Adrenergic vasoconstriction as a cause of inadequate hypotensive response to beta-adrenergic blockade.
This overview is concerned with the causes of nonresponsiveness to the hypotensive action of beta-adrenergic blocking drugs. The overall hemodynamic response, i.e., a secondary decrease in peripheral vascular resistance, is unrelated to the primary decrease in cardiac output. The reduction in vascular resistance may be triggered by mechanisms residing in the central nervous system, the arterial baroreceptor area, or the prejunctional beta-receptor. None of these mechanisms seem to be entirely responsible. Studies in responders vs nonresponders tend to equate nonresponsiveness with alpha-adrenoceptor-mediated vasoconstriction. Although circulating catecholamines are relatively poor indices of sympathetic activity, studies focusing on the renal-neural area appear to show clearly differential profiles between responders and nonresponders. Such findings, in relation to experimental data on the renal nerves as selective neural amplifiers, may provide a renewed interpretation of the centrally mediated hypotensive mechanism of beta-adrenergic blockade.
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects*; D002302:Cardiac Output / Q000187:drug effects; D002395:Catecholamines / Q000097:blood; D006801:Humans; D007668:Kidney / Q000098:blood supply / Q000187:drug effects*; D011311:Pressoreceptors / Q000187:drug effects; D012039:Regional Blood Flow; D012083:Renin / Q000097:blood; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects*
D000319:Adrenergic beta-Antagonists; D002395:Catecholamines; D012083:Renin