title: Differentiated response of the sympathetic nervous system to angiotensin-converting enzyme inhibition in hypertension.
abstract: Hypertension with renal artery stenosis is associated with both an activated renin-angiotensin system and elevated sympathetic activity. Therefore, in this condition it may be favorable to use a therapeutic modality that does not reflexly increase heart rate, renin secretion, and sympathetic nervous activity. The purpose of the present study was to assess overall, renal, and muscle sympathetic activity after short-term administration of an angiotensin-converting enzyme inhibitor (enalaprilat) and a nonspecific vasodilator (dihydralazine) to hypertensive patients with renal artery stenosis. Forty-eight patients undergoing a clinical investigation for renovascular hypertension were included in the study. An isotope dilution technique for assessing norepinephrine spillover was used to estimate overall and bilateral renal sympathetic nerve activity. In 11 patients simultaneous intraneural recordings of efferent muscle sympathetic nerve activity were performed. Thirty minutes after dihydralazine administration, mean arterial pressure fell by 15%, whereas plasma angiotensin II, muscle sympathetic nerve activity, heart rate, and total body norepinephrine spillover increased (P<0.05 for all). In contrast, after enalaprilat administration a fall in arterial pressure similar to that for dihydralazine was followed by decreased angiotensin II levels and unchanged muscle sympathetic nerve activity, heart rate, and total body norepinephrine spillover, whereas renal norepinephrine spillover increased by 44% (P<0.05). Acute blood pressure reduction by an angiotensin-converting enzyme inhibitor provokes a differentiated sympathetic response in patients with hypertension and renal artery stenosis, inasmuch that overall and muscle sympathetic reflex activation are blunted, whereas the reflex renal sympathetic response to blood pressure reduction is preserved.
authors.affiliation: Department of Clinical Physiology, Göteborg University, Sahlgrenska University Hospital, Göteborg, Sweden.
authors.forename: M
authors.initials: M
authors.lastname: Johansson
authors.forename: M
authors.initials: M
authors.lastname: Elam
authors.forename: B
authors.initials: B
authors.lastname: Rundqvist
authors.forename: G
authors.initials: G
authors.lastname: Eisenhofer
authors.forename: H
authors.initials: H
authors.lastname: Herlitz
authors.forename: G
authors.initials: G
authors.lastname: Jensen
authors.forename: P
authors.initials: P
authors.lastname: Friberg
mesh_terms: D000804:Angiotensin II / Q000097:blood; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage*; D001794:Blood Pressure / Q000187:drug effects; D004078:Dihydralazine / Q000008:administration & dosage*; D004594:Electrophysiology; D015773:Enalaprilat / Q000008:administration & dosage*; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D006978:Hypertension, Renovascular / Q000188:drug therapy* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000294:innervation; D009638:Norepinephrine / Q000378:metabolism; D010543:Peroneal Nerve; D012078:Renal Artery Obstruction / Q000150:complications / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000378:metabolism
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000804:Angiotensin II; D015773:Enalaprilat; D004078:Dihydralazine; D009638:Norepinephrine