β-Adrenergic Activation of the Renin-Angiotensin System Following α2-, α1-, or Nonselective α-Blockade in Conscious Dogs

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Abstract
The role of the renin-angiotensin system following .alpha.2-, .alpha.1- or nonselective .alpha.-blockade in an intact organism in which both postsynaptic .alpha.-adrenoceptor types contribute to adrenergic vasoconstriction was investigated. In conscious dogs, .alpha.2-blockade (0.3 mg/kg rauwolscine, n = 10) increased mean arterial pressure by 40 mm Hg, while hypotension by 8 mm Hg occurred following nonselective .alpha.-blockade (1.5 mg/kg phentolamine, n = 9) and by 20 mm Hg following .alpha.1-blockade (1.2 mg/kg prazosin, n = 10). Plasma angiotensin II (pg/ml) rose by 103 .+-. 28 AEM [standard error of the mean], 143 .+-. 48, and 58 .+-. 15 following .alpha.2-nonselective .alpha.-, or .alpha.1-blockade, respectivley. While .alpha.2- or nonselective .alpha.-blockade induced tachycardia and substantial elevations of plasma catecholamines, .alpha.1-blockade did not. .beta.-Blockade (2 mg/kg nadolol) attenuated the elevations of angiotensin following .alpha.2- or nonselective .alpha.-blockade by 100 and 88%, respectively, without affecting the .alpha.1-blockade-induced elevation, which is mainly mediated by the hypotension. Pretreatment with 3 mg/kg captopril reduced the pressure increase induced by .alpha.2-blockade from 40 to 13 .+-. 10 mm Hg and aggravated the decline in blood pressure induced by nonselective .alpha.-blockade from 8 to > 50 mm Hg. In anesthetized, spinalized dogs, both types of .alpha.-blockade copetitively antagonized the pressor effect of the .alpha.2-agonist azepexole by the same degree. In the intact animal, the central and peripheral presynaptic augmentation of sympathoexcitation induced by .alpha.2- or nonselective .alpha.-blockade evidently leads to a strong .beta.-adrenergic activation of the renin-angiotensin system, independent of the concomitant changes in blood pressure. The constrictive action of the activation contributes substantially to the compensation of the vascular adrenoceptor blockade induced by nonselective or .alpha.2-selective blockade in the intact organism.

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