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Differential Effect of Slow‐Pressor Angiotensin II on Contractile Responses to Norepinephrine in Arteries with and without Sympathetic Innervation
Author(s) -
Kopf Phillip G,
Johnson Alan Kim,
Phelps Laura E,
Schupbach Chad D,
Peuler Jacob D
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.1011.2
Subject(s) - angiotensin ii , norepinephrine , medicine , endocrinology , mesenteric arteries , artery , renin–angiotensin system , aorta , vascular resistance , angiotensin iii , blood vessel , sympathetic nervous system , vascular smooth muscle , angiotensin receptor , receptor , hemodynamics , blood pressure , dopamine , smooth muscle
There is evidence that chronically elevated circulating angiotensin II alters the function of the systemic vasculature. In the present study we examined the effect of two weeks of in vivo infusion of a slow‐pressor dose of angiotensin II on vascular responsiveness to exogenous angiotensin II and norepinephrine applied in vitro . As target vessels, we chose to isolate 1) the thoracic aorta, which in the rat is essentially free of sympathetic innervation, 2) a third order mesenteric resistance artery, which like all resistance vessels is densely innervated, and 3) the most proximal portion of the caudal artery, which is densely innervated, but functions in a thermo‐regulatory mode rather than as a resistance vessel. At the completion of the infusion there were no changes in contractile responses to angiotensin II itself in any of the three arterial tissue preparations (intact rings). However, we found that contractile responses to norepinephrine were significantly increased in aortic, but not in mesenteric or caudal arterial rings. For aorta, these increases were accompanied by a significant decrease in the half‐maximally effective concentration of norepinephrine from 48 ± 5 to 31 ± 5 nanomolar in vehicle versus angiotensin II treated rats (n =10 each). Therefore, we propose that long‐term systemic administration of a slow‐pressor dose of angiotensin II can potentially increase expression of alpha‐adrenergic receptors in arterial smooth muscle to increase responsiveness to norepinephrine. However, because it is likely that angiotensin II is acting through central mechanisms to increase arterial vascular sympathetic nerve activity, increased receptor expression may be prevented in densely innervated arterial vessels. Accordingly, our results suggest that angiotensin II‐induced hypertension, at least up to 2 weeks, may not involve increased responsiveness of resistance vessels to either angiotensin II itself or sympathetic nerve activity. Support or Funding Information University of Iowa and Midwestern University