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

Present knowledge of the mechanisms regulating release of renin is reviewed with particular emphasis on neural factors. Evidence is given for a direct effect of renal innervation on beta adrenergic receptors in juxtaglomerular cells, and for the involvement of reflex release of renin in conditions such as tilting and acute salt depletion. Participation of neural and nonneural mechanisms of control is also shown to occur in other conditions, such as aortic constriction and hemorrhage. The view is held that neural sympathetic factors might explain some of the renin disturbances found in essential hypertension. First, in patients with high renin hypertension part of the hypertension is renin-dependent, and these pressor levels of renin seem to be neurally induced since they can commonly be suppressed by beta adrenoreceptor blocking agents. Second, the hypothesis is presented that patients with low renin hypertension, at least those who have no volume disturbance, have a blunted sympathetic control of renin release. Therefore a sufficiently precise test of sympathetic activity, and possibly of body fluid volumes, should be associated with renin profiles for a better understanding of the pathophysiology of arterial hypertension and as a better guide to therapeutic management. Indeed, most of the available antihypertensive drugs act on sympathetic activity, body fluid volume or renin, and this multifaceted profile would provide more rational guidelines for treatment.
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PMID:Control of renin release: a review of experimental evidence and clinical implications. 0 64

With the wide range of medications available today it should be possible to obtain satisfactory control in the majority of hypertensive patients. However, there are various categories of patients who may present particular problems in management, as for example patients with cerebro-vascular and coronary disease, or with renal failure. A particularly important group is those presenting with severe resistant hypertension, and these patients may constitute about 5 to 10% of the hypertensive population. Considerations relevant to the management of patients presenting with such problems are discussed. Combined drug regimens employing clonidine or beta-blockers with peripheral vasodilators appear to be particularly useful.
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PMID:The difficult hypertensive. 0 88

The physician who understands the pathophysiology of angina pectoris can apply rational therapeutic measures based on an appreciation of the determinants of myocardial oxygen supply and demand. Most patients with angina secondary to coronary atherosclerosis can be treated conservatively using a systematic approach that includes correction or removal of underlying causes or precipitating factors and the judicious use of sublingual nitroglycerin. In patients with more resistant angina, use of oral or topical nitroglycerin or sublingual isosorbide dinitrite as well as propranolol can be advised. Aortocoronary bypass surgery can offer significant improvement in carefully selected patients with frequent angina poorly controlled by medical therapy. The most important consideration in the treatment of angina is protection of coronary blood flow reserve by primary prevention of the atherosclerotic process itself. All individuals from families prone to coronary artery disease should be evaluated for alterable risk factors, the most important being cigarette smoking, hypertension, and hypercholesterolemia. Considering the high risk of unheralded sudden death in previously asymptomatic patients with coronary atherosclerosis, angina can, in a sense, be considered a fortunate harbinger of coronary stenosis, identifying candidates for secondary preventive measures aimed at retarding the progression of vascular disease. More importantly, angina serves as an index for detecting families at high risk of coronary artery disease, in whom early application of primary prevention may afford a more promising outlook.
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PMID:Angina pectoris. Diagnosis and treatment. 0 83

Primary aldosteronism and renovascular hypertension are two different diseases in which renin determinations are necessary for establishment of diagnosis or therapeutic procedure. Low renin values which are not stimulated by acute stimuli combined with elevated plasma aldosterone concentrations confirm the diagnosis of primary aldosteronism. When in a patient with proven renal artery stenosis a significant difference in renal venous renin activity is observed between the two kidneys, a connection between hypertension and renal artery stenosis is likely when in addition the renin secretion of the unaffected kidney is suppressed. A favourable outcome for surgery can be predicted when the individual clinical picture in such a case is also considered. A similar view also holds for the connection between hypertension and unilateral small kidney not due to renal artery stenosis. In essential hypertension the plasma renin level makes it possible to a certain extent to predict whether a patient will benefit from diuretics or from beta-blocking agents. Despite this experience, however, renin determinations are not indicated in every case of essential hypertension. It has not been proven that the prognosis of this disease is improved by renin oriented monotherapy rather than by effective treatment with other antihypertensive agents.
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PMID:[The value of renin determination in the diagnosis of hypertension]. 0 81

