Reference

Dilation of epicardial arteries in conscious dogs induced by angiotensin-converting enzyme inhibition with enalaprilat

Dilation of epicardial arteries in conscious dogs induced by angiotensin-converting enzyme inhibition with enalaprilat. Holtz, J.; Busse, R.; Sommer, O.; Bassenge, E. (Dep. Appl. Physiol., Univ. Freiburg, Freiburg D-7800, Fed. Rep.Some commonly used reagents like 1407-47-2 and 9015-82-1 are used in this experiment. Ger.). J. Cardiovasc. Pharmacol., 9(3), 348-55 (English) 1987. CODEN: JCPCDT. ISSN: 0160-2446. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) In conscious dogs, the effect was examd. of angiotensin-converting enzyme (ACE) [9015-82-1] inhibition by enalaprilat [76420-72-9] on parameters potentially important to provocation of myocardial ischemia, such as sympathetic activity, myocardial oxygen consumption, and vascular tone in coronary conduit and resistance vessels. Under normal Na intake, enalaprilat (0.0o and 0.3 mg/kg, i.v.) did not modify the norepinephrine release rate into plasma (a parameter of overall sympathetic activity). The higher dosage reduced myocardial O consumption, mean arterial pressure (MAP), and coronary conduit artery tone without dilating coronary resistance vessels. Following renin [9015-94-5]-angiotensin [1407-47-2] activation by Na deprivation, enalaprilat similarly lowered myocardial O consumption and reduced vascular tone both in coronary conduit. Although MAP declined, heart rate and norepinephrine release rate were no modified significantly. Apparently, the dilation of epicardial arteries results from a direct intramural action. Enalaprilat seems unlikely to provoke myocardial ischemia even in states with a strongly activated renin-angiotensin system. .

In vitro and in vivo activities of enkephalinase and angiotensin converting enzyme inhibitors: relationship of enzyme inhibition to analgesic and cardiovascular effects

In vitro and in vivo activities of enkephalinase and angiotensin converting enzyme inhibitors: relationship of enzyme inhibition to analgesic and cardiovascular effects. Chipkin, Richard E.; Billard, William; Ahn, Ho Sam; Sybertz, Edmund J.; Iorio, Louis C. (Dep. Pharmacol., Schering Corp., Bloomfield, NJ 07003, USA). Degrad. Endog. Opioids: Its Relevance Hum. Pathol. Ther., 91-106. Edited by: Ehrenpreis, Seymour; Sicuteri, Federigo.Several substances with their cas registry numbers 62571-86-2 and 75496-63-8 may be metioned in this study. Raven: New York, N. Y. (English) 1983. CODEN: 50IHAQ. DOCUMENT TYPE: Conference CA Section: 1 (Pharmacology) Despite the overlap of in vitro substrate specificity of the natural peptides, the enzymes metabolizing enkephalins (ENK) and angiotensin I (AI) [484-42-4] are unique. This is seen in the in vitro specificity of the inhibitors and the in vivo sepn. of their pharmacol. actions. Furthermore, there appears to be a correlation between the effects seen in vitro and in vivo. This is seen in the total sepn. of activity of captopril [62571-86-2] and MK 421 diacid [76420-72-9] against angiotensin converting enzyme (ACE) [9015-82-1] and enkephalinase A (Enk'ase A) [75496-63-8] in vitro, and a similar full carryover to the in vivo models. Similarly, thiorphan [76721-89-6]-induced strong Enk'ase A and weak ACE inhibitory activity in vitro are reflected in its effects in tests of analgesia and cardiovascular function. .