Hypertension vasodilators

The antimycotic activity of a number of substituted 3-(3,3,3-trichloro-2-hydroxyprop-l-yl)benzofurans has been reported. Diuretic and other activities have been observed in a number of substituted aminobenzofuran-2-carboxylic acid derivatives. a- 2-Benzofuranyl) acrylic acid has exhibited a marked depressive ataratic and hypotensive activity (61MI31200), while 5-cinnamoylbenzofurans, e.g. (499), have been examined for hypertensive, vasodilating and spasmolytic activities (70GEP1933178). 

ANTI HYPERTENSIVE VASODILATORS, ACE INHIBITORS, ANGIOTENSIN II RECEPTOR BLOCKERS, AND CALCIUM CHANNEL BLOCKERS ... 

VASODILATOR ANTI HYPERTENSIVES VASODILATOR ANTI HYPERTENSIVES Profound, refractory J- BP may occur when diazoxide is co-administered with hydralazine Additive effect uncertain why the effect is so refractory to treatment Avoid co-administration of diazoxide with hydralazine... 

Key Words Crataegus oxyacantha heart failure hypertension vasodilation digoxin. 

Morphine triggers histamine release from mast cells in the skin. This reaction is not mediated by opioid receptors. This histamine can cause bronchospasm, hypertension, vasodilation, and facial flushing. True allergic reactions, including anaphylactic reactions, to opioids are rare but have been reported. 

They have adrenalin and vasodilating properties that can be utilized in the treatment of hypertension. 

Calcium channel blockers cause more pronounced lowering of blood pressure in hypertensive patients than in normotensive individuals. Generally, all calcium channel blockers cause an immediate increase in PRA during acute treatment in patients having hypertension but PRA is normalized during chronic treatment despite the sustained decrease in blood pressure. These agents also do not generally produce sodium and water retention, unlike the conventional vasodilators. This is because they produce diuretic effects by direct actions on the kidney. 

Nifedipine (Table 3) is a potent vasodilator that selectively dilates resistance vessels and has fewer effects on venous vessels. It does not cause reflex tachycardia during chronic therapy. Nifedipine is one of the first-line choices for black or elderly patients and patients having concomitant angina pectoris, diabetes, or peripheral vascular diseases. Nifedipine, sublingually, is also suitable for the treatment of hypertensive emergencies. Nifedipine does not impair sexual function or worsen blood Hpid profile. The side effects are flushing, headache, and dizziness. 

DHPs are potent arterial vasodilators. They act on resistance vessels and therefore reduce peripheral vascular resistance, lower arterial blood pressure, and antagonize vasospasms in coronary or peripheral arteries. By reducing afterload, DHPs also reduce cardiac oxygen demand. Together with their vascular spasmolytic effect, this explains most of the beneficial actions of DHPs in angina pectoris. Most DHPs are only licensed for the therapy of hypertension, some of them also for the treatment of angina pectoris and vasospastic (Prinzmetal) angina. 

In low doses, inhaled NO may have a beneficial therapeutic effect, since NO in the inspired air leads to pulmonary vasodilation. In persistent pulmonary hypertension of the newborn, NO inhalation has already been used with some success. NO inhalation as the treatment for acute respiratory distress syndrome, however, has been disappointing. Only transient improvements of oxygenation were detected and the outcome of placebo-controlled trials did not show any improvement... 

Vasodilators are a group of dtugs, which relax the smooth muscle cells of the blood vessels and lead to an increased local tissue blood flow, a reduced arterial pressure and a reduced central venous pressure. Vasodilators reduce the cardiac pre-load as well as after-load and thereby reduce cardiac work. They are used in a variety of conditions including hypertension, cardiac failure and treatment/prevention of angina pectoris. Major groups are Ca2+-channel blockers (e.g. dihydropyridines), NO-donators (e.g. organic nitrates), K+-channel openers (minoxidil), phosphodiesterase inhibitors (e.g. sildenafil), Rho-kinase inhibitors (e.g. Y27632) or substances with unknown mechanism of action (e.g. hydralazine). Inhibitors of the... 

Phentolamine (Regitine) is used for its vasodilating effect on peripheral blood vessels and therefore may be beneficial in the treatment of hypertension caused by... 

Vasodilating drags sometimes relieve die symptoms of vascular disease, but in some cases dragtherapy provides only minimal and temporary relief. Many of die vasodilating drug s are also used to treat hypertension. Their use as antihypertensives is discussed in Chapter 42. 

Increased intrahepatic resistance to portal flow increases pressure on the entire splanchnic bed an enlarged spleen (splenomegaly) is a common finding in cirrhotic patient and can result in thrombocytopenia due to splenic sequestration of the platelets. Portal hypertension mediates systemic and splanchnic arterial vasodilation through production of nitric oxide and other vasodilators in an attempt to counteract the increased pressure gradient. Nitric oxide causes a fall in systemic arterial pressure unfortunately, this activates both the renin-angiotensin-aldosterone and sympathetic nervous systems and... 

Only non-selective p-blockers reduce bleeding complications in patients with known varices. Blockade of P, receptors reduces cardiac output and splanchnic blood flow. 02-Adrenergic blockade prevents p2-receptor-mediated splanchnic vasodilation while allowing unopposed a-adrenergic effects this enhances vasoconstriction of both the systemic and splanchnic vascular beds. The combination of P, and P2 effects makes the non-selective p-blockers preferable to car-dioselective agents in treating portal hypertension.1,36,41... 

Wagner JA, Varga K, Jarai Z, Kunos G. Mesenteric vasodilation mediated by endothelial anandamide receptors. Hypertension 1999 33 429-34. 

Results of a more recent series of investigations suggest that lead may cause hypertension in rats by increasing reactive oxygen species, which act as vasoconstrictors, and decreasing nitric oxide, a vasodilator released by the endothelium. The reactive oxygen species may be the hydroxyl radical, and did not appear to be the superoxide anion (Ding et al. 1998). 

Hypertension, or a chronic elevation in blood pressure, is a major risk factor for coronary artery disease congestive heart failure stroke kidney failure and retinopathy. An important cause of hypertension is excessive vascular smooth muscle tone or vasoconstriction. Prazosin, an aradrenergic receptor antagonist, is very effective in management of hypertension. Because oq-receptor stimulation causes vasoconstriction, drugs that block these receptors result in vasodilation and a decrease in blood pressure. 

The vascular endothelium produces a number of substances that are released basally into the blood vessel wall to alter vascular smooth muscle tone. One such substance is endothelin (ET-1). Endothelin exerts its effects throughout the body, causing vasoconstriction as well as positive inotropic and chronotropic effects on the heart. The resulting increases in TPR and CO contribute to an increase in MAP. Synthesis of endothelin appears to be enhanced by many stimuli, including Ag II, vasopressin, and the mechanical stress of blood flow on the endothelium. Synthesis is inhibited by vasodilator substances such as prostacyclin, nitric oxide, and atrial natriuretic peptide. There is evidence that endothelin is involved with the pathophysiology of many cardiovascular diseases, including hypertension, heart failure, and myocardial infarction. Endothelin receptor antagonists are currently available for research use only. 

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