Heterogeneity of alpha-Adrenergic Responsiveness in Vascular Smooth Muscle: Role of Receptor Subtypes and Receptor Reserve

Flavahan, Nicholas A.; Vanhoutte, P. M.

doi:10.1007/978-1-4612-4582-7_9

Cited by 7 publications

(9 citation statements)

References 99 publications

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“…Partial activation of this influx by 012 occupation potentiates additional stretch-induced activation and confers strong sensitivity to inhibition by decreases in smooth muscle stretch. In contrast, evidence suggests that cii-tone is dependent on different calcium mobilizing mechanisms from ct2, in cluding mobilization of the phosphoinositide-sensitive calcium pool [2,28]. These coupling mechanisms may be less sensitive to modulation by myogenic stimuli that preferentially activate different calcium regulatory mech anisms [29][30][31].…”

Section: Discussionmentioning

confidence: 99%

“…A sec ond goal was to determine a-adrcnoccptor sensitivity of the isolated vessels for comparison with sensitivity deter mined previously under in vivo conditions. This was required for the myogenic studies and was also motivated by the suggestion that in vitro isolation might interfere with a2-adrenergic constriction [2],…”

Section: Introductionmentioning

confidence: 99%

“…Al though there are exceptions, in many tissues, adrenergic constriction of large conduit arteries utilizes a r adrenoceptors [1,2], while resistance vessels (small arteries and large arterioles) depend on both adrenoceptor types, and small terminal arterioles (precapillary sphincters) may rely predominantly on ay-adrenoceptors [3,4]. Myogenic responsiveness, i.e.…”

Section: Introductionmentioning

confidence: 99%

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In vitro Analysis of Alpha-Adrenoceptor Interactions with the Myogenic Response in Resistance Vessels

Ikeoka

Nishigaki²,

Ohyanagi³

et al. 1992

J Vasc Res

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The interaction of alpha 1- and alpha 2-adrenoceptor constriction of isolated rat cremaster small arteries (mean diameter +/- SEM, 114 +/- 5 microns) with the myogenic mechanism was examined with in vitro videomicroscopy. Microdissected vessels were double-cannulated with glass micropipets in a tissue bath, and intraluminal pressure was set at 65 mm Hg baseline pressure. Norepinephrine (NE) concentration-response curves were obtained alone and in the presence of prazosin or rauwolscine to establish the concentration of NE required to selectively stimulate alpha 1- or alpha 2-adrenoceptors. A bimodal response was produced by NE alone, indicating interaction with more than one receptor population. Rauwolscine and prazosin each produced dextral displacement at low (< 0.1 microM) NE concentrations. However, while prazosin exhibited competitive antagonism, rauwolscine did not antagonize NE at concentrations > or = EC50 value. Thus, both alpha 1- and alpha 2-adrenoceptors mediate constriction at low NE concentrations, but only alpha 1-receptors contributed to constriction at intermediate and high concentrations. These data are in contrast to previous findings for the same vessels studied in vivo. Diameter responses to increases and decreases in transmural pressure from baseline were examined in the relaxed (passive) state with nitroprusside present, during spontaneous intrinsic tone, and during induced alpha 1- or alpha 2-tone (EC20 concentration of NE plus rauwolscine or prazosin). Myogenic constriction during increases in lumen pressure and myogenic inhibition of tone during decreases in pressure were greatest during alpha 2-tone, less during intrinsic tone and least during alpha 1-tone.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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In vitro Analysis of Alpha-Adrenoceptor Interactions with the Myogenic Response in Resistance Vessels

Ikeoka

Nishigaki²,

Ohyanagi³

et al. 1992

J Vasc Res

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“…Catecholaminergic constriction is mediated by al-receptors for most large arteries and by both a1-and a2-receptors for resistance vessels, muscular venules, and veins. [36][37][38] We have found that constriction mediated by these two adrenoceptor populations exhibits very different sensitivities to modulation by humoral,3940 local metabolic,4' and myogenic38 regulation. This has led us to hypothesize that a differential distribution of a-adrenoceptor types and susceptibility to modulation among functionally distinct vascular segments may be important in determining the site of interaction of neural with humoral and local control mechanisms.…”

mentioning

confidence: 99%

Interaction between microvascular alpha 1- and alpha 2-adrenoceptors and endothelium-derived relaxing factor.

