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 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Based on analysis of 399 symptomatic patients with mitral valve prolapse (MVP) and the reported experience of others, we developed a clinical classification in order to improve nosology, provide better identification and promote insight into the mechanism of symptoms in patients with MVP. The heading of anatomic MVP designates those in whom symptoms or complications were primarily or directly related to valvular dysfunction and the heading of MVP syndrome designates those patients in whom symptoms cannot be explained on the basis of valvular dysfunction alone. Patients with MVP syndrome present with a symptom complex which results from various forms of neuroendocrine or autonomic dysfunction; the most common symptoms include chest pain, palpitations, cardiac arrhythmias, orthostatic phenomena, syncope, presyncope, fatigue, exercise intolerance, dyspnea and neuropsychiatric symptoms (Table 1). Mechanisms underlying the condition have been shown to include increased adrenergic activity, disturbances of catecholamine regulation, hyperresponsiveness to adrenergic stimulation, anomalous beta-adrenergic receptors, dysfunction of the parasympathetic portion of the autonomic nervous system, disturbances in renin-aldosterone regulation, decreased intravascular volume, diminished left ventricular diastolic volume in the upright position as well as abnormal secretion of atrial natriuretic factor (Table 2). In MVP syndrome, alterations of the heart, kidney, the adrenals and the autonomic nervous system coexist and interact, creating a complex "neuro-endocrine cardiovascular process" which may account for many of the symptoms otherwise unexplained on the basis of the valvular abnormality alone.
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PMID:Mitral valve prolapse syndrome: neuro-endocrinological aspects. 284 39

Water deprivation (WD) resulted in increased serum osmotic pressure (OP) and decreased body weight (WB); adrenal aldosterone content did not change. Adrenal corticosterone content tended to be elevated during early WD, indicating a stress response, but tended to decrease after seven days of WD, suggesting adrenal fatigue. During water restriction (WR), after the period of weight loss, adrenal corticosterone content and serum OP were elevated. As the birds began to gain weight, aldosterone levels did not change but adrenal corticosterone content and serum OP approached control values, suggesting that the birds were beginning to adapt to the WR. Adrenal sensitivity to ACTH was indicated by the elevated adrenal aldosterone and corticosterone content after ACTH injection.
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PMID:Adrenal responses to chronic and acute water stress in Japanese quail Coturnix japonica. 285 51

A 9-year-old boy who complained of fatigue, myalgias, and progressive weakness was found to have a markedly elevated serum creatine phosphokinase (CPK). He developed polyuria with polydipsia and was noted to be hypertensive and severely hypokalemic. Treatment with potassium and spironolactone alleviated his signs and symptoms and normalized the blood pressure and CPK. Initial studies revealed low plasma renin activity that did not increase with change from supine to upright position. Plasma aldosterone was consistently elevated in the supine position, decreased with upright posture, and was not suppressed by administration of dexamethasone. Plasma 18-hydroxycorticosterone also was elevated. Enhanced computerized tomography (CT) revealed a mass in the left adrenal that had not been seen on the initial unenhanced scan. Adrenal vein catheterization confirmed elevated plasma aldosterone on that side. Adrenalectomy was performed, and a well-encapsulated adenoma was found at examination of the surgical specimen. Postoperatively, suppression of plasma renin activity continued for many months without signs of aldosterone deficiency.
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PMID:Aldosterone-producing adenoma presenting with hypokalemic myopathy. Case report and review. 329 4

The cardiocirculatory actions of the oral vasodilator prazosin were evaluated by cardiac catheterization, forearm plethysmography, echocardiography, treadmill exercise, and symptoms in patients with advanced long-standing congestive heart failure. The administration of oral prazosin (2-7mg) reduced forearm venous tone and forearm vascular resistance. Concomitantly, mean systemic arterial pressure and left ventricular filling pressure decreased, and the cardiac index increased. These effects of a single dose of prazosin on left ventricular function were rapid in onset, maximal at 1 h, and sustained for the entire 6-h period of observation. After 2 weeks of outpatient therapy with 2-7 mg of prazosin four times daily, echographic end-diastolic dimension decreased, whereas the duration of treadmill exercise increased. Symptoms (dyspnea, fatigue, angina) were diminished throughout the course of prazosin therapy, and there was an improvement in the New York Heart Association functional class from 3.7 to 2.2. Thus, prazosin possesses sustained nitroprusside-like balanced dilator actions on the systemic arterial and venous beds, which are effectively translated into the beneficial hemodynamic effects of augmenting cardiac output and relieving excessive left ventricular end-diastolic pressure. The delayed vasodilator tolerance that occurs in 30% of the patients is prevented by the prior use of aldosterone antagonists, and is easily treated when present. Subacute hemodynamic suppression of beneficial prazosin vasodilator actions is transient and does not preclude successful sustained prazosin therapy of severe heart failure.
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PMID:Importance of neuroendocrine regulators of vascular tone and integral adrenoreceptor interaction during oral vasodilator therapy of severe congestive heart failure with prazosin. 617 36

