Drugs online research references
Neuroendocrinology. 1986;42(2):97-101.
Centrally administered inhibitors of the generation and action of angiotensin II do not attenuate the increase in ACTH secretion produced by ether stress in rats.
Buckner FS, Chen FN, Wade CE, Ganong WF.
The role of the brain renin-angiotensin system in the ACTH response to ether stress in rats was investigated by injecting the angiotensin II receptor blocking drug saralasin, the angiotensin II converting enzyme inhibitors enalaprilat and captopril, and the renin inhibitor L 363714 intraventricularly and measuring the ACTH and corticosterone concentration in plasma 10 min after ether stress. ACTH and corticosterone were elevated to at least the same level in rats treated with the inhibitors as they were in rats treated with the corresponding vehicles; indeed, ACTH values were somewhat greater in stressed rats treated with the converting enzyme inhibitors and the renin inhibitor. ACTH values in the absence of ether were not affected by saralasin, enalaprilat, and captopril and were increased by L 363714. The data do not support the hypothesis that the brain renin-angiotensin system is involved in the maintenance of ACTH secretion or that it mediates the increase produced by ether stress.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3005899&dopt=Abstract
Brain Res. 1992 May 8;579(2):261-9.
Effect of peptidase inhibition on the pattern of intraspinally released immunoreactive substance P detected with antibody microprobes.
Duggan AW, Schaible HG, Hope PJ, Lang CW.
Department of Preclinical Veterinary Sciences, University of Edinburgh Summerhall, UK.
Antibody microprobes bearing antibodies to the C-terminus of substance P (SP) were used to measure release of immunoreactive (ir) SP in the dorsal horn of barbiturate anaesthetized spinal cats. Electrical stimulation of unmyelinated primary afferents of the ipsilateral tibial nerve produced a relatively localised release of ir SP in the superficial dorsal horn. Prior microinjection of the peptidase inhibitors kelatorphan and enalaprilat in the dorsal horn resulted in ir SP being detected over the whole of the dorsal horn and the overlying dorsal column. This pattern had previously been observed with evoked release of ir neurokinin A and supports the proposal that a slow degradation results in a neuropeptide accessing many sites remote from sites of release.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1378348&dopt=Abstract
J Pharmacol Exp Ther. 1987 Oct;243(1):292-6.
Effect of pH on the inhibition of angiotensin converting activity by enalaprilat in the rat perfused mesenteric vascular bed.
Lindsey CJ, Bendhack LM, Paiva AC.
Department of Biophysics, Escola Paulista de Medicina, Sao Paulo, Brazil.
The previous finding that converting enzyme inhibitors (CEIs) potentiate bradykinin (BK), but do not inhibit conversion of angiotensin (ANG) I in isolated vessels, was explored further in the rat perfused mesenteric vascular bed. To investigate whether other peptidases besides angiotensin converting enzyme (ACE) might be involved in CEI-resistant ANG I conversion, synthetic angiotensinogen fragments (1-14, 1-11 and 2-14) were studied. Their vasoconstrictor activities were found to be about 80 times less than that of ANG I, and were not altered by the CEI enalaprilat, indicating that tonin-like enzymes do not play a role in the generation of ANG II by the arterial wall. The hypothesis that BK potentiation by CEI in arteries might be due to a direct effect on the receptors was not supported by the lack of potentiation, by enalaprilat, of the vasorelaxant effect of Lys-Lys-BK (an ACE-resistant BK homologue). Finally, the effect of pH in the perfusing solution on ACE inhibition by enalaprilat was studied. Whereas converting activity decreased with increasing pH in the range 6.8 to 8.1, enalaprilat did not affect the responses to ANG I at pH 7.5 or 7.8, but blocked them at pH 7.1. Our results indicate that arterial ACE shows substrate-specific inhibition and that, at physiological pH, converting activity is resistant to inhibition by CEIs, whose hypotensive action would be due mainly to inhibition of arterial wall kininase activity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2822902&dopt=Abstract
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