Responses of rabbit renal artery to histamine: receptor type and temperature dependence

1980 ◽  
Vol 58 (3) ◽  
pp. 306-309 ◽  
Author(s):  
D. A. Cook ◽  
D. M. Iwanow

The effects of histamine on spiral strips of rabbit renal artery have been recorded. Histamine causes dose-dependent contractions of this preparation which are not antagonized by the H2 receptor blocking agent metiamide, but which are blocked by the H1 antagonist diphenhydramine. The p42 for the latter agent is similar to that observed at 37 °C in intestinal smooth muscle. No evidence of a relaxant population of H2 receptors was encountered.Unlike that of intestinal smooth muscle, the response of strips of renal artery becomes progressively diminished at temperatures below about 20 °C, and the effect of reduced temperature on receptor subtype is thus more difficult to assess. It appears, however, that there is no change in type from the H1 receptor observed at 37 °C and thus the temperature-dependent transformation which has been reported previously does not occur in all H1 systems.

1986 ◽  
Vol 251 (1) ◽  
pp. G25-G33
Author(s):  
P. R. Kvietys ◽  
J. A. Barrowman ◽  
S. L. Harper ◽  
D. N. Granger

Blood flow, arteriovenous O2 difference, and lumen pressure were measured in isolated loops of canine ileum. Ileal pressure was increased by an intra-arterial infusion of either Met-enkephalin or acetylcholine. Pressures were quantitated using a motility index (MI = mean of the pressure peaks divided by number of contractions per minute). Both Met-enkephalin and acetylcholine increased MI in a dose-dependent fashion. The highest MI achieved with acetylcholine was 37.9 mmHg, while Met-enkephalin produced a maximal MI of 8.1 mmHg. Ileal oxygen uptake increased when MI reached values greater than 6. There was a direct linear relationship between oxygen uptake and MI. Distension of the lumen in the absence of motility resulted in a decrease in oxygen uptake when lumen pressure reached 15–20 mmHg. The results of these studies indicate that contractions of intestinal smooth muscle can increase intestinal oxygen uptake and may contribute to the overall oxygen demands of the gut under conditions of fasting and feeding. Furthermore, large (greater than 20 mmHg) increments in lumen pressure during enhanced motility may compromise intestinal oxygenation.


1992 ◽  
Vol 70 (12) ◽  
pp. 1571-1575 ◽  
Author(s):  
L. W. Kline ◽  
P. K. T. Pang

Calcitonin gene related peptide has been shown to relax vascular and intestinal smooth muscle. This study examines the effects of calcitonin gene related peptide on cholecystokinin-induced contraction of guinea pig gallbladder strips in vitro. Calcitonin gene related peptide was found to cause a dose-dependent relaxation of cholecystokinin-induced tension, which was blocked by the calcitonin gene related peptide receptor antagonist human calcitonin gene related peptide8–37. Previous studies demonstrated that calcitonin gene related peptide acted directly on guinea pig gallbladder smooth muscle to inhibit acetylcholine- or KCl-induced contraction. The present results further confirm that calcitonin gene related peptide acts directly on the smooth muscle. In addition, the use of L-NG-nitroarginine methyl ester, glibenclamide, and other agents strongly suggests that calcitonin gene related peptide also acts by way of the nonadrenergic noncholinergic nervous system, to induce the relaxation of cholecystokinin-induced contraction observed in the guinea pig gallbladder strips.Key words: calcitonin gene related peptide, gallbladder, cholecystokinin.


1984 ◽  
Vol 57 (5) ◽  
pp. 1551-1557 ◽  
Author(s):  
D. T. Tanaka ◽  
M. M. Grunstein

The contractile effects of substance P (SP) were studied in isolated rabbit tracheal smooth muscle (TSM) segments in vitro. Noncumulative administration of SP produced dose-dependent increases in TSM tension. The mean (+/- SE) peak isometric tension (Tmax) with SP was 35.7 (+/- 6.2%) of the corresponding Tmax response to methacholine. The dose of agonist producing 50% of Tmax (ED50) was significantly lower for SP, averaging 1.8 (+/- 0.4) X 10(-7) M, vs. 1.7 (+/- 0.32) X 10(-6) M for methacholine. Blockade of both parasympathetic ganglia with hexamethonium (10(-4) M) and neural transmission with tetrodotoxin (1 microgram/ml) had no effect on the TSM response to SP. On the other hand, TSM contraction to an ED50 dose of SP was 1) augmented by a mean (+/- SE) of 470 (+/- 110%) following pretreatment with the cholinesterase inhibitor, neostigmine (10(-6) M);2) inhibited by a mean (+/- SE) of 35 (+/- 15%) with the cholinergic antagonist, atropine (10(-4) M); and 3) also inhibited by a mean (+/- SE) of 45 (+/- 11%) following inhibition of acetylcholine synthesis with hemicholinium-3 (10(-4) M). Antagonists to 5-hydroxytryptamine, alpha 1-adrenergic, and histamine receptor binding had no effect on TSM contraction with SP. In contrast, the SP antagonist, D-Pro2,D-Trp7,9-SP, markedly inhibited TSM contraction to SP. Our findings indicate that rabbit TSM is sensitive to SP and its contraction is in part mediated by a peripheral cholinergic action, likely involving the accelerated release of acetylcholine at the airway neuromuscular junction.


1994 ◽  
Vol 28 (6) ◽  
pp. 726-729 ◽  
Author(s):  
Thomas G. Burnakis

OBJECTIVE: To report two cases in which patients were reputed to have exhibited thrombocytopenia secondary to the histamine-receptor blocking agent ranitidine. Evaluation and the associated time frame of events failed to confirm these observations. DESIGN: Two case studies. RESULTS: Ranitidine was ordered as part of the therapeutic course of two patients admitted to the medicine service. The development of thrombocytopenia in both patients was attributed to this agent and it was discontinued. In addition to ranitidine, both patients received several other agents with greater potential to cause thrombocytopenia, and had a time course of development of the adverse effect that would not support ranitidine as the offending agent. Both patients required histamine-receptor antagonists at some point following their discontinuation and, based on the available evidence, the pharmacy suggested that these agents be restarted. In neither case did restarting the histamine-receptor antagonist lead to recurrence of thrombocytopenia. CONCLUSIONS: Although ranitidine can cause thrombocytopenia, the reported incidence is very low. Spontaneous reporting of adverse effects is essential in establishing a true pattern of safety for a drug. However, reports need to be scrutinized before they are rolled into the collective intelligence. Overzealous or incomplete reporting will lead to cautions that are either unnecessary or, because they deny people necessary treatment, dangerous.


2001 ◽  
Vol 120 (5) ◽  
pp. A534-A534
Author(s):  
A ZHAO ◽  
D MULLOY ◽  
J URBANJR ◽  
W GAUSE ◽  
T SHEADONOHUE

Sign in / Sign up

Export Citation Format

Share Document