Alpha 1- and alpha 2-adrenoreceptor relationships in SHRs during hypotension.
Previous studies have suggested that spontaneously hypertensive rats (SHRs) are less able to tolerate the cardiovascular stress of hemorrhagic hypotension than normotensive WKYs. The present studies were designed to determine whether or not this deficiency on the part of the SHRs is related to a genetically derived inappropriate balance between the alpha 1- and alpha 2-adrenoreceptors in the peripheral vasculature. To answer this question, SHRs were divided into untreated controls and experimental rats, which were pretreated with either the relatively specific alpha 1-antagonist prazosin or the alpha 2-antagonist yohimbine. In another series, the adrenal medullae were removed 2-3 days before hemorrhage. The data indicate that alpha 1-receptor blockade might offer some degree of protection to SHRs subjected to hemorrhagic hypotension, whereas inhibition of the alpha 2-adrenoreceptors proved detrimental. We conclude that the innervated alpha 1-adrenoreceptors play a more dominant role in SHR blood pressure regulation than the extrasynaptic alpha 2-adrenoreceptors but that these alpha 1-receptors are unable to maintain the compensatory vasoconstrictor response as effectively as the alpha 2-adrenoreceptors.
D000313:Adrenal Medulla / Q000502:physiology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D007022:Hypotension / Q000503:physiopathology*; D008297:Male; D011224:Prazosin / Q000494:pharmacology; D011311:Pressoreceptors / Q000503:physiopathology; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D011918:Rats, Inbred SHR / Q000502:physiology*; D011919:Rats, Inbred Strains / Q000502:physiology*; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects / Q000502:physiology*; D012771:Shock, Hemorrhagic / Q000503:physiopathology
D011942:Receptors, Adrenergic, alpha; D011433:Propranolol; D011224:Prazosin