The effects of salt-induced hypertension on alpha1-adrenoreceptor expression and cardiovascular physiology in the rainbow trout (Oncorhynchus mykiss).
Experiments were conducted on rainbow trout to determine the impact of dietary salt on arterial blood pressure. After 4-6 wk, fish fed a salt-enriched diet exhibited a 37% elevation of dorsal aortic pressure (from 23.8 +/- 1.2 to 32.6 +/- 1.4 mmHg) and an 18% increase in ventral aortic pressure (from 33.0 +/- 1.5 to 38.9 +/- 1.3 mmHg). The hypertension presumably reflected the increase in cardiac output (from 31.0 +/- 0.8 to 36.4 +/- 2.2 ml.min(-1).kg(-1)) because systemic and branchial resistances were statistically unaltered by salt feeding. The chronic hypertension was associated with a decrease in the pressor responses of the systemic vasculature to catecholamines and hypercapnia in the salt-fed fish. The reduction in alpha-adrenergic responsiveness of the systemic vasculature is consistent with desensitization or loss of functional alpha-adrenoceptors (alpha-ARs). In support of this idea, the salt-fed fish exhibited significantly decreased levels of alpha(1D)-AR mRNA in the dorsal aorta and the afferent (ABA) and efferent branchial arteries (EBA). In contrast, however, the results obtained from norepinephrine dose-response curves for EBA and ABA vascular rings in vitro did not provide evidence for loss of function of branchial artery alpha(1)-ARs in the salt-fed fish. Indeed, the EC(50) for the EBA norepinephrine dose-response curve was significantly reduced (from 3.75 x 10(-7) to 2.12 x 10(-7) M) in the salt-fed fish, indicating an increase in the binding affinity of the alpha(1)-ARs.
Chen
Xi
X
Department of Biology, University of Ottawa, 10 Marie Curie, Ottawa, Ontario, Canada.
Moon
Thomas W
TW
Olson
Kenneth R
KR
Dombkowski
Ryan A
RA
Perry
Steve F
SF
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D001158:Arteries / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects; D002320:Cardiovascular Physiological Phenomena / Q000187:drug effects*; D002395:Catecholamines / Q000097:blood / Q000494:pharmacology; D002712:Chlorides / Q000097:blood; D004305:Dose-Response Relationship, Drug; D006973:Hypertension / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology*; D066298:In Vitro Techniques; D017686:Oncorhynchus mykiss / Q000502:physiology*; D011224:Prazosin / Q000494:pharmacology; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D018340:Receptors, Adrenergic, alpha-1 / Q000096:biosynthesis*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012964:Sodium / Q000097:blood; D012965:Sodium Chloride; D017673:Sodium Chloride, Dietary / Q000494:pharmacology
D000317:Adrenergic alpha-Antagonists; D002395:Catecholamines; D002712:Chlorides; D012333:RNA, Messenger; D018340:Receptors, Adrenergic, alpha-1; D017673:Sodium Chloride, Dietary; D012965:Sodium Chloride; D012964:Sodium; D011224:Prazosin