Cerebral hemispheric blood flow and metabolism were measured before and after therapy with intracarotid infusion of combined PBZ and PPL in 15 patients with recent cerebral infarction. HBF was unaltered despite decrease in cerebral perfusion pressure. Cerebral hemispheric oxygen comsumption and carbon dioxide production decreased while cerebral hemispheric lactate production increased. Biphasic cerebral uptake of tyrosine was observed during and immediately after PBZ and PPL infusion. CSF HVA increased, indicating altered DA turnover. CSF 5HIAA levels also increased, suggesting altered 5HT turnover after PBZ and PPL. Release of cyclic AMP from ischemic brain into cerebral venous blood seen in the steady state was abolished after therapy. Cerebral hemodynamic studies suggest a functional balance between monaminergic neurogenic influences in the control of cerebral circulation. Imbalance of such controlling factors in ischemic brain may lead to paradoxical vascular responses to induced hypertension and hypotension. PBZ and PPL enhance such responses perhaps by increasing central neurotransmitter turnover and release. Further shift toward cerebral anaerobic metabolism may occur in ischemic brain following the use of phenoxybenzamine and propranolol. Worsening of neurological deficit occurred in four cases. Combined therapy with PBZ and PPL does not appear beneficial in the therapy of patients with recent stroke.
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PMID:Influence of adrenergic receptor blockade on circulatory and metabolic effects of disordered neurotransmitter function in stroke patients. 0 7

When pathophysiological and pathogenetic aspects of hypertension are taken into consideration with special regard to diabetes mellitus the exhaustion of the "insulin enhancement" within the cerebrovisceral functional systems (Baumann) are discussed and the authors enter possible connections of diabetes mellitus to the renin-angiotensin-aldosterone system. After explanation of the diabetogenic and antidiabetogenic pharmacodynamic qualities of the antihypertensive drugs adequate therapeutic recommendations are proposed summarized in a figure. The authors conclude that for the present antihypertensive therapy in diabetics taking into consideration the references reported on there are sufficient possibilities of treatment for all degrees of severity of hypertension. Such preparations as Rausedan, Disotat, Dopegyt appear as particularly suitable; moreover, the beta receptor blockers, Haemiton, Depressan as well as Guanitil and Pargylin prove to be possible or without disadvantage, respectively. Especially when diuretics are described an exact control of the metabolism should be carried out.
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PMID:[Treatment of hypertonus in diabetes mellitus]. 0 29

In case of cranial trauma, early respiratory troubles either of central or peripheral origin often accelerate the deterioration of the neurological situation. The different values of PCO2, PO2, pH and alcaline reserve measured on samples of CSF in comatose patients prove the central acidosis related to metabolic and vascular disorders in the damaged areas. Our results confirm the correlation between the importance of this disturbances and the severity of the trauma. It is thus necessary to insure patients of satisfactory respiration conditions. The tracheobronchial cleansing is applicable to intubated or tracheotomized patients by an instillation of 5ml of simple or bicarbonated physiological serum 4 to 6 times a day, followed by repeated aspirations and associated to a preventive endotracheal instillation of 80 mg of Gentamycin 4 times a day. Moreover we use controlled respiration which does not modify the gazometric parameters in the CSF but which assures patients a normoxia and moderate hypocapnia with a decrease of intracranial hypertension. Treatment by controlled hyperventilation must be precocious, because the recuperation at the level of the damaged zones is very slow.
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PMID:Treatment of comatose patients by mechanical hyperventilation. 0 50

