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Showing papers by "Suzanne Oparil published in 1978"


Journal ArticleDOI
TL;DR: Ventricular performance and myocardial hypertrophy were studied in maturing spontaneously hypertensive and normotensive Kyoto-Wistar rats from 4 through 24 weeks of age to suggest that myocardials may be a manifestation of an underlyingMyocardial abnormality which could account for the hemodynamic alterations found in SH rats.

97 citations


Journal ArticleDOI
TL;DR: The loss of responsiveness of DOC to ACTH in the third trimester suggests that the maternal adrenals have undergone an alteration in their steroidogenic response to ACTh, but also may indicate that their output of DOC has reached a maximal rate.

85 citations


Journal ArticleDOI
TL;DR: The results support the proposition that the plasma free DOC fraction is increased because of displacement from corticosteroid-binding globulin by the ACTH-induced increment in cortisol, and could contribute to sodium retention and also would be available for hepatic metabolism.

49 citations


Journal ArticleDOI
TL;DR: The data give evidence for a direct action of AII on the juxtaglomerular cells independent of an interaction with either the sympathetic nervous system or the arteriolar baroreceptor and suggest that the intrarenal receptors that mediate AII-induced inhibition of renin release differ from AII receptors in the adrenal cortex.
Abstract: The mechanism and structural basis of the inhibition of renin release by angiotensin II (AII) were studied in rat kidney slices. Renin release was inhibited by AII and the (2–8), (3–8), (4–8), and (5–8) peptides of AII (5 X 10(-5) M). These constituent peptides of AII which share a common carboxyl terminus inhibited renin release with a sharp decrease in potency when the amino-terminal amino acid was removed. Saralasin attenuated the inhibition of renin release induced by equimolar concentrations of AII. Dose-response curves for AII and the (2–8) peptide [angiotensin III (AIII)] indicate that AII is a more potent inhibitor of renin release than is AIII. Depletion of renal norepinephrine by reserpine (10 mg/kg, i.p.) or pretreatment of slices with papaverine (1 X 10(-4) M) did not block the action of AII. The data give evidence for a direct action of AII on the juxtaglomerular cells independent of an interaction with either the sympathetic nervous system or the arteriolar baroreceptor and suggest that the ...

47 citations


Journal ArticleDOI
TL;DR: It is suggested that in this model NGFAS affects mitochondrial concentration either via its effect on arterial blood pressure and/or via some other, unidentified mechanism, and the decreased mitochondrial concentration in myocardial cells of untreated SH rats need not be causally related to the observed cardiac dysfunction.

14 citations


Journal ArticleDOI
TL;DR: Results indicate that conversion of des-Asp angiotensin I to angiotENSin III does occur in the pulmonary circulation of the dog but that hydrolysis of the des- asp peptide metabolites and tyrosine is so rapid that little circulating angiotenedin II and only a small pressor response appear.

13 citations