Hypertension alters the function of nitrergic and sensory innervation in mesenteric arteries from female rats.
OBJECTIVE
To investigate whether hypertension could modify the function of adrenergic, nitrergic, and sensory innervations involved in the electrical field stimulation-induced response in mesenteric arteries from female rats.


METHODS
Vascular reactivity experiments were performed in endothelium-denuded mesenteric arteries from normotensive, Wistar-Kyoto and spontaneously hypertensive female rats; protein expression was measured by western blot; nitric oxide release was measured by fluorometry; calcitonin gene-related peptide and noradrenaline release were determined by enzyme immunoassay.


RESULTS
The electrical field stimulation-induced contractions were significantly lower in segments from spontaneously hypertensive rats than those of Wistar-Kyoto rats. Hypertension did not modify either the response or release of noradrenaline. Preincubation with the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester increased the electrical field stimulation-induced contractions only in segments from Wistar-Kyoto rats. The relaxation induced by the nitric oxide donor sodium nitroprusside was similar in segments from both strains. The electrical field stimulation-induced nitric oxide release was decreased in segments from spontaneously hypertensive rats. The calcitonin gene-related peptide receptor antagonist CGRP(8-37) did not alter the electrical field stimulation-induced contractions in segments from Wistar-Kyoto rats but increased them in segments from spontaneously hypertensive rats. The calcitonin gene-related peptide-induced relaxation was increased in segments from spontaneously hypertensive rats. The expression of the 15-kDa active form of RAMP1 was increased in segments from spontaneously hypertensive rats.


CONCLUSIONS
In contrast to male rats, electrical field stimulation-induced contractions are decreased in hypertensive female rats. Nitrergic innervation plays a role in the development and/or maintenance of hypertension, whereas sensory innervation is a counteracting mechanism through the increased calcitonin gene-related peptide response.
del Campo
Lara
L
Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma de Madrid, Madrid, Spain.
Ferrer
Mercedes
M
Balfagón
Gloria
G
D000818:Animals; D015740:Calcitonin Gene-Related Peptide / Q000502:physiology*; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D005260:Female; D006973:Hypertension / Q000503:physiopathology*; D047908:Intracellular Signaling Peptides and Proteins / Q000032:analysis; D008297:Male; D008565:Membrane Proteins / Q000032:analysis; D008638:Mesenteric Arteries / Q000294:innervation* / Q000502:physiology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology*; D009638:Norepinephrine / Q000502:physiology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D058261:Receptor Activity-Modifying Proteins; D012727:Sex Characteristics; D014661:Vasoconstriction / Q000187:drug effects
D047908:Intracellular Signaling Peptides and Proteins; D008565:Membrane Proteins; D058261:Receptor Activity-Modifying Proteins; D009569:Nitric Oxide; D015740:Calcitonin Gene-Related Peptide; D019331:NG-Nitroarginine Methyl Ester; D009638:Norepinephrine