Mechanisms Leading to Increased Vasodilator Responses to Calcitonin-Gene-Related Peptide in Mesenteric Resistance Arteries of Early Pregnant Rats

2008 ◽  
Vol 45 (4) ◽  
pp. 350-356 ◽  
Author(s):  
H.W.F. van Eijndhoven ◽  
G.M.J. Janssen ◽  
R. Aardenburg ◽  
M.E.A. Spaanderman ◽  
L.L.H. Peeters ◽  
...  
Keyword(s):  
Calcitonin Gene Related Peptide ◽  
Resistance Arteries ◽  
Pregnant Rats ◽  
Related Peptide ◽  
Calcitonin Gene

Effects of calcitonin gene-related peptide on vascular resistance in rats: role of sex steroids

1999 ◽  
Vol 276 (6) ◽  
pp. H2063-H2068 ◽  
Author(s):  
Michelle Grewal ◽  
Janis Cuevas ◽  
Gautam Chaudhuri ◽  
Lauren Nathan
Keyword(s):  
Sex Steroids ◽  
Perfusion Pressure ◽  
Pressor Response ◽  
Calcitonin Gene Related Peptide ◽  
Ovariectomized Rats ◽  
Synthesis Inhibitor ◽  
Pregnant Rats ◽  
Related Peptide ◽  
Calcitonin Gene

It has been demonstrated in reflex-intact animals that the sensitivity to calcitonin gene-related peptide (CGRP) is increased during pregnancy and that this action is mediated by sex steroids but not by nitric oxide (NO). We assessed the effects of CGRP in the following groups of anesthetized ganglion-blocked rats: 1) pregnant, 2) ovariectomized, and 3) ovariectomized and treated with estradiol and progesterone. Changes in mean arterial pressure (MAP) were assessed after the administration of varying doses of CGRP. Decreases in MAP after CGRP administration were significantly greater in pregnant rats and ovariectomized rats administered sex steroids than in ovariectomized controls. The CGRP antagonist CGRP8–37 produced a pressor response of similar magnitude in both pregnant and ovariectomized rats. We also assessed the effects of CGRP and the modulating role of NO in the isolated uterine vascular bed preparation. CGRP reduced perfusion pressure to a greater degree in ovariectomized animals treated with sex steroids than in ovariectomized animals. This response was attenuated by pretreatment with an NO synthesis inhibitor. CGRP8–37 produced a similar increase in perfusion pressure in both groups. We conclude that 1) the increased vascular sensitivity observed during pregnancy or after treatment with sex steroids is in part mediated by NO, and 2) CGRP8–37 has a vasoconstrictor action of its own.

Effect of chronic sensory denervation on Ca2+-induced relaxation of isolated mesenteric resistance arteries

1998 ◽  
Vol 274 (5) ◽  
pp. H1655-H1661 ◽  
Author(s):  
Maria M. Mupanomunda ◽  
Yanlin Wang ◽  
Richard D. Bukoski
Keyword(s):  
Calcitonin Gene Related Peptide ◽  
Relaxation Response ◽  
Resistance Arteries ◽  
Related Peptide ◽  
Density Control ◽  
Calcitonin Gene ◽  
Perivascular Nerves ◽  
Sensory Denervation ◽  
Immunocytochemical Studies ◽  
Dose Dependent

We recently reported that Ca2+-induced relaxation could be linked to a Ca2+ receptor (CaR) present in perivascular nerves. The present study assessed the effect of chronic sensory denervation on Ca2+-induced relaxation. Mesenteric resistance arteries were isolated from rats treated as neonates with capsaicin (50 mg/kg), vehicle, or saline. The effect of cumulative addition of Ca2+ was assessed in vessels precontracted with 5 μM norepinephrine. Immunocytochemical studies showed that capsaicin treatment significantly reduced the density of nerves staining positively for calcitonin gene-related peptide (CGRP) and for the CaR (CGRP density: control, 51.1 ± 3.9 μm2/mm2; capsaicin treated, 31.4 ± 2.8 μm2/mm2, P = 0.01; control CaR density, 46 ± 4 μm2/mm2, n = 7; capsaicin-treated CaR density, 24 ± 4 μm2/mm2, n = 8, P = 0.002). Dose-dependent relaxation to Ca2+ (1–5 mM) was significantly depressed in vessels from capsaicin-treated rats (overall P < 0.001, n = 6 or 7), whereas the relaxation response to acetylcholine remained intact. These data support the hypothesis that Ca2+-induced relaxation is mediated by activation of the CaR associated with capsaicin-sensitive perivascular neurons.

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