Ohyanagi

Nishigaki

Faber

1992

Circulation Research

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Intravital microscopy was used to study the effect of endothelium-derived relaxing factor (EDRF) on microvascular adrenoceptor sensitivity in rat cremaster skeletal muscle. NG-Monomethyl L-arginine (L-NMMA, 1-300 ,uM), an inhibitor of EDRF formation, produced concentration-dependent constriction of arterioles and venules. When an intermediate amount of a-l versus a2-adrenoceptor tone was first produced with bath-added norepinephrine (NE) in the presence of rauwolscine or prazosin, L-NMMA caused constriction with greater potency and efficacy during aY2 than during crl tone. During localized arl or aY2 constriction along an arteriole by perivascular micropipette suffusion of NE in the presence of rauwolscine or prazosin, again, bath-added L-NMMA produced constriction with greater potency during a2 than during arl constriction. Like L-NMMA, disruption of EDRF release by microembolization caused baseline arteriole constriction and selectively increased aY2 sensitivity 75-fold. Although these findings support the hypothesis that endothelial cells possess ar2-adrenoceptors that promote EDRF release, a greater susceptibility of a2 than arl constriction to EDRF inhibition could also account for the results. In support of this latter possibility, a2 constriction was approximately 50-fold more susceptible than al constriction to inhibition by the EDRF-like nitrodilator nitroprusside. The similarity in magnitude of this difference in sensitivity with the difference obtained in the embolization experiments does not support the hypothesis that microvascular endothelial cells in skeletal muscle possess EDRF-promoting av2-adrenoceptors. However, these data do suggest that endogenous EDRF release modulates basal arteriole and venule tone and that aY2-adrenoceptor constriction is more sensitive than a, constriction to inhibition by EDRF. (Circulation Research 1992;71:188-200) KEY WoRDs * endothelium-derived relaxing factor * a-adrenergic receptors * arterioles venules * NG_monomethyl L-arginine * endothelial cells * microcirculation Since the discovery1 that acetylcholine (ACh) can stimulate endothelial cells to release a potent vasodilator substance-endothelium-derived relaxing factor (EDRF) -that is nitric oxide or a nitric oxide adduct,23 much has been learned about its synthesis, metabolism, release, and mode of relaxant action on vascular smooth muscle.45 On the other hand, the significance of EDRF in vascular regulation is not as well understood. The dilator properties of a number of vasoactive substances, e.g., ACh, bradykinin, and histamine, are mediated partly or entirely by EDRF.5 Also, flow-mediated dilation appears to involve a shearstress-induced increase in EDRF release.67 In certain8,9 but not all10-12 vessels, myogenic constriction may be mediated in part by endothelial cell vasoactive factors including EDRF. Inhibition of EDRF synthesis by substituted L-arginine compounds that serve as substrate inhibitors of EDRF synthetase13 produces increases in blood pressure and vascular resistance in

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“…Data from this study demonstrate that there exists both a 1 -and a 2 -adrenoceptor-like activity in the mesenSince b-adrenergic blockade may enhance a-adrener-are typically found in association with cutaneous arteries and/or on the venous side of the circulation [23]. Nonetheless, their presence was confirmed by the observation that the dramatic vasoconstrictor response to the selective a 2 -adrenoceptor agonist BHT-933 [24] was blunted by yohimbine, a known a 2 -adrenoceptor blocking agent [21,24].…”

Section: Fig 4 (A) Effect Of Intravenous Prazosin (Prz) and (B) Yohim-mentioning

confidence: 93%

Effect of Maturation on α-Adrenoceptor Activity in Newborn Piglet Mesentery

Hoang

Choe

Lippton

et al. 1996

Journal of Surgical Research

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Heterogeneity of alpha-Adrenergic Responsiveness in Vascular Smooth Muscle: Role of Receptor Subtypes and Receptor Reserve

Cited by 7 publications

References 99 publications

In vitro Analysis of Alpha-Adrenoceptor Interactions with the Myogenic Response in Resistance Vessels

In vitro Analysis of Alpha-Adrenoceptor Interactions with the Myogenic Response in Resistance Vessels

Interaction between microvascular alpha 1- and alpha 2-adrenoceptors and endothelium-derived relaxing factor.

Effect of Maturation on α-Adrenoceptor Activity in Newborn Piglet Mesentery

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