2. There is potentiation of sympathetic activity and the release of norepinephrine is attenuated. This action causes further vasodilatation and reduction in afterload. The effect on the sympathetic nervous system and increased vagal tone prevents the increase in heart rate that is observed with other vasodilating agents. This important action is helpful in the management of heart failure where tachycardia causes increased work for the heart, and in hypertensive patients it prevents hyper¬trophy. Other vasodilating drugs are deleterious in these two conditions.
3. There is a reduction in aldosterone secretion that promotes sodium excretion and potassium retention. This action also prevents or improves heart failure. Unfortunately, aldosterone secretion is not completely suppressed. Agents that completely suppress aldoste-rone are being investigated.
4. Converting enzyme is the same as kininase II, which causes degradation of bradykinin to inactive peptides. The accumulation of bradykinin appears to stimulate the release of the important vasodilator nitric oxide (NO) and prostacyclin, which protect the endothelial lining of arteries. This accumulation also contributes to arterial dilation and a further decrease in peripheral vascular resistance and afterload. Thus, ACE inhibitors are more beneficial than angiotensin receptor blockers that do not have this salutary effect on bradykinin. Excessive bradykinin, however, may cause angioedema in susceptible individuals.

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