The cardiocirculatory actions of prazosin (PZN) orally were evaluated by cardiac catheterization, forearm plethysmography, echocardiography, treadmill exercise, and symptoms in patients with advanced long-standing congestive heart failure (CHF). PZN orally (2 to 7 mg) reduced forearm venous tone and decreased forearm vascular resistance. Concomitantly mean systemic arterial pressure declined, left ventricular filling pressure (LVFP) decreased, and cardiac index (CI) was raised. These effects of a single dose of PZN on LV function were rapid in onset, maximal at 1 hour, and sustained for the entire 6 hours of observation. After 2 weeks of outpatient therapy with 2 to 7 mg PZN four times daily, echographic LV end-diastolic dimension decreased and the duration of treadmill exercise increased. Symptoms (dyspnea, fatigue, angina) were diminished throughout the course of PZN therapy, and New York Heart Association functional class improved for III to II. Thus PZN possesses sustained nitroprusside-like balanced dilator actions on the systemic arterial and venous beds, which are effectively translated into beneficial hemodynamics of augmenting lowered cardiac output and relieving excessive LVFP. Delayed vasodilator tolerance, occurring in 30% of patients, is prevented by prior use of aldosterone antagonists and is easily treated. Subacute hemodynamic suppression of beneficial PZN vasodilator actions is transient and does not preclude successful sustained PZN therapy of severe chronic CHF.
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PMID:Management of refractory congestive heart failure with prazosin. 626 22

Labetalol is a combined alpha- and beta-adrenoceptor blocking agent for oral and intravenous use in the treatment of hypertension. It is a nonselective antagonist at beta-adrenoceptors and a competitive antagonist of postsynaptic alpha 1-adrenoceptors. Labetalol is more potent at beta that at alpha 1 adrenoceptors in man; the ratio of beta-alpha antagonism is 3:1 after oral and 6.9:1 after intravenous administration. Labetalol is readily absorbed in man after oral administration, but the drug, which is lipid soluble, undergoes considerable hepatic first-pass metabolism and has an absolute bioavailability of approximately 25%. There are no active metabolites, and the elimination half-life of the drug is approximately 6 hours. Unlike conventional beta-adrenoceptor blocking drugs without intrinsic sympathomimetic activity, labetalol, when given acutely, produces a decrease in peripheral vascular resistance and blood pressure with little alteration in heart rate or cardiac output. However, like conventional beta-blockers, labetalol may influence the renin-angiotensin-aldosterone system and respiratory function. Clinical studies have shown that the antihypertensive efficacy of labetalol is superior to placebo and to diuretic therapy and is at least comparable to that of conventional beta-blockers, methyldopa, clonidine and various adrenergic neuronal blockers. Labetalol administered alone or with a diuretic is often effective when other antihypertensive regimens have failed. Studies have shown that labetalol is effective in the treatment of essential hypertension, renal hypertension, pheochromocytoma, pregnancy hypertension and hypertensive emergencies. In addition, preliminary studies indicate that labetalol may be of value in the management of ischemic heart disease. The most troublesome side effect of labetalol therapy is posture-related dizziness. Other reported side effects of the drug include gastrointestinal disturbances, tiredness, headache, scalp tingling, skin rashes, urinary retention and impotence. Side effects related to the beta-adrenoceptor blocking effect of labetalol, including asthma, heart failure and Raynaud's phenomenon, have been reported in rare instances.
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PMID:Labetalol: a review of its pharmacology, pharmacokinetics, clinical uses and adverse effects. 631 May 29

There is a close epidemiological association between obesity and elevated blood pressure for all age groups, although not every obese individual becomes hypertensive. In populations without age-related increases in body weight, an elevation of blood pressure with age is not seen. Mechanisms included in the development of hypertension in obesity are hyperinsulinemia, insulin induced sodium retention and increased sympathetic tone. Overnutrition with over intake of sodium and lack of physical exercise contribute to the metabolic syndrome of obesity. Thus, weight reduction by decreased energy uptake and increased physical exercise is recommended in the treatment of hypertension in obese patients. The resulting fall in insulin levels may lead to decreased sodium absorption in the kidney. Although treatment of obesity by weight loss decreases blood pressure substantially, a minority of patients do not respond to the weight loss. Blood pressure generally decreases before normal weight is achieved. Salt intake reduction does not appear to explain why weight reduction lowers blood pressure. Reduced levels of plasma renin activity, serum aldosterone levels, catecholamine levels and serum insulin levels may be involved in the blood pressure lowering associated with weight loss. Since the risk of cardiovascular disease in the hypertensive patient is not only determined by the blood pressure, an overall treatment which aims at reduction of other risk factors such as glucose intolerance and hyperlipoproteinemia is advocated. Thus, in any obese hypertensive patient normalization of excess body weight and increased physical activity appears to be the first and most important step of any rational therapeutic strategy.
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PMID:Obesity and hypertension: epidemiology, mechanisms, treatment. 636 45

