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The contribution of nitric oxide to cardiovascular status and responses to vasodilators in conscious, hypertensive, transgenic ((mRen-2)27) rats.
Br J Pharmacol. 1998 May; 124(2):299-306.BJ

Abstract

1. The aim of the study was to measure the regional haemodynamic responses to vasodilators, and the effects of nitric oxide (NO) synthase inhibition, in conscious, hypertensive, transgenic ((mRen-2)27) rats (TG rats) and normotensive, Hannover Sprague-Dawley (SD) rats. 2. The hypotensive response to acetylcholine was greater in TG than in SD rats, but the renal vasodilator responses were not different. 3. The responses to bradykinin were similar in the two strains, except that hindquarters vasodilatation occurred only in SD rats. 4. Salbutamol caused smaller renal and hindquarters vasodilatation in TG rats than in SD rats, and there was mesenteric vasodilatation only in the latter strain. 5. The hypotensive response to sodium nitroprusside was smaller, but the accompanying mesenteric vasodilatation was greater, in SD than in TG rats. 6. The contribution of NO to the vasodilator responses was taken as the difference between the responses in the presence of the NO synthase inhibitor, NG-nitro-L-arginine methylester (L-NAME), compared to those in the presence of a co-infusion of angiotensin II and vasopressin (to match the haemodynamic effects of L-NAME). 7. In TG rats, L-NAME caused a greater absolute pressor effect, but a smaller mesenteric vasoconstriction, than in SD rats. 8. L-NAME affected the vasodilator responses to all the challenges similarly in the two strains. 9. Collectively, the results provide no direct evidence for impaired NO-mediated vasodilator mechanisms in TG rats. It is feasible that the reduced hindquarters response to bradykinin and the reduced renal and hindquarters responses to salbutamol, in TG rats are due to abnormal beta2-adrenoceptor-mediated processes.

Authors+Show Affiliations

School of Biomedical Sciences, University of Nottingham Medical School, Queen's Medical Centre.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

9641546

Citation

Gardiner, S M., et al. "The Contribution of Nitric Oxide to Cardiovascular Status and Responses to Vasodilators in Conscious, Hypertensive, Transgenic ((mRen-2)27) Rats." British Journal of Pharmacology, vol. 124, no. 2, 1998, pp. 299-306.
Gardiner SM, March JE, Kemp PA, et al. The contribution of nitric oxide to cardiovascular status and responses to vasodilators in conscious, hypertensive, transgenic ((mRen-2)27) rats. Br J Pharmacol. 1998;124(2):299-306.
Gardiner, S. M., March, J. E., Kemp, P. A., & Bennett, T. (1998). The contribution of nitric oxide to cardiovascular status and responses to vasodilators in conscious, hypertensive, transgenic ((mRen-2)27) rats. British Journal of Pharmacology, 124(2), 299-306.
Gardiner SM, et al. The Contribution of Nitric Oxide to Cardiovascular Status and Responses to Vasodilators in Conscious, Hypertensive, Transgenic ((mRen-2)27) Rats. Br J Pharmacol. 1998;124(2):299-306. PubMed PMID: 9641546.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The contribution of nitric oxide to cardiovascular status and responses to vasodilators in conscious, hypertensive, transgenic ((mRen-2)27) rats. AU - Gardiner,S M, AU - March,J E, AU - Kemp,P A, AU - Bennett,T, PY - 1998/6/26/pubmed PY - 1998/6/26/medline PY - 1998/6/26/entrez SP - 299 EP - 306 JF - British journal of pharmacology JO - Br J Pharmacol VL - 124 IS - 2 N2 - 1. The aim of the study was to measure the regional haemodynamic responses to vasodilators, and the effects of nitric oxide (NO) synthase inhibition, in conscious, hypertensive, transgenic ((mRen-2)27) rats (TG rats) and normotensive, Hannover Sprague-Dawley (SD) rats. 2. The hypotensive response to acetylcholine was greater in TG than in SD rats, but the renal vasodilator responses were not different. 3. The responses to bradykinin were similar in the two strains, except that hindquarters vasodilatation occurred only in SD rats. 4. Salbutamol caused smaller renal and hindquarters vasodilatation in TG rats than in SD rats, and there was mesenteric vasodilatation only in the latter strain. 5. The hypotensive response to sodium nitroprusside was smaller, but the accompanying mesenteric vasodilatation was greater, in SD than in TG rats. 6. The contribution of NO to the vasodilator responses was taken as the difference between the responses in the presence of the NO synthase inhibitor, NG-nitro-L-arginine methylester (L-NAME), compared to those in the presence of a co-infusion of angiotensin II and vasopressin (to match the haemodynamic effects of L-NAME). 7. In TG rats, L-NAME caused a greater absolute pressor effect, but a smaller mesenteric vasoconstriction, than in SD rats. 8. L-NAME affected the vasodilator responses to all the challenges similarly in the two strains. 9. Collectively, the results provide no direct evidence for impaired NO-mediated vasodilator mechanisms in TG rats. It is feasible that the reduced hindquarters response to bradykinin and the reduced renal and hindquarters responses to salbutamol, in TG rats are due to abnormal beta2-adrenoceptor-mediated processes. SN - 0007-1188 UR - https://www.unboundmedicine.com/medline/citation/9641546/The_contribution_of_nitric_oxide_to_cardiovascular_status_and_responses_to_vasodilators_in_conscious_hypertensive_transgenic___mRen_2_27__rats_ L2 - https://doi.org/10.1038/sj.bjp.0701838 DB - PRIME DP - Unbound Medicine ER -