Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although verapamil is a well-established treatment for angina, cardiac arrhythmias and cardiomyopathies, this review reflects current interest in calcium antagonists as anti-hypertensive agents by focusing on the role of verapamil in hypertension. Verapamil is a phenylalkylamine derivative which antagonises calcium influx through the slow channels of vascular smooth muscle and cardiac cell membranes. By reducing intracellular free calcium concentrations, verapamil causes coronary and peripheral vasodilation and depresses myocardial contractility and electrical activity in the atrioventricular and sinoatrial nodes. Verapamil is well suited for the management of essential hypertension since it produces generalised systemic vasodilation resulting in a marked reduction in systemic vascular resistance and, consequently, blood pressure. Evidence from clinical studies supports the role of oral verapamil as an effective and well-tolerated first-line treatment for the management of patients with mild to moderate essential hypertension. Clinical studies have shown that verapamil is more effective the higher the pretreatment blood pressure and some authors have found a more pronounced antihypertensive effect in older patients or in patients with low plasma renin activity. Sustained release verapamil formulations are available for oral administration which, as a single daily dose, are as effective in lowering blood pressure over 24 hours as equivalent doses of conventional verapamil formulations given 3 times daily. As a first-line antihypertensive agent, oral verapamil is equivalent to several other calcium antagonists, beta-blockers, diuretics, angiotensin-converting enzyme (ACE) inhibitors and other vasodilators, and is not associated with many of the common adverse effects of these treatments. Verapamil may be preferred as an alternative first-line antihypertensive treatment to diuretics in elderly patients because it has similar efficacy in these patients without causing the adverse effects commonly linked with diuretic treatment. Furthermore, because verapamil does not cause bronchoconstriction, it may be used in preference to beta-blockers in patients with asthma or chronic obstructive airway disease. Reflex tachycardia, orthostatic hypotension or development of tolerance is not evident following verapamil administration. As a second- or third-line treatment for patients refractory to established antihypertensive regimens, verapamil produces marked blood pressure reductions when combined with diuretics and/or ACE inhibitors, beta-blockers and vasodilators such as prazosin.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Verapamil. An updated review of its pharmacodynamic and pharmacokinetic properties, and therapeutic use in hypertension. 267 May 11

Emerging evidence has suggested that with minimal prerequisite training, slow deep breathing around 0.10 Hz can acutely enhance cardiovagal baroreflex sensitivity (BRS) in humans. Such reports have led to the speculation that behavioral interventions designed to reduce breathing frequency may serve a therapeutic role in ameliorating depressed baroreflex function in conditions such as chronic heart failure, essential hypertension, and obstructive airway disease. This study sought to test the hypothesis that slow controlled breathing acutely enhances cardiovagal baroreflex function in young healthy volunteers. Distinct from earlier studies, however, baroreflex function was examined (n = 30) using the classical pharmacological modified Oxford method, which enabled the assessment of cardiovagal BRS through experimentally driven baroreceptor stimulation across a wide range of blood pressures. For a comparison against existing evidence, spontaneous cardiovagal BRS was also assessed using the alpha-index and sequence method. Compared with fast breathing (0.25 Hz), slow breathing (0.10 Hz) was associated with an increase in the alpha-index (8.1 +/- 14 ms/mmHg, P < 0.01) and spontaneous up-sequence BRS (10 +/- 11 ms/mmHg, P < 0.01). In contrast, BRS derived from spontaneous down sequences and the modified Oxford method were unaltered by slow breathing. The lack of change in BRS derived from the modified Oxford method challenges the concept that slow breathing acutely augments arterial baroreflex function in otherwise healthy humans. Our results also provide further evidence that spontaneous BRS may not reflect the BRS determined by experimentally driven baroreceptor stimulation.
 ...
PMID:Respiratory modulation of cardiovagal baroreflex sensitivity. 1960 28