Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1 Cardioselective and non-selective beta-blockers affect to a different degree several aspects of the circulatory homeostasis. The evidence available in this regard has been evaluated and the possible clinical importance of these differences has been discussed. 2 Venous return in partly regulated by beta-receptors (possibly of the beta 2 type) in the venous resistance vessels. Differences in blockade of venous return by the two classes of beta-blockers may, therefore, influence the degree of increase in left ventricular size, left ventricular end diastolic BPs and stroke volume during beta-blockade. 3 At the first part of the dose-reponse curve, non-selective beta-blockers seem to block more effectively renin release than cardioselective beta-blockers. 4 The direction and the extent to which beta-blockers 'directly' affect total peripheral resistance (TPR), is determined by the resultant of the degree of decrease in TPR by blockade of renin release and the extent of the increase in TPR by blockade of the beta 2-receptors in the arteriolar wall. 5 The clinical relevance of these differences could be that--especially in the low doses range--non-selective beta-blockers may be more 'safe' in patients with compromised cardiac function and may be more appropriate for the therapy of high renin hypertension than cardioselective blockers, whereas the latter may be more appropriate for the majority of hypertensive patients who have low to normal renin hypertension.
 ...
PMID:Possible significance of the pharmacological differentiation of beta-blockers for therapy of hypertension. 3 72

Renovascular hypertension and high renin hypertension were found to be associated with an excess prevalence of carotid artery atherosclerotic lesions and to a higher risk of stroke, respectively, as compared to low-to-normal renin hypertension. Primary aldosteronism, being characterized by hypertension and a chronically suppressed plasma renin activity, should be accompanied by a low prevalence of carotid artery lesions. To verify this hypothesis we investigated prospectively, by a high resolution duplex ultrasound technique, the prevalence of extracranial carotid artery lesions in a case-controlled study of 34 (22 women and 12 men, aged 22 to 76 years) patients with no history or symptoms of cerebrovascular disease. Primary aldosteronism was diagnosed in 17 patients; 12 had a surgically confirmed unilateral aldosterone-secreting adenoma; and 5 had idiopathic hyperaldosteronism. Each primary aldosteronism patient was individually matched with a control with primary hypertension for sex, race, age, body mass index, casual blood pressure levels, duration of hypertension, smoking, diabetes mellitus, total serum cholesterol, and triglycerides. After the matching, the two groups were similar in terms of demographic features and overall cardiovascular risk profile (all P = NS). However, plasma renin activity and aldosterone levels were significantly lower and higher, respectively, in primary aldosteronism than in primary hypertensive patients. In primary aldosteronism the overall prevalence of carotid artery lesions at duplex was 59%, not significantly different from that (53%) found in primary hypertensives. Thus, at variance with renovascular hypertension, primary aldosteronism is not associated with an excess prevalence of carotid artery lesions.
 ...
PMID:Prevalence of extracranial carotid artery lesions at duplex in primary aldosteronism. 842 67

In order to lower arterial blood pressure, antihypertensive drugs decrease cardiac output, total peripheral resistance or both. Diuretics, beta-blockers, and central adrenergic inhibitors decrease cardiac output. ACE inhibitors, angiotensin II antagonists, calcium antagonists, alpha-blockers, central adrenergic inhibitors, and after a delay also diuretics and beta-blockers decrease peripheral resistance. Diuretics are first line therapy for treating low renin hypertension. Beta blockers are used for treating high renin hypertension and patients suffering additional coronary artery disease. ACE inihibitors can be given for treating high renin hypertension particularly in conjunction with diabetes, heart failure or left ventricular hypertrophy. Combining ACE inhibitors with diuretics potentiates the antihypertensive effect. Angiotensin II antagonists exert fewer side effects and better renal protection than ACE inhibitors. The main indication for calcium antagonists is low renin hypertension, their advantages being strong blood pressure reduction as well as in preventing stroke. Central alpha2 receptor agonists and other vasodilators are chosen only in selected cases and mostly in combination with other antihypertensive drugs.
 ...
PMID:[Pharmacological basis of antihypertensive drug therapy]. 1519 36

In the 1970s, pharmacological therapy interrupting the renin-angiotensin system was considered beneficial for patients with high-renin hypertension. This gave rise to the development of ACE inhibitors. Surprisingly, the ACE inhibitors proved to be effective not only in patients with high renin hypertension, but also in many patients with normal levels of plasma renin activity. At present ACE inhibitors have a significant position in a wide range of chronic illnesses such as atherosclerosis, hypertension, myocardial infarction, diabetic complications, stroke etc. They are combined safely with drugs like angiotensin receptor blockers, calcium channel blockers and thiazides with varying degree of benefits. Though they are safe drugs, patients need monitoring for renal insufficiency, hypotension, hyperkalemia etc. The safety of these drugs in paediatrics patients is not established. It is better to avoid these drugs during pregnancy.
 ...
PMID:Therapeutic dimensions of ACE inhibitors--a review of literature and clinical trials. 1865 May 98