Detail of "5979-11-3"

Reference

Modification by capsaicin and compound 48/80 of dye leakage induced by irritants in the rat

Modification by capsaicin and compound 48/80 of dye leakage induced by irritants in the rat. Arvier, P. T.; Chahl, Loris A.; Ladd, R. J. (Dep. Physiol., Univ. Queensland, St. Lucia, Aust.). Br. J. Pharmacol., 59(1), 61-8 (English) 1977. CODEN: BJPCBM. DOCUMENT TYPE: Journal CA Section: 3 (Biochemical Interactions) In rats pretreated with capsaicin [404-86-4] (50 mg, s.c., over 4 days), Evans blue dye leakage induced by intracutaneous (i.c.) injection of capsaicin (5 .times. 10-5-4 .times. 10-4M), formalin [50-00-0] (0.036-0.3M), HCl (7.5 .times. 10-4-6 .times. 10-3M), KCl (0.013-0.1M), PGE1 [745-65-3] (7.25 .times. 10-7-6 .times. 10-6M), bradykinin triacetate [5979-11-3] (1.25 .times. 10-6-10-5M), and bradykinin with PGE1 (10-6M) was greatly reduced. Dye leakage induced by i.c. injection of histamine diphosphate [51-74-1] (5 .times. 10-5-4 .times. 10-4M) and 5-hydroxytryptamine creatinine sulfate [971-74-4] (6.25 .times. 10-7-5 .times. 10-6M) was slightly reduced by capsaicin pretreatment whereas dye leakage induced by ATP [56-65-5] (5 .times. 10-4-4 .times. 10-3M) and 48/80 (0.25-2.0 .mu.g/mL) was unaffected. Pretreatment with i.c. injections of 48/80 (0.5 .mu.g, 24 and 48 h previously) reduced the responses to ATP, 48/80, HCl, KCl, PGE1, and bradykinin but did not affect those to histamine, 5-hydroxtryptamine or bradykinin with PGE1. Thus prodn. of neurogenic edema involves both sensory nerves and most cells.

Studies of the hemopoietic microenvironment

Studies of the hemopoietic microenvironment. VI. Regulatory mechanisms in the splenic microvascular system of mice. Reilly, Frank D.; McCuskey, Robert S. (Coll. Med., Univ. Cincinnati, Cincinnati, Ohio, USA). Microvasc. Res., 13(1), 79-90 (English) 1977. CODEN: MIVRA6. DOCUMENT TYPE: Journal CA Section: 2 (Hormone Pharmacology) Various concns. of several vasoactive substances alone or in combination with appropriate blocking agents were administered topically to the spleens of anesthetized mice while changes in the microvasculature were measured using in vivo microscopic methods. The results suggested the presence of both .alpha.- and .beta.-adrenergic receptors were sparse or absent throughout the microvasculature. Histamine (I) [51-45-6] elicted arteriolar dilation which was antagonized by metiamide, suggesting the presence of H2 receptors in these vessels. Serotonin oxalate [3036-16-6] elicited only venular constriction. Lactic acid [50-21-5] caused arteriolar constriction; bradykinin triacetate [5979-11-3] and PGE2 [363-24-6] and PGF2.alpha. [551-11-1] elicited arteriolar constriction, but only at high concns. The microvascular response to lactic acid, PGE2, and PGF2.alpha. was partially or completely antagonized by blockade of .alpha. receptors. I, bradykinin, serotonin, PGE2, and PGF2.alpha. caused a redn. in blood flow through the red pulp. Although adenine nucleotides, guanosine, inosine, Na phosphate, and KCl elicited no response, adenosine (II) [58-61-7] was a potent vasodilator. The dilation was not blocked by adrenergic or cholinergic antagonists. Of the substances studied, only I, isoproterenol-HCl [51-30-9], and II induced arteriolar dilation. Of these, only isoproterenol and II increased the linear velocity of blood flow and the no. of vessels with flow in them. Since no known .beta. agonist occurs naturally in the spleen and II was the most potent arteriolar dilator in physiol. doses, II is suggested as candidate for the functional hyperemia reported in the erythropoietically stimulated murine spleen.