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At least 145 records · Page 8Linked to original sources
PubMed1989

Functional relationship between platelet alpha 2-adrenoceptors and sympathetic nerve activity in man.

Functional relationships between platelet alpha 2-adrenoceptors and sympathetic nerve activity were studied in patients with essential hypertension (n = 23), primary aldosteronism (n = 10), and normal subjects (n = 12). The maximum number of binding sites (Bmax) and the dissociation constant (Kd) of 3H-yohimbine on platelet membranes and resting plasma norepinephrine (NE) were similar among these groups of subjects. In all subjects combined, Bmax values were correlated positively (r = 0.471, p less than 0.01) to resting plasma NE and negatively (r = -0.531, p less than 0.01) to the changes in plasma NE when subjects were moved from lying to standing. A 2-4 week treatment with guanabenz or bethanidine induced a parallel fall of both Bmax and plasma NE, whereas administration of reserpine caused a similar fall of plasma NE but Bmax remained unchanged. Kd values were not changed after any of these treatments. The results support the view that platelet alpha 2-adrenoceptor density is functionally regulated in parallel with sympathetic nerve activity rather than plasma NE per se. This hypothesis seems quite reasonable when it is extended to the presynaptic alpha 2-adrenoceptors; otherwise, the negative feedback function on NE release should be lessened and contradictory to its physiological role.

Adult↗
PubMed1981

Withdrawal syndromes and the cessation of antihypertensive therapy.

A review of the available literature concerning sudden withdrawal of antihypertensive drugs shows that withdrawal syndromes after cessation of such agents have occurred with beta-blockers, methyldopa, clonidine hydrochloride, guanabenz, and bethanidine sulfate. Most commonly, these syndromes are limited to nervousness, tachycardia, headache, and nausea 36 to 72 hours after cessation of the drug. In rare cases, serious exacerbation of myocardial ischemia (beta-blockers) or hypertension (clonidine, methyldopa) may occur in the posttreatment period. The withdrawal syndromes generally respond promptly to reinstitution of antihypertensive therapy. The infrequent occurrence of withdrawal syndromes should not discourage use of these efficacious agents.

Adrenergic beta-Antagonists↗
PubMed1980

Factors influencing over and under-consumption of anti-hypertensive drugs.

Using a self-administered questionnaire, 817 patients attending two hypertension clinics were questioned about the number of tablets of different hypotensive drugs they took every day. The answers were compared with the number of tablets they should have been taking to determine the proportion who were not compliant with individual drug therapy. Ten per cent reported they were taking less than they should and seven per cent were taking more. Obsessionality was determined from a psychological questionnaire and non-compliant patients had a lower average score than compliant patients. Symptomatic side-effects associated with bethanidine appeared to induce non-compliance. Two symptoms were associated with failure to take the prescribed number of tablets, faintness on standing and a lessened interest in sex. This latest survey showed an improvement in compliance with most drugs compared with previous unpublished surveys conducted in 1971 to 1976. Once daily diuretic regimes were associated with better compliance than more complicated drug regimens.

Antihypertensive Agents↗
PubMed1984

New directions in antiarrhythmic drug therapy.

Cardiac arrhythmia causing sudden cardiac death is a serious worldwide public health problem. Antiarrhythmic agents have been available for therapy, but the conventional agents cause a high degree of intolerable side effects. The recent development of many new experimental antiarrhythmic agents has increased our capacity to effectively treat cardiac arrhythmias. Using a multifaceted approach of programmed electrical stimulation studies, drug level determinations, exercise testing and 24-hour ambulatory Holter monitoring, it can reasonably be decided which patient needs therapy and if therapy is going to be effective. Both aspects of the sudden death equation, ectopy frequency (triggering mechanism) and the ability to propagate sustained ventricular tachycardia (substrate), may be examined. Careful follow-up is needed to determine continued drug efficacy and the presence of side effects that may compromise patient compliance with therapy. If side effects intervene that may cause continued therapy to be intolerable, changing the antiarrhythmic agent, as opposed to decreasing the dosage to an ineffective range, may be appropriate. A comprehensive approach to arrhythmia management may begin to reduce the high incidence of sudden death due to fatal arrhythmias.

Adrenergic beta-Antagonists↗
PubMed1976

Patterns of blood-pressure during chronic administration of postganglionic sympathetic blocking drugs for hypertension.

Continuous recording of intra-arterial blood pressure in 11 ambulant patients taking postganglionic blocking drugs for the treatment of hypertension has shown an alternating pattern of high pressures at rest and very low pressures associated with exertion during normal daily activities. In 4 patients there was evidence of decreased cerebral or myocardial blood-flow during hypotensive episodes. It is suggested that these agents may predispose towards cerebral and myocardial infarction.

Adult↗
PubMed1979

Relationship between exchangeable sodium and blood pressure in different forms of hypertension in man.

1. Arterial pressure and exchangeable sodium (NaE) were measured in patients with Conn's syndrome, essential hypertension, renal artery stenosis and chronic renal failure. Comparison was made with a control group. Urine sodium excretion was measured separately from the two kidneys in patients with renal artery stenosis. 2. Compared with control, mean NaE was significantly increased in Conn's syndrome, and was normal in essential hypertension, renal artery stenosis and chronic renal failure. 3. The correlation of arterial pressure with NaE was positive and significant in Conn's syndrome, essential hypertension and chronic renal failure. 4. In contrast the correlation was significantly negative in unilateral renal artery stenosis. Patients with lowest NaE had hyponatraemia, hypokalaemia and secondary hyperaldosteronism. 5. Urinary sodium excretion from the unaffected kidney in unilateral renal artery stenosis correlated positively with arterial pressure, possibly reflecting the phenomenon of pressure-natriuresis. Patients subsequently responding least well to surgery excreted least sodium from the untouched kidney for a given arterial pressure. 6. The findings suggest important roles for arterial pressure in the regulation of sodium balance (predominant in renal artery stenosis), and for sodium balance in the regulation of arterial pressure (predominant in Conn's syndrome). The observations in essential hypertension are compatible either with an exact balance between these mechanisms or with the existence of some other mechanism raising blood pressure.

Adult↗
PubMed1986

Potassium channel blockade: A mechanism for suppressing ventricular fibrillation.

The suppression of ventricular fibrillation by antidysrhythmic drugs is well correlated with their ability to block potassium channels in nerve and cardiac membranes. Blockade of potassium channels reduces electrical inhomogeneities in action potential and conduction parameters that lead to ventricular fibrillation. These actions tend to effectively decrease the electrical size of the heart, which suggests a mechanism for antifibrillatory drug action. The receptor sites for antifibrillatory drug action (IK blockade) appear to be on the outside of the cardiac membrane whereas receptors for antiarrhythmic drug action (INa blockade) appear to be on the inside of the cardiac membrane.

4-Aminopyridine↗
PubMed1975

The influence of age and the level of arterial blood pressure on the changes in forearm blood flow resulting from sudden alterations in local vascular transmural pressure.

Forearm blood flow was measured by venous occlusion plethysmography in normotensive subjects of various ages and in patients with treated or untreated hypertension. Brief exposure of one forearm to pressures below atmospheric was used to study the transient local changes in arterial inflow which occurred with changes in transmural pressure induced in this way. The increase in initial arterial inflow with such an exposure to suction in a group of young normotensive women was only slightly reduced in two groups of older women. However, a group of subjects with untreated hypertension showed a significantly smaller initial inflow during the suction. There was some indication that adequate treatment of high blood pressure might reverse this effect.

Adult↗
PubMed1982

Psychiatric side effects of antihypertensive drugs other than reserpine.

The psychiatric side effects of the major antihypertensive drugs other than reserpine are reviewed, including centrally acting drugs such as methyldopa and clonidine, peripheral adrenergic drugs such as guanethidine, beta-adrenoceptor blockers such as propranolol, and diuretics. Problems with differential diagnosis and with the interpretation of case reports make assessment of psychiatric side effects difficult. Sedation and sleep disturbances are the most common side effects, occurring with methyldopa, clonidine, and propranolol. Only methyldopa is clearly associated with depression. Other reported effects are toxic confusional states and psychotic reactions. These are rare, however, and no clear patterns of development have been recognized.

Adrenergic beta-Antagonists↗
PubMed1984

Changes in active and inactive renin and in angiotensin II across the kidney in essential hypertension and renal artery stenosis.

Investigations were performed in 26 patients with essential hypertension and 24 with unilateral renal artery stenosis. In each patient blood was drawn simultaneously and in triplicate, from both renal veins and aorta, for measurement of plasma concentrations of active and inactive renin and of angiotensin II. In 19 patients estimates of individual renal plasma flow were obtained in order to calculate secretion rates for active and inactive renin, and to assess the contribution of renin secretion rate and of renal plasma flow to the renal vein renin ratio. In patients with essential hypertension there was evidence that the kidney secreted active renin (18% mean increase in renal vein concentration above that of arterial plasma; P less than 0.001), but no evidence of secretion of inactive renin (4% mean increase; NS). There was a tendency for the kidney to extract angiotensin II (8% mean decrease in renal vein concentration below that of arterial plasma; P = 0.07). The affected kidney in patients with renal artery stenosis showed marked secretion of active renin (364% mean increase; P less than 0.001) and also secreted inactive renin (80% mean increase; P less than 0.05) with net generation of angiotensin II across the renal circulation (100% mean increase; P less than 0.05). The contralateral kidney exhibited suppressed secretion of active renin (3% mean increase; NS) with no evidence of secretion of inactive renin (2% mean increase; NS), and marked extraction of angiotensin II (50% mean decrease; P less than 0.001). The correlation between combined secretion rate of active renin by both kidneys and the arterial concentration of active renin in patients with essential and renovascular hypertension taken together was strongly positive (r = 0.82; P less than 0.01). The same correlation for inactive renin was weak (r = 0.32; NS). The correlation between the combined secretion rates of active renin by both kidneys and the circulating plasma concentration of angiotensin II (r = +0.60; P less than 0.05) was both significant and positive. By contrast, the total 'secretion' rate of angiotensin II by both kidneys was inversely related to arterial plasma angiotensin II (r = -0.92; P less than 0.001). This latter relationship suggests an important role for the kidney in clearing angiotensin II from the circulation, this being more marked the higher the arterial angiotensin II concentration.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1981

Abrupt discontinuation of antihypertensive therapy.

The abrupt cessation of antihypertensive medication is usually without immediate consequence but may be associated with symptoms and signs of enhanced sympathetic activity, severe hypertension, morbid ischemic cardiovascular events, or death. This syndrome is more common after discontinuation of high doses of centrally acting antiadrenergic and beta-adrenergic blocking drugs or combination antihypertensive therapy, but it also occurs with numerous antihypertensive agents. Predisposing factors include ischemic heart disease, severe hypertension, renovascular or high renin hypertension, and high doses of multiple antihypertensive drugs. Gradual tapering of antihypertensive medications over seven to ten days will prevent symptoms and marked elevation of blood pressure. Should a discontinuation syndrome develop, re-administration of the drug previously discontinued is the most appropriate treatment.

Adrenergic beta-Antagonists↗