use of these agents in the future.
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PMID:Calcium channel blockers and cardiac surgery. 297 80

Intracoronary injection of acetylcholine has been shown to induce coronary spasm in patients with variant angina. To examine its sensitivity and specificity, incremental doses of acetylcholine (20, 50 and 100 micrograms into the left coronary artery and 20 and 50 micrograms into the right coronary artery) were injected into the coronary artery or arteries in 70 patients with variant angina (Group 1) (mean age 57 years) and 93 patients without variant angina or angina at rest (Group 2) (mean age 54 years). Forty patients of the latter group had atypical chest pain, 16 cardiomyopathy, 14 arrhythmia, 11 valvular disease, 7 stable effort angina due to advanced coronary artery disease, 3 congenital heart disease and 2 hypertension. A temporary cardiac pacemaker set at 40 to 50 beats/min was positioned in the right ventricle. Coronary spasm was defined as total occlusion or severe vasoconstriction associated with chest pain or ischemic ST changes on the electrocardiogram or both. In Group 1, acetylcholine induced spasm in 63 (90%) of the 70 patients in the artery or arteries predicted to be responsible for spontaneous attacks. In Group 2, acetylcholine induced coronary spasm only in one patient with effort angina and advanced coronary artery disease although lesser degrees of vasoconstriction (less than or equal to 75% of the luminal diameter) occurred in most patients after acetylcholine (specificity of acetylcholine thus was 99%). In conclusion, intracoronary injection of acetylcholine is sensitive and reliable for the induction of coronary spasm.
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PMID:Sensitivity and specificity of intracoronary injection of acetylcholine for the induction of coronary artery spasm. 304 96

Heroin, cocaine, amphetamines, sympathomimetic drugs can cause cerebral angiopathy. We report 2 patients with cerebrovascular disorders after ingestion of a nasal vasoconstrictor containing phenylpropanolamine (P.P.A.). The first patient had two acute repetitive attacks of severe headache and vomiting, occurring after a daily treatment with 180 mg of P.P.A. during 6 weeks. The second patient had an intracerebral hemorrhage, occurring some hours after taking for the first time 120 mg of P.P.A. In both cases, cerebral angiography, performed in the next week, demonstrated segmental narrowing and dilatations of medium-size intracranial arteries. None of the usual causes of cerebral vasculitis were present. The outcome was favorable and follow-up angiograms showed the disappearance of the beading pattern. P.P.A. is widely used over the counter in diet pills and stimulants. Cerebral vascular complications have been rarely reported, always hemorrhagic and often associated with cerebral vasculitis. They are unrelated to duration or dosage of treatment. The mechanism is unclear but could result from several factors: chronic or paroxystic high blood pressure, immuno-allergic vasculitis, arterial spasm, direct "toxic" effect of the P.P.A. on the arterial wall may be increased by other drugs and caffeine.
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PMID:[Benign cerebral angiopathies and phenylpropanolamine]. 304 37

It is a well-known fact that systemic hypertension is one of the major risk factors for myocardial infarction (MI). Extensive studies on hypertensive rats revealed that calcium is excessively elevated in the myocytes, as well as in the coronary artery wall of these animals, which results in a higher resting tension and a stronger contractile response of those muscle strips. Over many years coronary spasm has been claimed by various authors to be greatly involved in the pathophysiology of early phase of acute MI (AMI). It can be shown that thrombocytes that aggregate at the injured vessel wall next to atherosclerotic plaques release vasoconstrictive factors that induce series of severe spasms at the sites with defective endothelium that end up in myocardial infarction; the pathophysiologic pathway is called the thrombo-ischemic reentry mechanism. This local contractile response may be enhanced in the presence of systemic hypertension since intracellular calcium is elevated in the coronary smooth muscle. On the other hand, it has been shown that heart muscle fibers undergo severe alterations finally resulting in necrotization, as soon as free calcium ions penetrate excessively through the sarcolemma membrane into the myoplasm so that the capacities of the calcium binding or extrusion processes become overpowered; this is especially the case during ischemia. Since free intracellular calcium is already ten times elevated in the myocytes in systemic hypertension, the myocardium may be more vulnerable to further calcium overload owing to the ischemia and necrotization is augmented. The elevation of intracellular Ca of the myocytes of the cardiovascular system in systemic hypertension enhances the pathologic response of the coronary arteries and the myocardium. This work gives a complete overview of the pathophysiologic principles involved in AMI occurring with systemic hypertension.
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PMID:The interdependence of hypertension, calcium overload, and coronary spasm in the development of myocardial infarction. 304 54


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