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Acute intravenous injection and short-term oral administration of N(G) -nitro-L-arginine methyl ester to the rat provoke increased pressor responses to agonists and hypertension, but not inhibition of acetylcholine-induced hypotensive responses.
Fundam Clin Pharmacol. 2011 Jun; 25(3):333-42.FC

Abstract

In experiments in vivo, we studied whether the endothelial dysfunction induced by nitric oxide (NO) synthesis inhibition is simultaneously or sequentially manifested as a reduced level of endothelium-dependent agonist-induced vasodilatation, an increased responsiveness to vasoconstrictors, and hypertension. Vascular responses to acetylcholine, phenylephrine, and angiotensin II were measured in pithed rats after acute intravenous injection (100 mg/kg) and short-term oral administration of N(G) -nitro-L-arginine methyl ester (L-NAME; 60 mg/kg per day) for 1 and 3 days (L-NAME(1d) and L-NAME(3d), respectively). Pithed rats were chosen because drug-induced cardiovascular responses reflect only peripheral effects. Parallel experiments examined mean arterial pressure (MAP) values in anesthetized rats. After short-term L-NAME(1d) and L-NAME(3d) treatments, the MAP was significantly elevated in anesthetized but not pithed rats. Acute intravenous administration of L-NAME elevated MAP in pithed rats. Intravenous infusion of phenylephrine was used to compensate for the pressor response induced by L-NAME in pithed animals. The maximum decrease and duration of the hypotensive responses to acetylcholine were unaltered by the acute and both short-term L-NAME treatments in pithed rats. These treatments, on the other hand, increased phenylephrine- and angiotensin II-induced pressor responses in pithed animals. In isolated aortic rings prepared from pithed rats treated acutely and short-term with L-NAME, acetylcholine-induced relaxations were inhibited. Thus, the inhibition of NO-dependent vasodilator tone after acute intravenous injection and short-term oral L-NAME administration may be associated with vascular smooth muscle hyper-responsiveness to pressor agonists and hypertension, whereas the hypotensive responses to acetylcholine could not be associated with the L-NAME-induced endothelial dysfunction in pithed rats.

Authors+Show Affiliations

Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, México, D.F., México.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20608990

Citation

López, Ruth M., et al. "Acute Intravenous Injection and Short-term Oral Administration of N(G) -nitro-L-arginine Methyl Ester to the Rat Provoke Increased Pressor Responses to Agonists and Hypertension, but Not Inhibition of Acetylcholine-induced Hypotensive Responses." Fundamental & Clinical Pharmacology, vol. 25, no. 3, 2011, pp. 333-42.
López RM, Pérez T, Castillo C, et al. Acute intravenous injection and short-term oral administration of N(G) -nitro-L-arginine methyl ester to the rat provoke increased pressor responses to agonists and hypertension, but not inhibition of acetylcholine-induced hypotensive responses. Fundam Clin Pharmacol. 2011;25(3):333-42.
López, R. M., Pérez, T., Castillo, C., Castillo, M. C., & Castillo, E. F. (2011). Acute intravenous injection and short-term oral administration of N(G) -nitro-L-arginine methyl ester to the rat provoke increased pressor responses to agonists and hypertension, but not inhibition of acetylcholine-induced hypotensive responses. Fundamental & Clinical Pharmacology, 25(3), 333-42. https://doi.org/10.1111/j.1472-8206.2010.00852.x
López RM, et al. Acute Intravenous Injection and Short-term Oral Administration of N(G) -nitro-L-arginine Methyl Ester to the Rat Provoke Increased Pressor Responses to Agonists and Hypertension, but Not Inhibition of Acetylcholine-induced Hypotensive Responses. Fundam Clin Pharmacol. 2011;25(3):333-42. PubMed PMID: 20608990.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Acute intravenous injection and short-term oral administration of N(G) -nitro-L-arginine methyl ester to the rat provoke increased pressor responses to agonists and hypertension, but not inhibition of acetylcholine-induced hypotensive responses. AU - López,Ruth M, AU - Pérez,Teresa, AU - Castillo,Carlos, AU - Castillo,María C, AU - Castillo,Enrique F, PY - 2010/7/9/entrez PY - 2010/7/9/pubmed PY - 2011/8/11/medline SP - 333 EP - 42 JF - Fundamental & clinical pharmacology JO - Fundam Clin Pharmacol VL - 25 IS - 3 N2 - In experiments in vivo, we studied whether the endothelial dysfunction induced by nitric oxide (NO) synthesis inhibition is simultaneously or sequentially manifested as a reduced level of endothelium-dependent agonist-induced vasodilatation, an increased responsiveness to vasoconstrictors, and hypertension. Vascular responses to acetylcholine, phenylephrine, and angiotensin II were measured in pithed rats after acute intravenous injection (100 mg/kg) and short-term oral administration of N(G) -nitro-L-arginine methyl ester (L-NAME; 60 mg/kg per day) for 1 and 3 days (L-NAME(1d) and L-NAME(3d), respectively). Pithed rats were chosen because drug-induced cardiovascular responses reflect only peripheral effects. Parallel experiments examined mean arterial pressure (MAP) values in anesthetized rats. After short-term L-NAME(1d) and L-NAME(3d) treatments, the MAP was significantly elevated in anesthetized but not pithed rats. Acute intravenous administration of L-NAME elevated MAP in pithed rats. Intravenous infusion of phenylephrine was used to compensate for the pressor response induced by L-NAME in pithed animals. The maximum decrease and duration of the hypotensive responses to acetylcholine were unaltered by the acute and both short-term L-NAME treatments in pithed rats. These treatments, on the other hand, increased phenylephrine- and angiotensin II-induced pressor responses in pithed animals. In isolated aortic rings prepared from pithed rats treated acutely and short-term with L-NAME, acetylcholine-induced relaxations were inhibited. Thus, the inhibition of NO-dependent vasodilator tone after acute intravenous injection and short-term oral L-NAME administration may be associated with vascular smooth muscle hyper-responsiveness to pressor agonists and hypertension, whereas the hypotensive responses to acetylcholine could not be associated with the L-NAME-induced endothelial dysfunction in pithed rats. SN - 1472-8206 UR - https://www.unboundmedicine.com/medline/citation/20608990/Acute_intravenous_injection_and_short_term_oral_administration_of_N_G___nitro_L_arginine_methyl_ester_to_the_rat_provoke_increased_pressor_responses_to_agonists_and_hypertension_but_not_inhibition_of_acetylcholine_induced_hypotensive_responses_ L2 - https://doi.org/10.1111/j.1472-8206.2010.00852.x DB - PRIME DP - Unbound Medicine ER -