The report of the 4th Joint National Committee on detection, evaluation and treatment of high blood pressure medication recommended to start with the destination of any of the diuretics Cove, adrenoblokatorov ( -blockers), Ca antagonists (calcium channel blockers) or inhibitor angiotensin-converting enzyme (ACE). When choosing a suitable drug, one should take into account the patient’s age, the presence of concomitant diseases, as well as conditions that can either serve as contraindications to the use of certain drugs (for example, chronic obstructive pulmonary diseases when prescribing -blockers), or determine the special indications to the use of certain drugs (e.g. -blockers or Ca antagonists for angina).
These are vasodilators that reduce blood pressure by reducing general peripheral resistance without causing reflex tachycardia . They reduce blood pressure in a wide range of patients with hypertension, regardless of plasma renin activity. ACE inhibitors suppress the activity of the renin-angiotensin system, preventing the inactive octapeptide, angiotensin I from converting to angiotensin II, a powerful potential vasoconstrictor and aldosterone stimulator. In addition, ACE inhibitors prevent degradation of the vasodilator bradykinin, inhibiting kininase II, an enzyme that inactivates bradykinin. Bradykinin levels increase, which increases the synthesis of various prostagglandins (also having a vasodilator action). Thus, ACE inhibitors have a combined effect by reduced production of angiotensin II and increased levels of bradykinin and various prostaglandins .
ACE inhibitors are the drugs of choice in combination with diabetes mellitus and arterial hypertension with IHD, myocardial infarction, systolic and diastolic heart failure, impaired function of the sinus node, cardiac conduction system, pulmonary hypertension, Raynaud’s disease. There are indications of reverse development of left ventricular hypertrophy and improvement of its perfusion. Reverse development of left ventricular hypertrophy is mainly associated with a decrease in pre- and afterload on the heart. The basis of stimulation of protein synthesis by angiotensin II, which contributes to the development of hypertrophy of intact myocardium due to the local renin-angiotensin system (RAS) in the heart. It has been shown (Hansson, 1998)that in patients with diabetes mellitus the risk of myocardial infarction and other fatal cardiovascular complications is significantly reduced in the group treated with ACE inhibitor compared with the group treated with Б -blockers and diuretics.
Contraindications are expressed forms of mitral and aortic stenosis, stenosis of the carotid and renal arteries. Undesirable for pregnancy and renal failure. Side effects include a dry cough due to bradykininin irritation of nerve endings. ACE inhibitors are well tolerated by patients. Unlike other antihypertensive drugs, they do not adversely affect carbohydrate, lipid or purine metabolism, combined with diuretics, б -blockers, and Ca antagonists. ACE inhibitors have a positive effect on carbohydrate metabolism by reducing peripheral resistance to glucose, an improvement in insulin sensitivity by 40%, which, most likely, can be explained by an increase in the muscular digestibility of glucose. It is known that ACE is identical to kinase II, the enzyme responsible for the destruction of bradykinin. A higher level of kinin entails a possible increase in insulin sensitivity.