Simultaneous perfusion of rat isolated superior mesenteric arterial and venous beds: comparison of their vasoconstrictor and vasodilator responses to agonists
- PMID: 2328405
- PMCID: PMC1917370
- DOI: 10.1111/j.1476-5381.1990.tb14720.x
Simultaneous perfusion of rat isolated superior mesenteric arterial and venous beds: comparison of their vasoconstrictor and vasodilator responses to agonists
Abstract
1. A new isolated perfused preparation is described that allows a direct comparison to be made of the responses of the perfused arterial and retrogradely perfused venous circulations of the rat superior mesenteric vascular bed. 2. In experiments comparing the responses of the intact arterially perfused mesentery and small intestine to those of the same preparation following removal of the intestine and division of the circulations, the increases in perfusion pressure produced by arginine-vasopressin (30 pmol) and noradrenaline (1 nmol) were retained by the arterial circulation and those induced by angiotensin II (30 pmol) by the venous circulation. Endothelin-1 (30 pmol) constricted both portions of the vasculature but the prolonged nature of its response was associated with only the venous vessels. 3. In the simultaneously perfused arterial and venous preparation arginine vasopressin (3-100 pmol) was a selective constrictor of the arterial circulation and angiotensin II (3-100 pmol) of the venous circulation. In addition, noradrenaline (0.3-10 nmol), 5-hydroxytryptamine (0.3-10 nmol) and KCl (1-60 micromol) were more active as constrictors of the arterial than the venous vessels, and U46619 (10-300 pmol) a more active constrictor of the venous than the arterial vessels. Endothelin-1 (3-100 pmol) constricted both the arterial and venous portions of the vasculature but was significantly longer acting as a venoconstrictor than an arterioconstrictor. 4. Angiotensin I (300 pmol) caused constrictions of the venous circulation which were dependent upon the presence of angiotensin converting enzyme for captopril (10 microM) abolished constrictions caused by angiotensin I but not by angiotensin II. 5. In preparations preconstricted by U46619 (0.3-3 microM), acetylcholine (0.01-100 nmol), bradykinin (0.001-nmol), sodium nitroprusside (0.01-lOnmol) or isoprenaline (1-l00pmol) produced dose-related dilatations of both the arterial and the venous vasculatures, whereas adenosine diphosphate (ADP, 0.01-lOOnmol) caused dose-dependent dilatations of the arterial circulation but principally constrictions of the venous circulation. The dilatations caused by acetylcholine and bradykinin in both portions of the circulation, and by ADP in the arterial circulation, were endothelium-dependent as they were inhibited by gossypol (3 microM), whereas dilatations to sodium nitroprusside were not. 6. This preparation allows the responses of the arteries and veins of a single perfused mesenteric bed to be compared. In addition, with this preparation it is possible to demonstrate that veins, as well as arteries, show significant endothelium-dependent relaxations. It is concluded that the venous portion of the vasculature is significantly involved in the responses of the intact circulation.
Similar articles
-
Characterization of receptors for endothelins in the perfused arterial and venous mesenteric vasculatures of the rat.Br J Pharmacol. 1993 Oct;110(2):687-92. doi: 10.1111/j.1476-5381.1993.tb13866.x. Br J Pharmacol. 1993. PMID: 8242241 Free PMC article.
-
Characterization of receptors for kinins and neurokinins in the arterial and venous mesenteric vasculatures of the guinea-pig.Br J Pharmacol. 1995 Aug;115(7):1319-25. doi: 10.1111/j.1476-5381.1995.tb15043.x. Br J Pharmacol. 1995. PMID: 7582563 Free PMC article.
-
Endothelium-dependent vascular activities of endothelin-like peptides in the isolated superior mesenteric arterial bed of the rat.Br J Pharmacol. 1990 Sep;101(1):81-8. doi: 10.1111/j.1476-5381.1990.tb12093.x. Br J Pharmacol. 1990. PMID: 2282471 Free PMC article.
-
[Mechanisms underlying enhanced vasodilator responses to various vasodilator agents following endothelium removal in rat mesenteric resistance arteries].Yakugaku Zasshi. 2007 Apr;127(4):729-33. doi: 10.1248/yakushi.127.729. Yakugaku Zasshi. 2007. PMID: 17409704 Review. Japanese.
-
Inhibition of vasoconstrictor and vasodilator responses by PGE1 in the intestinal vascular bed of the cat.Prostaglandins Med. 1981 Dec;7(6):537-52. doi: 10.1016/0161-4630(81)90044-6. Prostaglandins Med. 1981. PMID: 6798592 Review.
Cited by
-
Effects of endothelin-1 on vascular permeability in the conscious rat: interactions with platelet-activating factor.Br J Pharmacol. 1991 Dec;104(4):797-804. doi: 10.1111/j.1476-5381.1991.tb12509.x. Br J Pharmacol. 1991. PMID: 1667286 Free PMC article.
-
Acute pro-inflammatory actions of endothelin-1 in the guinea-pig lung: involvement of ETA and ETB receptors.Br J Pharmacol. 1995 May;115(2):227-36. doi: 10.1111/j.1476-5381.1995.tb15868.x. Br J Pharmacol. 1995. PMID: 7670725 Free PMC article.
-
Characterization of receptors for endothelins in the perfused arterial and venous mesenteric vasculatures of the rat.Br J Pharmacol. 1993 Oct;110(2):687-92. doi: 10.1111/j.1476-5381.1993.tb13866.x. Br J Pharmacol. 1993. PMID: 8242241 Free PMC article.
-
Role of R-type calcium channels in the response of the perfused arterial and venous mesenteric vasculature of the rat to platelet-activating factor.Br J Pharmacol. 1994 Aug;112(4):1202-8. doi: 10.1111/j.1476-5381.1994.tb13211.x. Br J Pharmacol. 1994. PMID: 7952882 Free PMC article.
-
Effects of the ETA/ETB receptor antagonist, bosentan on endothelin-1-induced myocardial ischaemia and oedema in the rat.Br J Pharmacol. 1995 Sep;116(2):1745-50. doi: 10.1111/j.1476-5381.1995.tb16657.x. Br J Pharmacol. 1995. PMID: 8528554 Free PMC article.
References
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources