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Bolus injection of human UII in conscious rats evokes a biphasic haemodynamic response.
Br J Pharmacol. 2004 Oct; 143(3):422-30.BJ

Abstract

A biphasic cardiovascular response to bolus i.v. injection of human urotensin II (hUII, 3 nmol kg(-1)) in conscious, male, Sprague-Dawley (SD) rats was identified and underlying mechanisms were explored. Initially (0-5 min) there was tachycardia, hypotension and mesenteric and hindquarters vasodilatation; later (30-120 min), tachycardia, hindquarters vasodilatation and a modest rise in blood pressure occurred. Pretreatment with indomethacin or N(G) nitro-l-arginine methylester (l-NAME) reduced the mesenteric vasodilator response to hUII, and abolished the late tachycardia and hindquarters vasodilatation. Indomethacin also abolished the hypotension and early hindquarters vasodilatation, and substantially reduced the initial tachycardia. Indomethacin and l-NAME together prevented all haemodynamic responses to hUII. Inhibition of inducible NOS had no effect on responses to hUII, whereas inhibition of neuronal NOS reduced the delayed tachycardic response to hUII but did not significantly affect the vasodilatation. Only the initial tachycardic response to hUII was antagonised by propranolol. In spontaneously hypertensive rats (SHR), the initial haemodynamic responses to hUII were qualitatively similar to those in SD rats, although there was also a modest renal vasodilatation. The secondary response comprised a smaller tachycardia and a small rise in blood pressure, with no significant hindquarters vasodilatation. Haemodynamic responses to hUII were not enhanced by endothelin and angiotensin receptor antagonism in either SD rats or in SHRs. One interpretation of these results is that the primary response to bolus injection of hUII is prostanoid- or prostanoid- and NO-mediated (mesenteric vasodilatation) and that this triggers secondary events, which are dependent on eNOS (hindquarters vasodilatation) and neuronal NOS (tachycardia).

Authors+Show Affiliations

Centre for Integrated Systems Biology & Medicine, School of Biomedical Sciences, University of Nottingham, Nottingham. sheila.gardiner@nottingham.ac.ukNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

15339862

Citation

Gardiner, Sheila M., et al. "Bolus Injection of Human UII in Conscious Rats Evokes a Biphasic Haemodynamic Response." British Journal of Pharmacology, vol. 143, no. 3, 2004, pp. 422-30.
Gardiner SM, March JE, Kemp PA, et al. Bolus injection of human UII in conscious rats evokes a biphasic haemodynamic response. Br J Pharmacol. 2004;143(3):422-30.
Gardiner, S. M., March, J. E., Kemp, P. A., & Bennett, T. (2004). Bolus injection of human UII in conscious rats evokes a biphasic haemodynamic response. British Journal of Pharmacology, 143(3), 422-30.
Gardiner SM, et al. Bolus Injection of Human UII in Conscious Rats Evokes a Biphasic Haemodynamic Response. Br J Pharmacol. 2004;143(3):422-30. PubMed PMID: 15339862.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Bolus injection of human UII in conscious rats evokes a biphasic haemodynamic response. AU - Gardiner,Sheila M, AU - March,Julie E, AU - Kemp,Philip A, AU - Bennett,Terence, Y1 - 2004/08/31/ PY - 2004/9/2/pubmed PY - 2005/1/19/medline PY - 2004/9/2/entrez SP - 422 EP - 30 JF - British journal of pharmacology JO - Br J Pharmacol VL - 143 IS - 3 N2 - A biphasic cardiovascular response to bolus i.v. injection of human urotensin II (hUII, 3 nmol kg(-1)) in conscious, male, Sprague-Dawley (SD) rats was identified and underlying mechanisms were explored. Initially (0-5 min) there was tachycardia, hypotension and mesenteric and hindquarters vasodilatation; later (30-120 min), tachycardia, hindquarters vasodilatation and a modest rise in blood pressure occurred. Pretreatment with indomethacin or N(G) nitro-l-arginine methylester (l-NAME) reduced the mesenteric vasodilator response to hUII, and abolished the late tachycardia and hindquarters vasodilatation. Indomethacin also abolished the hypotension and early hindquarters vasodilatation, and substantially reduced the initial tachycardia. Indomethacin and l-NAME together prevented all haemodynamic responses to hUII. Inhibition of inducible NOS had no effect on responses to hUII, whereas inhibition of neuronal NOS reduced the delayed tachycardic response to hUII but did not significantly affect the vasodilatation. Only the initial tachycardic response to hUII was antagonised by propranolol. In spontaneously hypertensive rats (SHR), the initial haemodynamic responses to hUII were qualitatively similar to those in SD rats, although there was also a modest renal vasodilatation. The secondary response comprised a smaller tachycardia and a small rise in blood pressure, with no significant hindquarters vasodilatation. Haemodynamic responses to hUII were not enhanced by endothelin and angiotensin receptor antagonism in either SD rats or in SHRs. One interpretation of these results is that the primary response to bolus injection of hUII is prostanoid- or prostanoid- and NO-mediated (mesenteric vasodilatation) and that this triggers secondary events, which are dependent on eNOS (hindquarters vasodilatation) and neuronal NOS (tachycardia). SN - 0007-1188 UR - https://www.unboundmedicine.com/medline/citation/15339862/Bolus_injection_of_human_UII_in_conscious_rats_evokes_a_biphasic_haemodynamic_response_ L2 - https://doi.org/10.1038/sj.bjp.0705954 DB - PRIME DP - Unbound Medicine ER -