• Corpus ID: 24450689

Role of receptor reserve in the inhibition of alpha-1 adrenoceptor-mediated pressor responses by calcium antagonists in the pithed rat.

@article{Jim1986RoleOR,
  title={Role of receptor reserve in the inhibition of alpha-1 adrenoceptor-mediated pressor responses by calcium antagonists in the pithed rat.},
  author={Kam F. Jim and Richard A. Macia and William D. Matthews},
  journal={The Journal of pharmacology and experimental therapeutics},
  year={1986},
  volume={238 1},
  pages={
          89-94
        }
}
The effect of the calcium channel antagonists nifedipine and FR 34235 on the vasopressor response to alpha-1 adrenoceptor stimulation in the pithed normotensive rat was investigated. The maximal pressor response elicited by the full alpha-1 adrenoceptor agonist SK&F l-89748 was slightly but significantly reduced by 1-mg/kg doses of nifedipine (21 +/- 2%) and FR 34235 (34 +/- 4%). In comparison, the maximal pressor response to alpha-1 adrenoceptor stimulation by the partial alpha-1 agonist SK&F… 
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12 Citations

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Citation Type

Equal potency of nifedipine to inhibit α1-(dobutamine and BDF 6143) and α2-adrenoceptor (B-HT 920) induced pressor responses in pithed rats; lack of effect of phenoxybenzamine
Differential effects of calcium antagonists and Bay K 8644 on contractile responses to exogenous noradrenaline and adrenergic nerve stimulation in the rabbit ear artery
TLDR
The differential effects of the calcium antagonists on NA‐ and ENS‐induced contractions were not related to differences in α‐adrenoceptor subtype (α1/α2), receptor reserve or response amplitude, but may rather reflect temporal and spatial differences between the responses.
High alpha 1-adrenoceptor occupancy decreases relaxing potency of nifedipine by increasing myosin light chain phosphorylation.
TLDR
Results from the present study support the hypothesis that the decreased potency of Ca2+ channel blockers to produce relaxation in vascular tissues contracted at high alpha 1-adrenoceptor occupancy may be caused by activation of spare receptors and provide a cellular explanation for the phenomenon.
Decreased α1-Adrenoceptor Reserve in Arteries from Spontaneously Hypertensive Rats
TLDR
A receptor reserve for the α1-adrenoceptor-mediated contraction decreased inSHR mesenteric artery as compared with WKY, which may lead to the greater inhibitory effect of nifedipine on phenylephrine-induced contractions and may contribute to the enhancement of vasoconstrictor responsiveness in SHR.
Role of the sympathetic nervous system in blood pressure maintenance and in the antihypertensive effects of calcium antagonists in spontaneously hypertensive rats.
TLDR
Results indicate that, in conscious adult SHR, norepinephrine released by peripheral sympathetic nervous terminals and humorally borne epinephrine stimulate almost exclusively post-junctional alpha 1-adrenergic receptors.
High a1-Adrenoceptor Occupancy Decreases Relaxing Potency of Nifedipine by Increasing Myosin Light Chain Phosphorylation
TLDR
The results suggest that the unique relation between stress and myosin light chain phosphorylation may play a role in determining the sensitivity of relaxing agents.
Benextramine and nifedipine distinguish between sub-classes of α1-adrenoceptors
Hypotension induced by growth-hormone-releasing peptide is mediated by mast cell serotonin release in the rat.
Forearm vascular α1‐adrenergic blockade by verapamil
TLDR
Verapamil‐induced attenuation of forearm vasoconstriction elicited by phenylephrine indicates that, in humans, in vivo verapamIL forearm vasodilating effects are, in part, a result of α1‐adrenergic blockade.
Effect of Early Diabetes on the Expression of Alpha-1 Adrenergic Receptors in Aorta and Carotid Arteries of Wistar Kyoto and Spontaneously Hypertensive Rats
TLDR
It is suggested that early diabetes modifies the expression of alpha-1 adrenergic receptors in aorta and carotid arteries of both WKY and SHR strains in a different way.
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