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Diseases of the cardiovascular system.
Serum vasoconstrictor, serotonin; isolation and characterization.
Baroceptor Function in Chronic Renal Hypertension
TLDR
The results of these experiments indicate that the carotid and aortic baroceptor mechanisms are reset to the hypertensive pressure levels of animals with chronic perinephritic hypertension and are, presumably, an important component in the mechanism of chronic renal hypertension.
Increased Cardiac Output as a Contributory Factor in Experimental Renal Hypertension in Dogs
TLDR
Increased cardiac output probably has a contributory role in the development of renal hypertension, and absence of change in plasma volume and increase in mean circulatory pressure measured in a separate series of 7 dogs suggest that the initial increase in cardiac output preceding rise in pressure was due to enhanced venous return consequent to constriction of capacitance vessels.
A CRYSTALLINE PRESSOR SUBSTANCE (ANGIOTONIN) RESULTING FROM THE REACTION BETWEEN RENIN AND RENIN-ACTIVATOR
TLDR
Renin reacts with renin-activator to form a strong pressor substance which is heat-stable, water- and alcohol-soluble, fluorescent, acid- stable, and alkali-labile, and it is suggested that this substance be called angiotonin.
Atherosclerosis and the Fat Content of the Diet
A report to the American Heart Association and to the American Society for the Study of Arteriosclerosis the Nutrition Committee of the Council on Community Service and Education of the American
Cardiovascular Actions of Sodium Nitroprusside in Animals and Hypertensive Patients
TLDR
Sodium nitroprusside is a powerful hypotensive agent when given intravenously tohypertensive patients, but is no more effective than the sodium thiocyanate into which it is converted when given by mouth.
Arterial Hypertension Elicited by Subpressor Amounts of Angiotensin
TLDR
This indirect action of angiotensin to increase total peripheral resistance and arterial pressure by an action on the sympathetic nervous system, along with an upward resetting of the carotid sinus buffering mechanism, might logically account for the neural component of chronic renal hypertension.
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