The premenstrual symptom complex many women experience in a moderate to severe form can be divided into four subgroups. Because there is more than one syndrome and nervous tension is one of the most common symptoms, the term premenstrual tension syndromes (PMTS) is used. The most common subgroup, PMT-A, consists of premenstrual anxiety, irritability and nervous tension, sometimes expressed in behavior patterns detrimental to self, family and society. Elevated blood estrogen and low progesterone have been observed in this subgroup. Administration of vitamin B6 at doses of 200-800 mg/day reduces blood estrogen, increases progesterone and results in improved symptoms under double-blind conditions. Women in this subgroup consume an excessive amount of dairy products and refined sugar, and progesterone may be of value in them. The second-most-common subgroup, PMT-H, is associated with symptoms of water and salt retention, abdominal bloating, mastalgia and weight gain. The severe form of PMT-H is associated with elevated serum aldosterone. Vitamin B6 at high dosage suppresses aldosterone and results in diuresis and clinical improvement. Vitamin E helps the breast symptoms. Methylxanthines and nicotine should be curtailed and sodium limited to 3 gm/day. PMT-C is characterized by premenstrual craving for sweets, increased appetite and indulgence in eating refined sugar followed by palpitation, fatigue, fainting spells, headache and sometimes the shakes. PMT-C patients have increased carbohydrate tolerance and low red-cell magnesium. Adequate magnesium replacement results in improved glucose tolerance tests and decreased PMT-C symptoms. Deficiency of the prostaglandin PGE1 may also be involved in PMT-C. PMT-D is the least common but most dangerous because suicide is most frequent in this subgroup. The symptoms are depression, withdrawal, insomnia, forgetfulness and confusion. In ten PMT-D patients the mean blood estrogen was lower and the mean blood progesterone higher than normal during the midluteal phase. Elevated adrenal androgens are observed in some hirsute PMT-D patients. Two PMT-D patients with normal blood progesterone and estrogens had high lead levels in hair tissue and chronic lead intoxication. This subgroups needs careful medical attention when the symptoms are severe. Therapy should be individualized according to the results of the evaluation.
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PMID:Nutritional factors in the etiology of the premenstrual tension syndromes. 668 67

Thirty-two patients with primary hypertension were studied in a double-blind cross-over comparison between the cardioselective beta 1-blocking agent atenolol and the combined alpha- and beta-blocking agent labetalol. The doses used were atenolol 50--150 mg twice daily and labetalol 200--600 mg twice daily. Both drugs effectively reduced blood pressure and heart rate. Dose increments every second week resulted in a higher proportion of patients with normal blood pressure (les than or equal to 150/90 mm Hg) with both drugs. Labetalol was somewhat more effective in lowering upright blood pressure while atenolol caused a more pronounced heart-rate reduction. Both agents decreased plasma renin activity and urinary aldosterone excretion. Scalp tingling on labetalol (2 patients) and cold fingers with atenolol (1 patient) caused withdrawal of the drugs. Cold fingers were reported in another four patients during treatment with atenolol and in one when on labetalol. Tiredness and postural symptoms were more common during intake of labetalol.
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PMID:Antihypertensive and metabolic effects of increasing doses of atenolol and labetalol. A comparative study in primary hypertension. 676 Jun 79

1. Prizidilol (SKF 92657), a new antihypertensive drug with combined precapillary vasodilator and non-selective beta-adrenoceptor-blocking actions, was given to 24 patients with essential hypertension in a placebo-controlled, dose-titration study, Incremental doses from 200 to 800 mg were given once daily. Supine and standing blood pressure measured 24--27 h after drug intake was reduced during treatment with prizidilol (400--800 mg/day). Slight but significant decreases in heart rate were seen after moderate doses (mean: 447 mg once daily) of prizidilol. A more pronounced blood pressure reduction was noticed 2--7 h after drug administration. 2. Maximal blood pressure reduction coincided with peak plasma concentration of prizidilol, which was measured by a newly developed assay. 3. Plasma renin activity and 24 h urinary excretion of aldosterone and methoxycatecholamines were reduced after the highest doses (mean: 700 mg once daily) of prizidilol. 4. Prizidilol was well tolerated, although dizziness and tiredness were reported by four patients and oedema by two.
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PMID:Prizidilol (SKF 92657) in primary hypertension. 718 85


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