Recent studies demonstrated that epinephrine causes significant pulmonary A-V shunting. This study reports the effect of alpha and beta adrenergic blockade on this shunting. Sixty-three anesthetized mongrel dogs were ventilated with a mechanical respirator. Measurements of (1) the pulmonary shunt, (2) cardiac output, (3) mean pulmonary artery, pulmonary capillary wedge and systemic pressures, and (4) pulmonary and systemic vascular resistances were obtained at 5, 15 and 30 minute intervals during the first hour and hourly for 5 hours. Fifteen dogs received no treatment. All others received epinephrine hydrochloride, 2 mug/kg/min for 5 hours. Ten received epinephrine only. Ten were pretreated with propranolol hydrochloride, 250 mug/kg, 12 with phenoxybenzamine, 1 mg/kg, and 16 with phenoxybenzamine and propranolol. Propranolol significantly decreased the epinephrine induced pulmonary shunt at all times and was the most effective drug. Phenoxybenzamine decreased the early shunting, but less than propranolol, and did not decrease the late shunting. Blockade with propranolol and phenoxybenzamine was less effective than propranolol alone. Based on the observed hemodynamic changes it was suggested that beta blockade is effective in reducing epinephrine induced pulmonary insufficiency by favorably altering the flow and distribution of pulmonary blood flow which in turn decreases epinephrine induced ventilation-perfusion inequalities and capillary hypertension both of which result in shunting. Conversely phenoxybenzamine has an unfavorable effect on the pulmonary flow. These studies support previous work in animals and man which showed that beta adrenergic stimulation is important in the pathogenesis of pulmonary insufficiency. Because the amounts of epinephrine used produce blood levels observed in critical illness, these studies add support to a relationship between the increased catecholamine stimulation of critical illness and the associated and often unexplained pulmonary insufficiency.
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PMID:Effect of alpha and beta adrenergic blockade on epinephrine induced pulmonary insufficiency. 0 61

There is evidence that hypersensitivity of vascular muscle to neurotransmitters contributes to the development of hypertension. Comparison of the caudal arteries of spontaneously hypertensive rats (SHR) and their genetically related Kyoto-Wistar normotensive control rats (KNR) showed that although there is no difference in membrane potential under unstimulated conditions, greater depolarization of the SHR vascular muscle cells by norepinephrine occurs at concentrations which cause greater contraction. The mechanism for the increased depolarization and resulting increase in contraction appears to be a lower intracellular potassium ion activity in SHR vascular muscle cells, which results in a lower contribution of potassium gradient to membrane potential. Experiments to determine the sensitivity of isolated, dispersed chick omphalomesenteric vascular muscle cells to neurotransmitters showed remarkably low thresholds to the neutransmitters norepinephrine, serotonin, and acetylcholine, but not potassium chloride. The high sensitivity of isolated cells to neurotransmitters suggests that factors in the intact vessel may cause thresholds to be high, possibly implying that alterations in a neurotrophic mechanism might be responsible for changes in vascular muscle sensitivity in situ.
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PMID:Cellular basis for increased sensitivity of vascular smooth muscle in spontaneously hypertensive rats. 0 7

Briefly trained physicians assistants using protocols (clinical algorithms) for diabetes, hypertension, and related chronic arteriosclerotic and hypertensive heart disease abstrated information from the medical record and obtained history and physical examination data on every patient-visit to a city hospital chronic disease clinic over a 18-month period. The care rendered by the protocol system was compared with care rendered by a "traditional" system in the same clinic in which physicians delegated few clinical tasks. Increased thoroughness in collecting clinical data in the protocol system led to an increase in the recognition of new pathology. Outcome criteria reflected equivalent quality of care in both groups. Efficiency time-motion studies demonstrated a 20 per cent saving in physician time with the protocol system. Coct estimates, based on the time spent with patients by various providers and on the laboratory-test-ordering patterns, demonstrated equivalent costs of the two systems, given optimal staffing patterns. Laboratory tests were a major element of the cost of patient care,and the clinical yield per unit cost of different tests varied widely.
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PMID:Quality, efficiency, and cost of a physician-assistant-protocol system for managment of diabetes and hypertension. 0 25


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