Angiotensin blood pressure affected

Lisinopril is an angiotensin-converting enzyme (ACE) inhibitor and ACE inhibitors should be avoided during pregnancy. ACE inhibitors may adversely affect fetal and neonatal blood pressure control and renal function. They may also cause neonatal skull defects. 

Captopril-lysozyme did not significantly affect systemic blood pressure whereas an equimolar dose of captopril alone decreased blood pressure significantly. Whereas free captopril (5 mg kg ) completely prevented an angiotensin-I-induced blood pressure increase, an equimolar amount of captopril-lysozyme did not. However, in line with the direct ACE activity measurements in renal tissue and plasma, in captopril-lysozyme-treated rats the an-giotensin-I-induced blood pressure increase was lower than in untreated rats, suggesting that systemic activity was not fully prevented. 

The inhibition of ACE, located in different tissues (e.g., plasma, lung, kidney, heart, skeletal muscle, pancreas, brain) may influence various regulatory systems (Ondetti and Cushman, 1984). ACE plays a pivotal role in two independent humoral systems that affect blood pressure, since it is responsible for the generation of a vasopressor agent, angiotensin II, and for the inactivation of a vasodepressor agent, bradykinin. Many specific ACE-inhibitors have been developed for use as a potent, orally administered antihypertensive drug (Wyvratt and Patchett, 1985). 

Blood pressure is also regulated via the hormonal feedback loop shown in Figure II-1-3. The system is affected only by decreases in mean blood pressure (hypotension), which result in decreased renal blood flow. Decreased renal pressure causes the release of renin, which promotes formation of the angiotensins. Angiotensin II increases aldosterone release from the adrenal cortex, which, via its mineralocorticoid actions to retain sodium and water, increases blood volume. Increased venous return results in an increase in cardiac output. Angiotensin II also causes vasoconstriction, resulting in an increase in TPR. 

Phthalide 30 did not affect mean arterial blood pressure in normal anesthetized rats [313] or subarachnoid hemorrhaged rats [329, 330], In spontaneous hypertensive rats, however, 30 elicited a transient reduction in systolic blood pressure without affecting the activities of plasma and tissue angiotensin converting enzymes or urine output, which were diuresis indicators [354]. 

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