Contrasting views on the action of atrial peptides: lessons from studies of conscious animals.
In a rather short time, a consensus seems to have emerged among researchers regarding the mechanisms of the natriuretic and hypotensive actions of atrial natriuretic factor (ANF). According to the by now classic view, the natriuresis induced by ANF is mediated by changes in renal hemodynamics; vasorelaxation is proposed as the primary mechanism of its hypotensive action. Recent evidence, mostly from experiments with conscious animals, does not support this view. Results from experiments performed with chronically instrumented spontaneously hypertensive rats and normotensive (Wistar-Kyoto and Wistar) rats show that the natriuresis induced by a synthetic ANF is not accompanied by increases in glomerular filtration rate or renal blood flow. Measurement of cardiac output (CO) and blood pressure indicate that a decrease in CO, not a fall in total peripheral resistance, is the cause of the decrease in blood pressure. Based on this and other available evidence, a hypothetical scheme for the biological role of ANF is proposed.
D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D009320:Atrial Natriuretic Factor / Q000097:blood / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D005110:Extracellular Space / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects; D007678:Kidney Glomerulus / Q000187:drug effects; D051381:Rats; D012079:Renal Circulation / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
D000959:Antihypertensive Agents; D009320:Atrial Natriuretic Factor